Cov txiaj ntsig thiab cov txheej txheem ntawm Polysaccharides Los ntawm Tuam Tshoj Medicinal Herbs Rau Kev Kho Mob Osteoporosis
Mar 25, 2022
Hu rau: Audrey Hu Whatsapp / hp: 0086 13880143964 Email:audrey.hu@wecistanche.com
Shan shan Lei a, 1, Jie Su d, 1, Yang Zhang, 1, Xiao wen Huang a, Xu ping Wang a, Min Cong Huang b,*, Bo Li c,*, Dan Shou a, d,**
a * Department of Medicine, Zhejiang Academy ntawm Tsob Ntoo Suav Tshuaj, Hangzhou, Zhejiang 310007, PR Tuam Tshoj
b * Chaw soj ntsuam kev nyab xeeb, Hangzhou Medical College, Hangzhou, Zhejiang 310053, PR Tuam Tshoj
c * Zhejiang University of Technology, Hangzhou, Zhejiang 310014, PR Tuam Tshoj
d * Zhejiang Suav Medical University, Hangzhou, Zhejiang 310053, PR Tuam Tshoj
Abstract
Osteoporosis yog ib hom kab mob metabolic pob txha uas muaj qhov tshwm sim ntau ntxiv. Suav tshuaj ntsuab muaj keeb kwm ntev ntawm kev kho mob pob txha. Polysaccharides yog ib pawg tseem ceeb ntawm phytochemicals hauv Suav tshuaj ntsuab, thiab lawv cov txiaj ntsig kev noj qab haus huv tau nce kev txaus siab ntawm cov pej xeem. Ntau cov kev tshawb fawb tau qhia tias polysaccharides muaj kev cuam tshuam los tiv thaiv pob txha los ntawm kev sib npaug ntawm cov pob txha resorption thiab tsim cov pob txha, tab sis cov ncauj lus kom ntxaws thiab cov txheej txheem tsis tau sau tseg. Peb tau ua tiav kev tshuaj xyuas cov ntaub ntawv txhawm rau txheeb xyuas cov kev tshawb fawb rau lub sijhawm 2000-2021 los ntawm kev tshawb nrhiav hluav taws xob ntawm PubMed, CNKI, VIP, thiab Wanfang databases. Nyob rau hauv tag nrho, polysaccharides los ntawm 19 hom tshuaj suav tshuaj hauv 54 kev tshawb fawb tau pom cov pob txha homeostasis tiv thaiv. Hauv vivo thiab hauv vitro thwmsim tau pom tias polysaccharides tam sim no muaj zog hauv kev kho mob postmenopausal osteoporosis, senile osteoporosis, thiab glucocorticoid-induced secondary osteoporosis, tshwj xeeb tshaj yog postmenopausal osteoporosis. Ntxiv mus, ib tug xov tooj ntawm kev taw qhia txoj kev, xws li Wnt/ -catenin signaling pathway, BMP/SMAD/RUNX2 signaling pathway, OPG/RANKL/RANK signaling pathway, apoptosis pathway, thiab transcription factors, yog tswj los ntawm polysaccharides thiab koom rau hauv kev txhim kho pob txha. homeostasis. Qhov kev tshuaj xyuas no yuav muab kev nkag siab zoo dua ntawm kev tiv thaiv osteoporotic cuam tshuam ntawm polysaccharides thiab cov kev sib txuas ua ke ntawm kev taw qhia txoj hauv kev.
Ntsiab lus:Polysaccharides, Suav tshuaj ntsuab, Mechanisms, Pob txha homeostasis
Suav tshuaj ntsuab tshuaj ntsuab --Cistanche, zoo rau kev tiv thaiv pob txha
1. Taw qhia
Osteoporosis yog ib qho kab mob hauv cov pob txha uas muaj cov kab mob metabolic uas tshwm sim los ntawm microarchitectural deterioration, cov pob txha qis, thiab muaj kev pheej hmoo ntawm pob txha. Raws li cov txiaj ntsig ntawm thawj qhov kev soj ntsuam kab mob qog noj ntshav tau ua los ntawm National Health Commission ntawm Tuam Tshoj hauv xyoo 2018, qhov feem ntau ntawm cov pob txha ntawm cov poj niam hnub nyoog 50 xyoo tau nce mus txog 32.1 feem pua, thaum cov poj niam hnub nyoog tshaj 65 xyoo yog 51.6 feem pua. Kwv yees li ntawm 10 lab tus tib neeg hnub nyoog tshaj 50 xyoo hauv Tebchaws Meskas muaj mob pob txha, thiab 34 lab tus tib neeg muaj kev pheej hmoo ntawm tus kabmob no. Hauv tebchaws Askiv, 50 feem pua ntawm cov poj niam hnub nyoog 50 xyoo thiab 20 feem pua ntawm cov txiv neej raug kev txom nyem los ntawm pob txha pob txha [1]. Kev puas tsuaj los ntawm pob txha pob txha tuaj yeem ua rau muaj kev mob hnyav ntxiv thiab kev tuag, ua rau muaj kev cuam tshuam loj heev [2].
Ib qho kev tsis sib haum xeeb hauv cov pob txha homeostasis yog paub zoo tias yog tshwm sim los ntawm ntau cov pob txha osteoclast-mediated resorption dua li osteoblast-mediated pob txha tsim ua rau osteoporosis. Ntau yam ua rau cov pob txha homeostasis, tab sis cov txheej txheem tseem ceeb yog qhov tsis sib xws ntawm osteoblasts thiab osteoclasts, suav nrog (i) txo qis osteoblast (OB) qhov sib txawv thiab kev ua haujlwm, ua rau txo cov pob txha deposition; (ii) nce osteoclast (OC) qhov sib txawv thiab kev ua haujlwm, ua rau cov pob txha resorption ntau dhau; thiab (iii) o thiab oxidative xwm txheej [3]. Tsis tas li ntawd, kev ua haujlwm ntawm OB thiab OC tau tswj hwm los ntawm ntau yam kev hloov pauv thiab cov kev taw qhia.
Hauv Suav teb, ntau cov tshuaj suav tshuaj suav tshuaj uas muaj cov haujlwm yooj yim rau cov pob qij txha thiab ntxiv dag zog rau cov pob txha thiab cov leeg tau siv los kho cov pob txha pob txha rau ntau pua xyoo. Polysaccharides yog ib qho ntawm cov khoom tseem ceeb ntawm ntau cov tshuaj suav tshuaj, xws li Polygonatum sibiricum Delar. ex Redoute, Angelica sinensis (Oliv.) Diels thiab Morinda Officinalis How. Lub caij no, polysaccharides tau raug pov thawj tias muaj ntau lub zog, xws li antioxidant [4], immunomodulation [5], thiab tiv thaiv qaug zog [6]. Txog niaj hnub no, ntau cov kev tshawb fawb tau qhia tias polysaccharides muaj kev tiv thaiv kab mob osteoporosis los ntawm kev sib npaug ntawm cov pob txha resorption thiab tsim cov pob txha, tab sis cov ncauj lus kom ntxaws thiab cov txheej txheem tsis tau sau tseg.
Hauv kev tshuaj xyuas no, peb tau sau tag nrho ntawm 54 qhov kev tshawb fawb ntawm polysaccharides ntawm kev tiv thaiv pob txha los ntawm 2000 txog 2021 xyoo, thiab polysaccharides los ntawm 19 hom tshuaj suav tshuaj tau tshawb fawb. Cov kev tshawb fawb no suav nrog 25 hauv vivo kev tshawb fawb thiab 40 hauv vitro kev sim. Cov qauv tsiaj sim muaj xws li ovariectomized (OVX) nas, SAMP6 nas, thiab glucocorticoid-induced osteoporosis (GIOP) zebrafish. MCET3-E1 hlwb, BMSCs, dexamethasone-induced OB, thiab RANK-induced BMM cell qauv tau siv dav hauv kev sim vitro. Cov txheej txheem ntawm crude polysaccharides los yog purified polysaccharides ntawm kev tiv thaiv pob txha yog tsom rau OB los yog OC proliferation, sib txawv, nrog rau kev qhia ntawm transcription yam, inflammatory yam, teeb liab txoj kev xws li Wnt / -catenin signaling pathway, BMP / SMAD / RUNX2 signaling pathway, OPG / RANKL / RANK qhia txoj hauv kev, thiab lwm yam. Peb tau tshuaj xyuas cov kev tiv thaiv kab mob osteoporosis thiab cov txheej txheem ntawm polysaccharides los ntawm 19 hom tshuaj suav tshuaj thiab sau cov ntsiab lus no hauv Table 1.
2. Polysaccharides muab los ntawm Suav tshuaj ntsuab tshuaj tiv thaiv osteoporosis
Ntawm 19 hom tshuaj ntsuab, 13/19 yog los ntawm rhizome ib feem, 1/19 los ntawm paj, 2/19 los ntawm nplooj nplooj, 1/19 los ntawm cov txiv hmab txiv ntoo, thiab 2/19 los ntawm fungus. Tag nrho cov pov thawj ntawm polysaccharides los ntawm cov tshuaj suav tshuaj suav tshuaj no los txhim kho cov pob txha homeostasis thiab txwv cov pob txha poob yog qhia nyob rau hauv kab lus hauv qab no.
2.1. Polysaccharides muab tau los ntawm rhizomes ntawm Suav tshuaj ntsuab
Achyranthes bidentata Blume (AC, "Niu xi"), Morinda Officinalis How (MO, "Ba-Ji-Tian"), Curculigo orchioides Gaertn (CO, "Xian Mao"), Cynomorium solarium Rupr. (CY, "Suo yang"), Cistanche deserticola Ma (CD, "Rou Cong Rong"), thiab Cibotium barometz (L.) J. Sm (CB, "Gou Ji") yog Suav tshuaj ntsuab uas "tone lub raum thiab ntxiv dag zog rau cov pob txha" thiab tshwj xeeb tshaj yog siv rau kev kho mob ntawm postmenopausal osteoporosis. Cov ntsiab lus tseem ceeb ntawm polysaccharides tau tshaj tawm tias muaj txiaj ntsig zoo rau kev tiv thaiv pob txha hauv OVX nas qauv. Crude polysaccharides los ntawm AC [7,8], MO [9–11], CO [12], CY [17], thiab ABPB-3 [13] (a purified polysaccharide los ntawm AC) tau raug tshaj tawm kom cov pob txha mineral density (BMD), txhim kho biomechanical indices ntawm femurs nyob rau hauv OVX nas, thiab tswj lub microarchitecture ntawm trabecular pob txha tom qab tas mus li kev tswj xyuas yuav luag 3 lub hlis. Lub caij no, ABPB-3 kuj tseem tuaj yeem ua rau cov ntshav qab zib osteocalcin (OCN) [13], pob txha glutamate protein (BGP), thiab cov zis deoxypyridinol (DPD) qib [15]. Hauv kev sim hauv vitro, polysaccharides los ntawm CB (CBP) thiab ib qho tshiab homogeneous heteropolysaccharide COP70-3 los ntawm CO nce alkaline phosphatase (ALP) kev ua haujlwm thiab txhim kho cov mineralization tus nqi [12] [16]. Lwm purified polysaccharide, COP90-1, los ntawm CO txhawb kev loj hlob thiab kev sib txawv ntawm thawj nas OB [17]. Tsis tas li ntawd, ob qhov tshiab polysaccharides ntawm ABW50-1 thiab ABPB-3 los ntawm AC qhov tseem ceeb nce pob txha loj hauv GIOP zebrafish qauv [18] [13]. Polysaccharides los ntawm CD (CDP) zoo kawg nkaus ameliorated pob txha histopathological puas thiab txhawb kev tsim cov pob txha tshiab hauv SAMP6 nas [45].
Astragali Radix (AS, "Huang qi"), Angelica sinensis (Oliv.) Diels (AN, "Dang Gui"), thiab Hedysarum Polyporus Tes.-Mazz. (HP, "Hong qi") yog Suav tshuaj ntsuab uas "supple qi thiab nourish ntshav". AS polysaccharides (ASP) tau tshaj tawm tias muaj peev xwm thim rov qab qhov txo qis hauv pob txha, nce ntshav ALP thiab BGP, thiab tswj hwm biomechanical indices ntawm femur hauv OVX nas thiab Dex-induced thiab stress-induced osteoporosis nas nyob rau hauv ib koob tshuaj. kev [20,21]. Polysaccharides los ntawm AN (ANP) nce tus naj npawb ntawm trabeculae thiab txhawb kev kho pob txha raug mob hauv hom 2 mob ntshav qab zib nas. Hauv kev tshawb nrhiav vivo, 40 mg / L ASP nce cov calcium nodule tus lej thiab ALP kev ua haujlwm hauv BMSCs raug ntxias los ntawm 25.5 mmol / L qabzib [22]. ANP thiab polysaccharides los ntawm HP (HPP) tshwm sim los txhim kho qhov kev loj hlob ntawm OB thiab txhim kho ALP kev ua haujlwm nyob rau hauv koob tshuaj [23,24].
Polygonatum sibiricum Delar. ex Redoute (RP, "Huang Jing") thiab Dendrobium officinale Kimura thiab Migo (DO, "Tie pi shi hu") yog cov tshuaj suav tshuaj uas "nourish Yin". Hauv vivo cov kev tshawb fawb tau pom tias polysaccharides los ntawm RP (RPP) tuaj yeem ua rau tag nrho BMD thiab txhim kho cov pob txha trabecular microstructure ntawm OVX nas tom qab kev tswj hwm tas li [25,26] thiab tuaj yeem txhim kho cov tsos mob hauv tus qauv osteoporotic puas [27]. DO polysaccharides (DOP) tiv thaiv kev degradation ntawm trabecular microstructural thiab txhim kho BS / TV, Tb. N, thiab qhov txo qis hauv Tb.Sp age-induced osteoporosis model [28]. Ib yam li ntawd, kev tswj hwm txhua hnub ntawm polysaccharides los ntawm Gastrodia elata Bl. (GA, "Tian ma") thiab Saposhnikovia divaricata (Turcz.) Schischk. (SA, "Fang Feng") kuj nce BMD [29,30] thiab ntshav Ca2 ntxiv, Mg2 ntxiv, thiab P2− qib [31] hauv OVX qauv.
cistanche tubolosa cov txiaj ntsig
2.2. Polysaccharides muab tau los ntawm nplooj ntawm Suav tshuaj ntsuab
Epimedium brevicornum Maxim (EB, "Yin Yang Huo") yog nplooj nrov heev, ib txwm siv los kho pob txha kab mob thiab gonad dysfunction hauv Suav tshuaj rau ntau txhiab xyoo. EB tuaj yeem txo cov tsos mob tom qab menopausal thiab inhibit osteoporosis thiab lwm yam kab mob pob txha. Kev tshawb fawb hauv vitro tsis ntev los no tau qhia tias EB polysaccharide (EBP) tuaj yeem txhawb nqa thiab txhim kho kev loj hlob thiab kev sib txawv ntawm OB hlwb raug ntxias los ntawm dexamethasone [32].
Hairyvein Agrimonia Herb thiab Bud (AP, "Xian he cao") belongs rau Rosaceae thiab yog siv los ua Suav tshuaj rau kev kho mob ntshav qab zib thiab arrhythmia. Ib qho dej-soluble polysaccharide (APP-AW) raug cais los ntawm AP, thiab peb sulfated derivatives (S1, S2, thiab S3) los ntawm APP-AW tuaj yeem tiv thaiv apoptosis hauv dexamethasone-induced OB qauv [33].
2.3. Polysaccharides muab tau los ntawm fungi thiab nceb ntawm Suav tshuaj ntsuab
Suav tshuaj ntawm Poria cocos (Schw.) Hma. (PO, "Fu ling") tau muaj koob npe nrov tau siv rau kev noj haus txhua hnub thiab tshuaj hauv Suav teb thiab lwm lub tebchaws Esxias txij li xyoo pua. Raws li classical anti-oxidant tus neeg saib xyuas, PO tsis ntev los no tau nthuav tawm cov txiaj ntsig rau kev kho mob ntawm angina pectoris, kub siab, thiab cov pob txha metabolism. PO polysaccharide (POP) yog ib qho tseem ceeb thiab tseem ceeb sib xyaw muab rho tawm los ntawm PO. Ib qho kev tshawb fawb hauv vivo tau qhia tias kev kho POP cuam tshuam RANKL-vim OC tsim nyob rau hauv RAW264.7 thiab BMMS hlwb nyob rau hauv ib qho kev noj tshuaj thiab txo qis kev ua haujlwm ntawm resorption [34].
Polystictus versicolor (L.) Fr. (TV, "Yun Zhi") yog ib qho ntawm cov tshuaj ntsuab nceb nrov tshaj plaws los ntawm Coriolus Versicolor (L. ex Fr.) Quel vim nws cov khoom siv lom neeg ntau yam. Polysaccharopeptides los ntawm TV (TVP) tau pom tias muaj kev tiv thaiv kab mob hauv lub cev thiab hom I ntshav qab zib mellitus (DM) nas. Ib txoj kev tshawb fawb tsis ntev los no tau pom tias TVP yog ib qho kev kho mob zoo rau cov kab mob osteoporosis hauv cov nas mob ntshav qab zib mellitus. Piv nrog rau pawg qauv, TVP txo qis DM-vim cov pob txha tsis zoo, raws li kev txiav txim siab los ntawm kev ua kom cov pob txha ntim ntawm cov tibia proximal, trabecular tooj, thiab femoral pob txha muaj zog (11 feem pua qhov siab tshaj plaws, 22 feem pua stiffness, thiab 14 feem pua modulus) thiab los ntawm txo cov femoral cortical porosity los ntawm 25 feem pua [35].
2.4. Polysaccharides muab tau los ntawm lwm cov tshuaj suav tshuaj
Lycium chinense Miller (LY, "Gou qi"), uas yog Lycium barbarum L., yog dav faib nyob rau sab qaum teb sab hnub poob ntawm Tuam Tshoj, thiab nws cov txiv hmab txiv ntoo tau sau tseg los ua lub luag haujlwm hauv kev cuam tshuam hauv cov metabolism hauv postmenopausal. Cov qauv nas ntawm postmenopausal estrogen deficiency-induced osteoporosis thiab dexamethasone-induced osteoporosis tau qhia tias LYP tuaj yeem muab kev kho mob zoo rau pob txha. Hauv vivo cov kev tshawb fawb tau pom tias LY polysaccharide (LYP) nce ntxiv
lumbar BMD thiab qhov hnyav qhuav ntawm femurs hauv OVX nas tom qab kev kho mob rau 12 lub lis piam, txhim kho cov pob txha pob txha, thiab txo qis lacunal absorption [24]. Ntxiv mus, LYP kuj nce ntshav calcium, ALP cov ntsiab lus, thiab BMD nyob rau hauv glucocorticoid-induced osteoporosis nas [36].
Carthamus Flos (SF, "Hong Hua") los ntawm Carthamus tinctorius L. tau siv los ua suav tshuaj rau kev kho mob stroke thiab mob plawv. Cov kev sim tshuaj niaj hnub no kuj tau pom tias polysaccharides cais tawm ntawm SF (SFP) muaj peev xwm kho tau tus nqi rau kev kho mob ntawm osteogenesis tsis zoo thiab pob txha. Cov kev tshawb fawb hauv vitro tau pom tias SFP tuaj yeem siv tshuaj raws li kev txhim kho kev loj hlob ntawm thawj OB thiab mineralization thiab qhov kev txhim kho no tau nrog los ntawm kev ua haujlwm ALP thiab collagen synthesis qhia [37].
3. Mechanism uas polysaccharides txhim kho pob txha homeostasis los ntawm kev tswj OB thiab OC
3.1. Mechanism uas polysaccharides txhawb osteoblast-mediated pob txha tsim
OB tau txais plaub theem hauv kev tsim cov pob txha, suav nrog osteoblast proliferation, extracellular matrix maturation, extracellular matrix mineralization, thiab osteoblast apoptosis. Ntau yam, xws li kev taw qhia txoj hauv kev thiab cov kev hloov pauv tuaj yeem tswj cov theem no thiab thaum kawg tswj cov pob txha tsim. Ntawm no, peb sau cov ntsiab lus ntawm kev hloov pauv thiab cov cim qhia txoj hauv kev uas polysaccharides cuam tshuam rau pob txha tsim hauv OB. Cov txheej txheem ntawm OB-mediated pob txha tsim thiab polysaccharide kev tswj hwm ntawm OB muaj nuj nqi uas koom nrog hauv peb cov kev tshawb fawb tau pom hauv daim duab. 1 thiab 2.
Fig. 1. Cov ntsiab lus ntawm cov txheej txheem ntawm cov pob txha pob txha uas koom nrog hauv peb txoj kev tshawb fawb. Txhawb (→), inhibit (⊥). Hauv BMSCs, kev sib txuas ntawm Wnt proteins nrog cov membrane-bound frizzles receptors thiab LRP5/6 co-receptor pib Axin1 complex inhibit qhov ubiquitination thiab degradation ntawm -catenin thiab ceev nws translocation rau hauv lub nucleus [38]. Qhov no nuclear -catenin khi rau thiab co-activates cov tswv cuab ntawm T-cell factor / lymphoid-enhancing factor tsev neeg ntawm transcription factor (TCF/LEF) qhib cov noob caj noob ces, xws li Runx2 thiab Osterix (Osx), yog li ua rau kev nce qib. rau kev sib txawv thiab kev loj hlob ntawm OBs [32]. DKK-1 inhibits Wnt khi rau frizzled receptors thiab LRP5/6, wnt/ -catenin signaling pathway raug thaiv. Hauv OB, pob txha morphogenetic proteins (BMP) khi rau BMP receptor (BMPR), qhib SMAD1/5/8 proteins uas nkag mus rau hauv lub nucleus, ces tswj RUNX2 noob qhia. Runx2 tuaj yeem ua ke nrog cov ntsiab lus sib txuas los tsim cov qauv heterologous dimer thiab tom qab ntawd khi rau DNA, ua rau kev nthuav qhia ntawm cov pob txha tsim cov noob caj noob ces, xws li Osx, pob txha glutamate protein (BGP), thiab ALP. PIP3 tsim los ntawm PI3K ua kom khi rau PH sau ntawm N-kawg ntawm Akt, hloov Akt mus rau cov ntshav plasma, uas catalyzes Akt ser473 thiab Thr308 qhov chaw phosphorylation. Tom qab Akt activation, nws txhawb cov kev qhia ntawm downstream pro-apoptotic yam ntawm bax-2, caspase 3 thiab inhibits qhov anti-apoptotic yam ntawm BCL-2. Hauv pre-OC, IL-1, IL-6, thiab TNF- nquag NF-κB, uas txhim kho kev hloov pauv ntawm NF-κB mus rau hauv lub nucleus, uas ua rau muaj kev sib txawv ntawm pre-OC mus rau OC. Hauv OC, IL-6 khi rau interleukin 6 receptor (IL-6R), TNF- khi rau TNF- receptor (TNFR), RANKL khi rau RANK thiab ntxiv cov neeg ua haujlwm TNFR-txog yam xwm txheej (TRAFs) los pib cov kev taw qhia downstream cascades, suav nrog NF-κB phosphorylation, p38 phosphorylation, JNK, thiab ERK1/2. Qhov kawg tshwm sim ntawm RANKL-RANK signaling yog qhov ua kom muaj osteoclast transcription yam, xws li NF-κB, activator protein 1 (AP{ {55}}), Proto-oncogene protein (FOS), thiab activated nuclear factor of activated T-cells (NFATc1). NFATc1 induced qhov kev qhia ntawm osteoclast-specific genes xws li tartrate-resistant acid phosphatase (TRAP) thiab cathepsin K (Ctsk), uas ua rau kev sib txawv thiab txhawb OC maturation.
Fig. 2. Cov ntsiab lus ntawm polysaccharides thiab cov txheej txheem ua tau uas koom nrog hauv kev kho mob pob txha. ACP: polysaccharide los ntawm Achyranthes bidentata Blume; ASP: polysaccharide los ntawm Astragali Radix; ANP: polysaccharide los ntawm Angelica Sinensis (Oliv.) Diels; APP: polysaccharide los ntawm Hairyvein Agrimonia Tshuaj ntsuab thiab Bud; COP: polysaccharide los ntawm Curculigo orchioides Gaertn; CYP: polysaccharide los ntawm Cynomorium songaricum Rupr; CDP: polysaccharide los ntawm Cistanche deserticola Ma; CBP: polysaccharide los ntawm Cibotium barometz (L.) J. Sm; DOP: polysaccharide los ntawm Dendrobium officinale Kimura thiab Migo; EBP: polysaccharide los ntawm Epimedium brevicornum Maxim; WSS25: polysaccharide los ntawm Gastrodia elata Bl.; HPP: polysaccharide los ntawm Hedysarum Polyporus Tes.-Mazz.; LYP: polysaccharide los ntawm Lycium chinense Miller; MOP: polysaccharide los ntawm Morinda Officinalis Yuav ua li cas; POP: polysaccharide los ntawm Poria cocos (Schw.) Hma.; RPP: polysaccharide los ntawm Polygonatum sibiricum Delar. ex rov; SAP: polysaccharide los ntawm Sap oshnikovia divaricata (Turcz.) Schischk.; SFP: polysaccharide los ntawm Carthami Flos. TVP: polysaccharide los ntawm Polystictus Versicolor (L.) Fr.
3.1.1. Transcription yam
Osteogenic sib txawv ntawm BMSCs yog tswj hwm los ntawm ntau yam kev hloov pauv, xws li Runt-related transcription Factor 2 / core binding factor 1 (Runx2 / Cbfa1) thiab osterix. Cbf 1, tseem hu ua polyomavirus enhancer-binding protein 2 A (PEBP2 A) los yog mob myeloid leukemia Factor 3 (AML3), yog ib qho kev hloov pauv ntawm cov tsev neeg cov noob caj noob ces. Osterix, qhov tseem ceeb tshaj plaws uas tswj hwm cov phiaj xwm hauv cov pob txha tsim, yog tus tswj hwm qhov tseem ceeb ntawm OB qhov sib txawv thiab yog qhov ntxov tshaj plaws thiab tshwj xeeb tshaj plaws ntawm kev sib txawv ntawm OB.
MOP-mediated serum intervention ntawm BMSCs rau 14 hnub upregulated kev qhia ntawm Cbf 1 mRNA thiab txhawb osteogenic sib txawv [39]. Lwm txoj kev tshawb fawb tau pom tias qhov kev qhia ntawm Cbf 1 mRNA nyob rau hauv nas calvarial OB tau nce-tswj tom qab kev kho mob nrog ib tug dej extract ntawm Morinda Officinalis thiab MOP-muaj kuab tshuaj rau 72 h, thiab cov nyhuv ntawm MOP yog zoo dua li cov nyhuv ntawm ib tug dej extract. Morinda Officinalis [40]. MOP muab rau OVX osteoporosis nas rau 30 hnub nce qhov kev qhia ntawm tibial noob Cbf 1 thiab DMP1 [10]. Ib qho tshiab inulin fructan MOW90-1 cais los ntawm MO90 nce- tswj kev qhia ntawm Runx2 thiab Osterix thiab txhawb kev loj hlob, sib txawv, thiab mineralization ntawm MC3T3-E1 hlwb [14].
Kev tshawb fawb hauv vitro tsis ntev los no tau soj ntsuam cov txiaj ntsig ntawm HPP ntawm kev sib txawv ntawm osteogenic ntawm MC3T3-E1 osteoblastic hlwb thiab pom tias HPP txhawb nqa ALP kev ua haujlwm ntawm kev siv tshuaj ntau ntxiv thiab nce kev qhia thiab kev ua haujlwm ntawm Runx2 thiab Osterix, Ob lub tswv yim ntawm OB sib txawv [24] Liao et al pom tias ANP tuaj yeem tsim kho qhov kev qhia mRNA ntawm CyclinD1, Runx2, thiab Osterix [22,23]. ASP kuj tau nce qhov kev qhia ntawm CyclinD1 thiab txhawb kev loj hlob [41].
3.1.2. Wnt/ -catenin signaling txoj kev
Wnt/ -catenin signaling pathway plays lub luag haujlwm tseem ceeb hauv kev rov ua dua tshiab ntawm tus kheej, kev taw qhia sib txawv, preosteoblast proliferation, OB tsim, thiab apoptosis ntawm BMSCs. Hauv cov txheej txheem ntawm kev txhawb nqa OB qhov sib txawv, Wnt tswj OB qhov sib txawv ntawm cov noob los ntawm kev tswj cov qib ntawm -catenin hauv BMSCs. Activated Wnt signaling tuaj yeem txhawb nqa -catenin aggregation, ua rau OB sib txawv thiab tsim pob txha. Kev qhia ntawm Wnt3a thiab Wnt10b hauv BMSCs tuaj yeem qhib Wnt / -catenin signaling txoj hauv kev thiab txhawb kev loj hlob ntawm BMSCs [42]. DKK-1 yog ib qho inhibitor ntawm Wnt signaling pathway, inhibits pob txha tsim, thiab ua rau osteoporosis thaum antagonizing DKK-1 tuaj yeem nce pob txha loj [43].
MOP nce qhov kev loj hlob ntawm OBs hauv vitro, nce ALP kev ua haujlwm, thiab txo qis cov protein qhia ntawm DKK-1 [44]. Ntxiv rau hauv vivo kev tshawb fawb ntawm cov txheej txheem molecular tom qab cov tshuaj tiv thaiv osteoporosis ntawm CDP qhia tias qhov txo qis ntawm cov pob txha degeneration yog txuam nrog kev ua kom Wnt / -catenin signaling pathway [45]. RPP kev cuam tshuam tau txhim kho ALP kev ua haujlwm ntawm BMSCs nyob rau hauv koob tshuaj, ua kom muaj peev xwm ua kom muaj peev xwm ntawm cov hlwb, nce kev nthuav qhia ntawm ALP, Runx2, thiab Osteocalcin genes hauv BMSCs, nce kev tswj hwm kev qhia ntawm -catenin, thiab txhawb nqa. qhov kev nthuav qhia siab ntawm TCF khi qhov chaw. Lub tshuab yuav cuam tshuam txog kev ua kom Wnt / -catenin signaling txoj hauv kev thiab txhawb kev sib txawv ntawm BMSCs rau hauv OBs [46], tab sis RPP tsis cuam tshuam rau txoj hauv kev BMP. Kev tshawb pom kuj pom tau tias RPP txhawb nqa OB qhov sib txawv thiab kev ntxhia los ntawm kev tswj hwm ERK/GSK-3 / -catenin signaling pathway [47]. Li et al. pom tias BMP9 yog lub hom phiaj ncaj qha ntawm miR-152, thiab ASP tuaj yeem txo qis- tswj miR{18}} cov lus qhia thiab txhawb nqa BMP9 kev tswj hwm, yog li ua kom PI3K / AKT thiab Wnt / -catenin txoj kev taw qhia hauv BMSCs [ 41] ib. ASP alleviated oxidative stress-induced osteoporosis los ntawm kev tswj cov FoxO3a/Wnt2/ -catenin signaling pathway [48]. LYP-mediated serum activates cov kev qhia ntawm Wnt signaling pathway-protein-catenin thiab Wnt10b txhawb kev sib txawv ntawm BMSCs rau hauv OB, thiab nce mineralized nodules [49].
cistanche tubolosa extract: kho cov kab mob ntshav qab zib
3.1.3. BMP/SMAD/RUNX2 teeb liab txoj kev
BMP / SMAD signaling pathway ua lub luag haujlwm tseem ceeb hauv kev ua kom cov pob txha tsim cov noob caj noob ces. Pob txha morphogenetic protein II (BMP2), ib tug tswv cuab ntawm TGF- superfamily, yog heev nthuav nyob rau hauv OB thiab tswj kev sib txawv nyob rau hauv vitro thiab nyob rau hauv vivo [50]. BMP khi heterodimeric receptors los qhib SMAD cov proteins, uas hloov cov noob caj noob ces ncaj qha lossis ntawm Runx2 [51]. Runx2 yog lub hom phiaj nqes dej ntawm BMP2 / Smad teeb liab hloov pauv mechanism thiab ib qho kev hloov pauv uas yuav tsum tau ua rau osteoblastogenesis. Runx2 tuaj yeem ua ke nrog cov ntsiab lus sib txuas los tsim cov qauv heterologous dimer thiab tom qab ntawd khi rau DNA, ua rau kev nthuav qhia ntawm cov pob txha tsim cov noob caj noob ces, xws li COL-І, BGP, thiab ALP.
Huang thiab al cais ob qhov tshiab polysaccharides, CBP70-1-1 thiab CBP70-1-2, los ntawm rhizomes ntawm Cibotium barometz thiab pom tias lawv tuaj yeem txhawb nqa OB proliferation ntawm qhov tsis tshua muaj siab. CBP70-1-1 ntawm 3.93 thiab 7. Ntxiv mus, CBP70-1-2 tau nce qhov kev qhia thiab kev hloov pauv ntawm BMP2, thiab qhov kev nthuav qhia ntau ntxiv ntawm BMP2 tom qab tau txhawb nqa cov noob caj noob ces Smad1. Lub phosphorylation ntawm Smad1 yog nce, uas ntxiv nkoos lub osteogenic marker gene Runx2 los txhawb cov pob txha tsim [50].
Lwm txoj kev tshawb fawb pom tau tias CEP tuaj yeem txhim kho cov ntaub ntawv pob txha los ntawm kev tswj cov protein qhia ntawm BMP2 / Smad1 thiab Smad5 / Runx2 [52]. Chen li al pom tias Gastrodia elata Bl. polysaccharide WSS25 tuaj yeem cuam tshuam qhov kev qhia ntawm BMP2 / Smad1 txoj hauv kev thiab inhibit osteoclastic sib txawv [29]. RPP txhawb kev tsim cov pob txha hauv OVX nas los ntawm kev nce qib ntawm ALP, OPG, thiab BGP thiab cov protein qhia ntawm BMP2 [26]. APP txhim kho ALP kev ua ub no, txhawb kev loj hlob thiab kev sib txawv ntawm OB, thiab nce OB qhov sib txawv cim cov proteins BMP2, Runx2, Osterix, thiab Osteocalcin. Lub tshuab molecular muaj feem xyuam nrog kev txhim kho miR-70 qhia [53] thiab kev tswj hwm ntawm Wnt/ -catenin signaling pathway [54].
3.1.4. Antiapoptosis kho txoj hauv kev
Apoptosis, ib daim ntawv ntawm kev tuag ntawm tes, ua lub luag haujlwm tseem ceeb hauv cov ntaub so ntswg homeostasis, thiab deregulation ntawm apoptosis tau cuam tshuam rau ntau yam kab mob pathological [55]. Proteins ntawm Bcl-2 tsev neeg muaj cov kev ua ub no pro- lossis antiapoptotic thiab tswj txoj hauv kev mitochondrial ntawm apoptosis los ntawm kev tswj mitochondrial txheej membrane permeabilization (MOMP). MOMP yog qhov xwm txheej tseem ceeb hauv txoj hauv kev apoptotic. Bax, uas koom nrog hauv kev tsim MOMPs, ua rau kev tso tawm cov ntsiab lus ntawm mitochondrial interemembrane chaw rau hauv cytoplasm. Qhov tso tawm cytochrome c khi rau cov cytosolic protein uas muaj cov caspase-recruitment domain (CARD) los tsim cov apoptosome thiab tom qab ntawd mus nrhiav ntau yam procaspase-9 molecules, thaum kawg ua rau cov neeg tua hluav taws hauv qab caspases xws li caspase-3. Anti-apoptotic proteins ntawm Bcl-2 thaiv cell tuag los ntawm kev tiv thaiv kev ua kom thiab homo-oligomerization ntawm Bax [56]. Ntxiv mus, Bax protein yog tswj los ntawm phosphorylation nyob rau hauv Akt-dependent yam, thiab qhov kev tshwm sim phosphorylation inhibits cov teebmeem ntawm Bax ntawm mitochondria los ntawm kev tswj nws nyob rau hauv lub cytoplasm [57].
Glucocorticoids tau dav siv los kho cov kab mob inflammatory thiab ua rau kwv yees li 30 feem pua ntawm OB cell apoptosis hauv cov neeg mob osteoporosis los ntawm kev siv ntau dhau ntawm glucocorticoids. Ib qho dej-soluble polysaccharide (APP-AW) raug cais tawm ntawm Agrimonia pilosa, thiab peb sulfated derivatives (S1, S2, thiab S3) los ntawm APP-AW inhibited apoptosis hauv dexamethasone-induced OB qauv [33], thim rov qab qhov nce hauv Bax. , cytochrome, thiab caspase-3 thiab txo Bcl-2 thiab c-Myc protein qhia hauv MC3T3-E1 hlwb. Ib qho kev tshawb fawb hauv vitro tau pom tias MOP inhibited OB apoptosis induced los ntawm all-trans retinoic acid [58]. SFP zoo nkaus li tiv thaiv OB hlwb los ntawm dexamethasone-induced apoptosis, tejzaum nws yog vim nws cov nyhuv ntawm reversing lub activation ntawm caspase -3 thiab cleavage ntawm PARP [37]. EBP tau tswj hwm qhov kev qhia ntawm Bcl-xl thiab Bcl-2 thiab txo qis Bax thiab caspase-3 qhia los ntawm PI3K/ Akt/mTOR signaling pathway in dexamethasone-induced OB [32].
3.1.5. Oxidative stress-mediated pathways
Kev txhim kho ntawm oxidative kev ntxhov siab thaum lub sij hawm laus tuaj yeem yog qhov tseem ceeb ua rau pob txha. Oxidative stress yog ib yam kab mob uas cuam tshuam txog kev tsim cov pa oxygen ntau dhau (ROS) nyob rau hauv cov xwm txheej thaum lawv tshem tawm raug txo. Raws li qhov taw qhia thiab kev tswj hwm ntawm kev puas tsuaj oxidative, lub nuclear factor erythroid 2- ntsig txog yam 2 (Nrf2)/Heme Oxygenase 1 (HO-1) txoj kev, uas tiv thaiv oxidative puas thiab cell tuag, tau qhov tseem ceeb ntawm kev tshawb fawb tau ntau xyoo. Ib qho kev tshawb fawb hauv vivo tau pom tias DOP tuaj yeem cawm H2O2- induced hloov ntawm BMSC sib txawv txoj hmoo thiab nce qhov kev qhia ntawm Nrf2, HO-1, thiab Nqo1 [28].
3.1.6. Txhawb cov pob txha tshwj xeeb matrix thiab pob txha mineralization
Pob txha sialoprotein (BSP), osteopontin, thiab osteocalcin yog cov cim phenotypic rau cov laus OB thiab cov cim tseem ceeb ntawm matrix mineralization. Osteopontin yog secreted los ntawm OB thiab koom nyob rau hauv lub mineralization ntawm cov pob txha matrix, uas muaj peev xwm ua ke nrog hydroxyapatite los ntawm ib cheeb tsam nplua nuj nyob rau hauv aspartic acid thiab koom nyob rau hauv lub mineralization ntawm cov pob txha matrix. BSP, ib tug loj extracellular noncollagenous matrix protein nyob rau hauv cov pob txha cov ntaub so ntswg nyob rau hauv lub mineralized matrix, yuav txhawb nqa nucleation ntawm hydroxyapatite mineralization nyob rau hauv vitro thiab nce calcium incorporation thiab nodule tsim. Osteocalcin, tsim thiab secreted yuav luag tshwj xeeb los ntawm OB, khi rau Ca2 ntxiv thiab yog lub luag hauj lwm rau cov mineralization ntawm cov pob txha matrix [59].
MOP (50 ug⋅mL-1) txhawb nqa MC3T3-E1 cell proliferation, txhawb kev tso tawm ntawm collagen hom 1 (COL-І) thiab Osteocalcin, thiab txhim kho ALP kev ua haujlwm [60]. RPP txhim kho cov khoom siv biomechanical thiab BMD ntawm pob txha pob txha pob txha hauv nas los ntawm kev txo cov ntsiab lus ntawm cov pob txha ALP, TRAPa, thiab TNF- hauv osteoporosis ntawm nas [25] thiab nce qib ntawm ALP, OPG, thiab BGP thiab cov protein qhia ntawm BMP2 [ 26] ib. Ib qho purified polysaccharide ABW70-1, cais tawm ntawm radix achyranthis bidentatae, txhawb kev loj hlob ntawm MC3T3-E1 hlwb, nce ALP kev ua haujlwm, tsim cov pob zeb hauv av, thiab cov noob qhia ntawm Osterix, Osteocalcin, thiab BSP, thiab txhawb nqa Kev sib txawv ntawm osteogenic [8]
Cistanche tubulosa pab cov pob txha
3.2. Mechanism uas polysaccharides inhibit osteoclast-mediated pob txha resorption
Pob txha resorption yog qhov tshwm sim ntawm kev sib cuam tshuam ntawm activated OC thiab cov pob txha matrix. Lub luag haujlwm ntawm OC hauv pob txha resorption suav nrog plaub theem: osteoclast adhesion thiab polarization, pob txha resorption microenvironment acidification, pob txha matrix degradation, thiab endocytosis thauj. Nyob rau hauv tus txheej txheem ntawm osteoclast adhesion thiab polarization, osteoclast precursors yog recruited rau saum npoo ntawm cov pob txha nyob rau hauv qhov kev txiav txim ntawm -integrin thiab sib txawv rau hauv OC stimulated los ntawm M-CSF, RANKL, thiab cytokines. Hauv cov txheej txheem no, cov txheej txheem hloov pauv thiab cytokines xws li IL-1 thiab IL-6 tuaj yeem txhawb kev sib txawv. Tom qab ntawd, OC tsim ib qho acidic microenvironment ntawm lub xov tooj ntawm tes thiab saum npoo ntawm cov pob txha [61] thiab mature OCs secrete ntau yam enzymes, xws li protein kinase K, matrix metalloproteinases (MMPs), thiab tartrate-resistant acid phosphatase [62] kom degrade. pob txha matrix. Cov txheej txheem ntawm osteoclast-mediated pob txha resorption thiab polysaccharide kev cai ntawm OC muaj nuj nqi uas koom nrog hauv peb cov kev tshawb fawb tau qhia hauv Fig. 1 thiab 2.
3.2.1. Transcription yam
Qhov sib txawv ntawm OC yog tswj hwm los ntawm ntau yam kev hloov pauv. Thaum lub sij hawm osteoclastogenesis, NFATc1, uas belongs rau NFAT transcription superfamily, feem ntau tau txais los ua ib qho tseem ceeb transcription yam uas tswj RANKL-induced osteoclastogenic noob qhia [63]. NFATc1 yog cov khoom siv hluav taws xob sab saud uas ua lub luag haujlwm tseem ceeb hauv kev tswj cov kev qhia ntawm ntau yam osteoclast-specific genes [64], xws li tartrate-resistant acid phosphatase (TRAP), 3- integrin, cathepsin K (Ctsk), thiab MMP-9, uas koom nrog kev tswj hwm ntawm kev sib txawv ntawm osteoclast, fusion, thiab ua kom muaj zog. Lub caij no, Ctsk thiab MMP-9 degrade cov organic pob txha matrix thiab ua rau cov pob txha resorptive kev ua haujlwm [65].
Ib qho kev tshawb fawb hauv vivo tau pom tias WSS25 (GAP) tuaj yeem cuam tshuam kev sib txawv ntawm osteoclastic thaum ntxov thiab inhibit qhov kev qhia ntawm osteoclast tsim tshwj xeeb cov noob TRAP, NFATc1, MMP-9, thiab CtsK hauv RANKL-induced RAW264.7 hlwb. Yuav ua li cas ua noj nyob rau hauv lub qhov cub [29] Kev tshawb fawb ntxiv pom tias cov txheej txheem molecular ntawm WSS25 hauv kev tsim osteoclast yog los ntawm inhibition ntawm kev qhia ntawm BMP2 / Smad1 txoj kev [29]. RPP down-regulated osteoclastic kev ua si nyob rau hauv ib koob tshuaj-nyob ntawm seb, nrog rau kev txo qis ntawm TRAP, MMP-9, CtsK, thiab NFATc1 hauv RANKL-induced RAW264.7 hlwb [66]. Tsis tas li ntawd, RPP down-regulated miR-1224 kev qhia thiab lub hom phiaj tseem ceeb molecule Limd1 hauv Hippo signaling pathway nyob rau hauv cov pob txha pob txha-derived macrophages (BMMs) [67]. Tsis tas li ntawd, ib qho kev tshawb nrhiav hauv vitro tau pom tias CDP inhibited RANKL-induced osteoclast txawv ntawm BMMs thiab suppressed osteoclast fusion los ntawm inhibiting hydroxyapatite resorption kev ua thiab downregulating osteoclast marker mRNA qib ntawm NFATC1, MMP9, Ctsk, thiab TRAP [19]. Lwm txoj kev tshawb fawb tau tshaj tawm tias RPP kuj tau txo qis cov kev qhia ntawm cov noob tshwj xeeb, suav nrog TRAP, MMP-9, CtsK, thiab NFATc1, thaum lub sijhawm tsim OC [66].
3.3.2. OPG/RANKL/RANK signaling txoj kev
OPG / RANKL / RANK axis system yog qhov tseem ceeb hauv kev tswj hwm kev sib txawv ntawm cov pob txha thiab pob txha resorption [68]. Qib, tseem hu ua TNFR superfamily tus tswv cuab 11a, ua lub luag haujlwm tseem ceeb hauv osteoclastogenesis. RANKL khi rau qeb duas thiab ntxiv cov neeg ua haujlwm TNFR-txog yam tseem ceeb los pib cov kev taw qhia qis qis, suav nrog p38, JNK, thiab ERK. Qhov kawg tshwm sim ntawm RANKL-RANK signaling yog ua kom cov osteoclast transcription yam xws li NF-κB, activator protein 1 (AP- 1), cyclic adenosine monophosphate teb cov ntsiab lus-binding protein (CREB), thiab activated t-nuclear. yam khoom-1 (NFATc1), txhua yam uas ua rau muaj kev qhia ntawm cov cim osteoclast, xws li TRAP, 3 integrin, thiab CtsK [69]. OPG yog ib tug tswv cuab ntawm TNF receptor superfamily thiab tseem hu ua osteoclastogenesis inhibitory factor (OCIF), uas tuaj yeem sib tw antagonize RANKL, yog li inhibiting qhov sib txawv ntawm OC [70].
ACP koob tshuaj-raws li nce cov pob txha tsim cov cim ntawm serum OC thiab BAP thiab txo cov pob txha resorption cov cim ntawm cov ntshav TPACP5b, NTX, thiab CTX hauv OVX nas, thiab cov txheej txheem yuav cuam tshuam txog qhov nce ntawm OPG thiab RANK protein qhia hauv cov pob txha pob txha thiab txo qis ntawm RANKL qhia, yog li ua rau inhibition ntawm pob txha resorption [7]. Ntxiv mus, ACP inhibited RANKL-induced phosphorylation ntawm MAPK txoj kev [71]. CYP [15] nce qib ntshav ntawm OPG thiab txo RANKL thiab qhov piv ntawm RANKL / OPG hauv OVX osteoporosis qauv nas. ASP nce qib ntawm OPG, txo RANKL thiab qhov piv ntawm RANKL / OPG, thiab txo qis qib ntawm TNF- thiab IL-2, uas ua rau inhibition ntawm osteoclast sib txawv ua haujlwm [20,21].
3.3.3. ERK/JNK signaling pathway
ERK/JNK signaling pathway yog koom nrog hauv cell proliferation thiab sib txawv, thiab phosphorylation-activated ERK1/2 translocates los ntawm lub cytoplasm mus rau lub nucleus, uas kho cov transcriptional activation ntawm AP-1, c-Fos, thiab c-Jun thiab txhawb kev loj hlob thiab kev sib txawv ntawm OC. Kev tswj hwm qis ntawm p38, ERK, thiab JNK inhibited kev qhia ntawm NFAcT1 thiab c-Fos hauv RANKL-induced osteoclastogenesis. Kev kho mob nrog ERK lossis JNK inhibitors txo qis tus naj npawb ntawm OC thiab IL-6 ntau lawm [72]. Cov txheej txheem muaj peev xwm ntawm POP hauv osteoclastogenesis tau sib phim rau JNK thiab ERK cov kev taw qhia (txo ERK1/2 phosphorylation, STAT3, thiab JNK1/2 qhia) [34]. Txhawm rau kom paub meej tias kev kho mob zoo rau cov pob txha, ntxiv rau hauv vivo kev tshawb fawb yog tsim nyog.
3.3.4. Regulated inflammatory yam
Ntau yam inflammatory yam txhawb OC qhov sib txawv los ntawm kev sib kho RANKL qhia [73]. TNF- yog lub zog muaj zog ntawm cov pob txha resorption thiab ua lub luag haujlwm tseem ceeb hauv cov pob txha metabolism, uas tuaj yeem cuam tshuam ncaj qha rau kev tsim ntawm OC los ntawm precursors OC nyob rau hauv lub xub ntiag ntawm M-CSF los yog tsis muaj RANKL los ntawm activating NF-κB signaling [74] thiab induce RANK qhia hauv OC precursors [75]. Tus pro-inflammatory cytokine IL-1 yog lub zog stimulator ntawm OC sib txawv thiab pob txha resorption los ntawm inducing RANKL qhia [76]. IL-6 induces osteoclastogenesis thiab OC activation ntawm induction ntawm RANKL qhia hauv OB thiab stromal hlwb [77].
Zhu et al. pom tias MOP txo cov ntshav IL-6 thiab TNF- qhia qib [10]. Ren et al. qhia tias LYP kev tswj hwm rau 90 hnub txo qis IL-6 cov ntsiab lus hauv cov ntshav qab zib [78]. ASP muaj kev tiv thaiv cov pob txha poob hauv OVX nas los ntawm kev txo qis ntawm TNF- thiab inhibiting osteoclastogenesis [20]. Tom qab kev kho mob nrog ASP, kev txhim kho qib ntawm TNF- thiab IL-2 tau txo qis hauv dexamethasone-induced osteoporosis nas qauv, thiab cov tshuaj tiv thaiv kab mob cuam tshuam nrog kev tswj cov hnyuv [21]. SA Polysaccharide (SAP) kev tswj hwm rau 70 hnub ua rau txo qis cov ntshav ntawm IL-6 thiab TNF- [30,31]. Lwm tus tau tshaj tawm tias RPP tuaj yeem cuam tshuam cov pob txha resorption los ntawm kev txo cov ntsiab lus ntawm TRAPa thiab ntshav IL-1, IL{19}}, thiab TNF- hauv cov nas osteoporotic [25,27].
Cistanche tubulosa anti-osteoporosis
4. Cov lus xaus
Hauv kev xaus, hauv vivo, thiab hauv vitro kev sim tau pom tias polysaccharides tam sim no muaj zog rau kev kho mob postmenopausal osteoporosis, senile osteoporosis, thiab glucocorticoid-induced secondary osteoporosis, tshwj xeeb tshaj yog postmenopausal osteoporosis, los ntawm kev txhawb nqa OBi kev sib txawv thiab kev ua ub no thiab kev ua haujlwm OC. Cov txheej txheem los ntawm polysaccharides txhim kho pob txha homeostasis suav nrog feem ntau Wnt / -catenin signaling pathway, BMP / SMAD / RUNX2 signaling pathway, OPG / RANKL / RANK signaling pathway, ERK / JNK signaling pathway, apoptosis pathway, thiab transcription factors. Qhov kev tshuaj xyuas no yuav muab kev nkag siab zoo ntawm cov tshuaj tiv thaiv osteoporotic ntawm polysaccharides thiab kev hloov kho ntawm cov kev taw qhia, uas yog qhov tseem ceeb rau kev muab cov txheej txheem theoretical ntawm polysaccharides rau kev siv tshuaj kho mob.
5. Kev cia siab yav tom ntej
Ntau qhov kev tshawb fawb tau qhia meej txog qhov muaj txiaj ntsig zoo ntawm polysaccharides ntawm kev mob pob txha hauv vitro thiab hauv vivo kev sim. Tam sim no, txawm hais tias tsis muaj kev tshawb fawb soj ntsuam tau qhia txog kev kho mob pob txha nrog polysaccharides los ntawm Suav tshuaj ntsuab, ntau cov kev siv tshuaj kho mob polysaccharides tau tshawb nrhiav thiab tshuaj xyuas hauv kev kho mob lwm yam kab mob, xws li qog nqaij hlav [79], Hom 2. Ntshav Qab Zib [80]. Ntawm lawv, Poria cocos polysaccharide, Astragali Radix polysaccharide, thiab Lycium chinense Miller polysaccharide tau pom zoo los ntawm CFDA ua raw khoom. Cov tshuaj suav tshuaj suav hais txog hauv daim ntawv no muaj keeb kwm ntev hauv kev kho mob ntawm cov pob txha kab mob, hauv vitro thiab hauv vivo kev sim kuj qhia tau tias cov polysaccharides muab rho tawm los ntawm cov tshuaj ntsuab no muaj kev cuam tshuam rau cov neeg mob pob txha. Yog li ntawd, peb txiav txim siab tias kev tshawb fawb soj ntsuam ntxiv kom paub meej tias lawv cov tshuaj tiv thaiv kab mob osteoporosis yuav pab txhawb kev tsim cov tshuaj suav tshuaj ntsuab polysaccharides rau hauv cov khoom noj lossis tshuaj.
Txawm li cas los xij, nyob rau hauv cov txheej txheem ntawm kev txhim kho polysaccharides los ntawm Suav tshuaj ntsuab tshuaj ntsuab, muaj ob peb lub ntsiab lus uas yuav tsum tau xav txog thiab kawm ntxiv. Ua ntej, polysaccharides muaj cov yam ntxwv ntawm qhov hnyav molecular loj thiab cov qauv nyuaj, kev tshawb fawb ntxiv los tshawb txog kev sib raug zoo ntawm cov dej num lom neeg ntawm polysaccharides thiab cov qauv tshuaj.
Tsis tas li ntawd, yuav tsum tau saib xyuas ntau ntxiv rau cov txiaj ntsig ntawm polysaccharides ntawm txoj hnyuv plab hnyuv. Polysaccharides yog sawv cev los ntawm lawv cov bioavailability tsawg, uas yog nyob ntawm degradation tshwm sim nyob rau theem ntawm thawj-pass metabolism thiab nqus los ntawm txoj hnyuv [81]. Ntau cov kev tshawb fawb tau pom tias kab mob plab hnyuv muaj feem cuam tshuam rau qhov tshwm sim thiab kev loj hlob ntawm osteoporosis [82–84]. Txawm hais tias thiab yuav ua li cas polysaccharides koom nrog hauv cov pob txha metabolism los ntawm kev tswj cov kab mob hauv plab tseem tsis paub meej thiab tuaj yeem nthuav tawm cov tswv yim tshiab polysaccharide rau kev kho mob pob txha.
Kev lees paub
Kev tshawb fawb ua haujlwm tau txais kev txhawb nqa nyiaj txiag los ntawm National Science Foundation of China (No. 82003977, 81803760, 82004022), Zhejiang Province Excellent Young Talents Fund Project of Traditional Chinese Medicine (No. 2020ZQ011), thiab Cov Haujlwm Tseem Ceeb ntawm Cov Tshuaj Hauv Suav Teb hauv Zhejiang Province (2018ZY003), Basic Public Welfare Research Program ntawm Zhejiang Province (LGF20H060006), Kev Kho Mob thiab Kev Noj Qab Haus Huv Science thiab Technology Program ntawm Zhejiang Province (2020KY507).
Suav tshuaj ntsuab tshuaj ntsuab --Cistanche, zoo rau kev tiv thaiv pob txha
Los ntawm: 'Cov txiaj ntsig thiab cov txheej txheem ntawm polysaccharides los ntawm Suav tshuaj ntsuab tshuaj tiv thaiv kab mob osteoporosis' los ntawmShan Shan Lei, et al.
---International Journal of Biological Macromolecules 193 (2021) 1996–2005
