Ntu 2: Acteoside Counteracts Interleukin -1 -Induced Catabolic Processes Los ntawm Kev Hloov Kho Ntawm Mitogen-Activated Protein Kinases Thiab NFκB Cellular Signaling Pathway
Mar 05, 2022
Hu rau: Audrey Hu Whatsapp / hp: 0086 13880143964 Email:audrey.hu@wecistanche.com
Hyang I Lim , 1 Do Kyung Kim , 1 Tae-Hyeon Kim , 1 Kyeong-Rok Kang ,
Osteoarthritis (OA) yog cov kab mob uas feem ntau degenerative sib koom ua ke nrog mob pob qij txha uas tshwm sim los ntawm kev loj hlob ntawm cov pob txha mos ntawm cov pob qij txha ntawm cov pob qij txha.Acteoside, caffeoylphenylethanoid glycoside, muaj ntau yam kev ua ub no xws li tshuaj tua kab mob, tshuaj tiv thaiv kab mob, tshuaj tiv thaiv kab mob, tshuaj tiv thaiv oxidative, cytoprotective, thiab neuroprotective effective. Ntxiv mus, qhov ncauj tswj hwm ntawmacteosidentawm qhov ntau npaum li cas tsis ua rau genotoxicity. Yog li ntawd, lub hom phiaj ntawm txoj kev tshawb fawb tam sim no yog txhawm rau txheeb xyuas cov txiaj ntsig ntawm anticatabolicacteosidetiv thaiv osteoarthritis thiab nws cov anticatabolic signaling txoj kev.Acteosidetsis txo qis qhov ua tau zoo ntawm nas fibroblast L929 hlwb siv los ua cov hlwb qub thiab thawj cov nas chondrocytes. Acteoside tiv thaiv IL-1 -induced proteoglycan poob nyob rau hauv chondrocytes thiab pob txha pob txha pob txha los ntawm suppressing kev qhia thiab ua kom cov pob txha mos-degrading enzyme xws li matrix metalloproteinase- (MMP-) 13, MMP-1, thiab MMP -3. Tsis tas li ntawd, acteoside suppressed cov lus qhia ntawm inflammatory mediators xws li inducible nitric oxide synthase, cyclooxygenase-2, nitric oxide, thiab prostaglandin E2 nyob rau hauv thawj nas chondrocytes kho nrog IL-1 . Tom qab ntawd, kev qhia ntawm proinflammatory cytokines tau txo qis los ntawm acteoside hauv thawj nas chondrocytes kho nrog IL-1 . Ntxiv mus, acteoside suppressed tsis yog tsuas yog cov phosphorylation ntawm mitogen-activated protein kinases nyob rau hauv thawj nas chondrocytes kho nrog IL-1 tab sis kuj translocation ntawm NFκB los ntawm lub cytosol mus rau lub nucleus los ntawm suppression ntawm nws phosphorylation. Kev tswj hwm qhov ncauj ntawm 5 thiab 10mg / kg acteoside txo qis kev loj hlob ntawm cov pob txha pob txha hauv cov qauv nas osteoarthritic tsim los ntawm destabilization ntawm medial meniscus. Peb qhov kev tshawb pom qhia tias acteoside yog ib qho kev cog lus muaj peev xwm tiv thaiv kab mob los yog ntxiv kom txo qis lossis tiv thaiv kev loj hlob ntawm cov pob txha mos.
Pls nyem qhov no rov qab mus rau Ntu 1
4. Kev sib tham
Lub synovial (diarthrosis) sib koom ua ke yog ib qho kev sib koom ua ke ntawm lub cev uas muaj ntau hom ntaub so ntswg nyob ntawm qhov chaw muaj peev xwm ntawm cov pob txha kom tso cai rau kev txav mus los thiab kev ruaj ntseg ntawm lub cev los ntawm kev tawm tsam qhov sib txawv ntawm kev siv tshuab thauj khoom thiab tswj kev txav mus los [16] . Raws li cov neeg laus coob zuj zus tuaj thoob ntiaj teb, OA tau tshwm sim los ua tus kab mob degenerative cuam tshuam nrog cov teeb meem kev puas siab puas ntsws thiab kev lag luam uas yuav tsum tau daws sai sai [17]. Hmoov tsis zoo, tseem tsis tau muaj cov tshuaj zoo rau OA; Yog li ntawd, kev tiv thaiv ntawm articular pob txha mos degeneration yog qhov tseem ceeb tshaj plaws los tswj cov neeg kho tshuab kev sib koom ua ke nrog rau kev tso cai ntawm lub cev txav mus los thiab ruaj khov.
Feem ntau, cov pob txha synovial yog tsim los ntawm ob pob txha los muab kev ruaj ntseg thiab txhawb cov leeg nqaij los ntawm ligament thiab tendons thiab yog nyob ib puag ncig los ntawm cov pob txha pob txha pob txha uas muaj cov kua dej synovial los txo kev sib txhuam ntawm cov pob txha pob txha nyob rau ntawm cov pob txha pob txha. [16]. Tshwj xeeb tshaj yog, extracellular matrix (ECM) ntawm pob txha pob txha pob txha yog tsim los ntawm hom II collagen thiab proteoglycans uas yog synthesized thiab tswj los ntawm cov hlwb tshwj xeeb hu ua chondrocytes. Lub homeostasis ntawm articular pob txha mos yog qhov sib npaug ntawm anabolism (synthesis ntawm ECM) thiab catabolism (degeneration ntawm ECM) hauv cov pob qij txha synovial [18]. Feem ntau, catabolic yam xws li proinflammatory cytokines thiab inflammatory medicators induce the progressive degeneration of articular carti- lage los ntawm kev qhia cov pob txha-degrading enzymes xws li matrix metalloproteinase (MMPs) thiab metallopro- teinase nrog thrombos (AMPs) drocytes [18]. Yog li no, cov tswv yim biochemical tsis ntev los no los tiv thaiv lossis txo qis kev loj hlob ntawm cov pob txha mos ntawm pob txha pob txha tau tsom mus rau kev tawm tsam ntawm pob txha mos-degrading enzymes, proinflammatory cytokines, thiab inflammatory mediators raws li kev nyab xeeb ntawm cov kab mob mus ntev hauv cov pob qij txha syno-vial [19, 20] Cov kev tshawb fawb tsis ntev los no qhia tau hais tias cov khoom ntuj tsim los ntawm cov tshuaj ntsuab lossis cov tshuaj oriental, muaj kev nyab xeeb nyob rau lub sijhawm ntev, tiv thaiv kab mob, thiab cov tshuaj tiv thaiv oxidative thiab tuaj yeem txhawb kev noj qab haus huv thiab tswj OA los ntawm kev tawm tsam kev tso tawm ntawm proinflammatory cytokines [21].
cistanche extract: acteoside
Acteoside (hu ua verbascoside; C29H36O15) yog glycosides uas cais tawm ntawm cov paj lossis nplooj ntawm ntau cov nroj tsuag xws li Scrophularia ningpoensis,Cistanche deserticola, Digitalis purpurea, thiab Osmanthus fragrans [22, 23]. Tsis ntev los no, Henn et al. tau tshaj tawm tias cov concentration siab (100ug / mL) ntawm acteoside cais tawm ntawm nplooj ntawm Plantago australis tsis tau tsuas yog qhia tsawg cytotoxicity nyob rau hauv V79 Suav hamster hlwb siv raws li ib txwm cell tab sis kuj tsis muaj mutagenic los yog genotoxic kev ua ub no thiab phototoxic zog [6] . Tsis tas li ntawd, Perucatti et al. tau tshaj tawm tias nyob rau hauv vivo cytogenetic kuaj uas pub 5mg / kg acteoside rau luav (Oryctolagus cuniculus) rau 80 hnub qhia tsis muaj tshuaj lom nrog lwm yam mutagenic, ua rau tsis muaj cytotoxicity rau cov tsiaj [24]. Cov kev tshawb fawb no qhia tias acteoside yog cov khoom siv bio-active uas tuaj yeem siv rau hauv cov tsiaj thiab tib neeg noj [6, 24]. Raws li pom nyob rau hauv daim duab 2, zoo ib yam li cov kev tshawb fawb yav dhau los, 100μM (62.459ug / mL) acteoside tsis cuam tshuam rau kev muaj peev xwm ntawm nas fibroblast cell kab L929 siv los ua ib lub xov tooj ntawm tes thiab thawj nas chondrocytes hauv txoj kev tshawb no. Yog li, cov ntaub ntawv no qhia tau hais tias acteoside yuav muaj peev xwm ua kom muaj kev nyab xeeb thiab tuaj yeem siv los ua ib qho ntxiv. ECM, ntau txog li 98 feem pua ntawm cov pob txha mos, yog ib qho kev sib koom ua ke ntawm hyaluronan, proteoglycans, thiab hom II collagen [25]. Tshwj xeeb tshaj yog, proteoglycans yog cov proteins glycosylated nrog sulfated glycosaminoglycan los ua ib qho kev sib sau ua ke uas tsim kom muaj cov nqi hluav taws xob zoo li qub rau kev tawm tsam compressive rog thaum lub sijhawm ua haujlwm ntawm cov pob qij txha synovial [25]. Yog li ntawd, qhov poob ntawm proteoglycan nyob rau hauv cov pob txha pob txha pob txha ntawm cov pob qij txha synovial ua rau muaj kev tsis taus ntawm cov neeg kho tshuab kev ua haujlwm [25]. Degeneration ntawm pob txha mos pob txha vim qhov poob ntawm proteoglycan ua rau muaj kev tsis sib haum xeeb ntawm cov txheej txheem anabolic thiab catabolic. Yog li no, cov tswv yim bio-logical tsis ntev los no cuam tshuam nrog kev tsim kho ntawm pob txha pob txha thiab kev tiv thaiv lossis txo qis ntawm cov pob txha pob txha loj zuj zus yog xav txog kev nce ntawm cov txheej txheem anabolic los ntawm kev sib txuas ntawm cov pob txha pob txha loj xws li proteoglycan thiab hom II collagen thiab nce ntawm Cov txheej txheem anticatabolic tawm tsam catabolic yam xws li proinflammatory cytokines, cov kab mob sib kis, thiab catabolic loj hlob yam. Raws li pom hauv daim duab 3, acteoside tsis tsuas yog rov qab tau cov ntsiab lus proteoglycan los ntawm kev tawm tsam tawm tsam proinflammatory cytokine IL-1 -induced proteoglycan depletion nyob rau hauv thawj nas chondrocytes tab sis kuj suppressed proteoglycan poob nyob rau hauv articular pob txha mos cov ntaub so ntswg{IL 23}} rau 7 hnub. Muab ua ke, cov ntaub ntawv no qhia tsis tu ncua tias acteoside tuaj yeem tiv thaiv lossis txo qis kev loj hlob ntawm cov pob txha mos los ntawm kev tawm tsam rau cov txheej txheem cytokine-induced catabolic hauv cov pob txha mos ntawm cov pob txha synovial.
Cov pob txha mos-degrading enzymes suav nrog MMP-1, MMP-3, MMP-13, ADMITS-4, thiab ADAMTS-5 hauv cov kua dej synovial ntawm cov neeg mob OA yog cov enzymes tseem ceeb ua lub luag haujlwm rau kev loj hlob ntawm cov pob txha pob txha los ntawm kev degradation ntawm collagen thiab ECM cov khoom [26, 27]. Yog li ntawd, qhov inhibition ntawm MMP kev qhia thiab kev ua kom zoo li yog ib qho kev zoo nkauj kho kom zoo nkauj los tiv thaiv thiab txo qis kev loj hlob ntawm cov pob txha mos rau kev tswj xyuas qhov kev ua haujlwm ntawm cov pob qij txha synovial [26]. Hauv txoj kev tshawb fawb tam sim no, acteoside tau cuam tshuam cov lus qhia thiab ua kom cov pob txha mos-degrading enzyme hauv thawj nas chondrocytes kho nrog proinflammatory cytokine IL-1 raws li qhia hauv daim duab 4. Cov ntaub ntawv no qhia tau hais tias acteoside tuaj yeem txo qis kev loj hlob ntawm cov kab mob. articular pob txha mos los ntawm suppressing kev qhia thiab ua kom cov pob txha mos articular nyob rau hauv synovial sib koom nrog catabolic mob.
Cov kab mob sib kis xws li iNOS, NO, COX-2, thiab PGE2 yog qhov tseem ceeb rau OA pathogenesis [28]. Tshwj xeeb tshaj yog, proinflammatory cytokines xws li IL-1 thiab TNF upregulate zus tau tej cov NO thiab PGE2 los ntawm kev nce ntawm iNOS thiab COX2, feem, nyob rau hauv lub synovial sib koom nrog OA [29, 30]. Upregulated NO inhibits cov synthesis ntawm ECM Cheebtsam xws li hom II collagen thiab proteoglycan. Tsis tas li ntawd, nce PGE2 inhibits kev loj hlob ntawm chondrocytes thiab txo cov synthesis ntawm ECM [28]. Yog li, kev tawm tsam ntawm cov kab mob sib kis tuaj yeem ua rau txo qis kev loj hlob ntawm cov pob txha mos los ntawm kev cuam tshuam ntawm ECM txo qis hauv synovial sib koom nrog OA. Hauv txoj kev tshawb fawb tam sim no, acteoside tau ua kom muaj txiaj ntsig zoo rau kev tswj hwm ntawm inflammatory mediators raws li qhia hauv daim duab 5. Cov ntaub ntawv no qhia tsis tu ncua tias acteoside tuaj yeem txo qis kev loj hlob ntawm cov pob txha pob txha los ntawm kev tawm tsam ntawm inflammatory mediators hauv synovial sib koom nrog OA.
Ntxiv mus, qhov overexpression ntawm proinflammatory cytokines los ntawm inflamed synovium thiab chondrocytes yog ib tug loj txaus ntshai pathogenic yam nyob rau hauv OA pathogenesis. Tshwj xeeb tshaj yog, qhov kev qhia ntawm proinflammatory cytokine yog xav tias yog tsim los ntawm cov synovial membrane ntawm theem ntawm OA pib. Raws li txoj cai, cov cytokines txhawb nqa kev ua haujlwm chondrocytes los qhia lawv tus kheej qhia thiab ua ke cov pob txha mos-degrading enzymes, chemokines, thiab inflammatory mediators [31]. Yog li ntawd, kev tawm tsam ntawm proinflammatory cytokines tuaj yeem tiv thaiv OA thiab tuaj yeem txo qis kev loj hlob ntawm cov pob txha mos los ntawm kev cuam tshuam ntawm lwm cov cytokines proinflammatory cytokines, inflammatory mediators, thiab pob txha mos-degrading enzymes. Nyob rau hauv txoj kev tshawb no, acteoside suppressed zus tau tej cov proinflammatory cytokines xws li CINC-2, CINC-3, CNTF, fractalkine, IL-1, IL-1, leptin, MCP{ {7}}, MIP-3 , thiab -NGF hauv thawj nas chondrocytes kho nrog IL-1 piv nrog IL-1 ib leeg, raws li pom hauv daim duab 6.
Gouze et al. qhia tias CINC-2 tau nce ntxiv hauv chondrocytes kho nrog IL-1 zoo ib yam li peb txoj kev tshawb fawb [32]. Txawm li cas los xij, ib txoj kev tshawb fawb tsis ntev los no tau pom tias kev ua haujlwm ntawm tus txha caj qaum ntawm cov kev mob tshwm sim tau raug hloov pauv zoo thaum OA pathogenesis [33]. Hais txog kev mob pob qij txha, CINC-2 thiab CINC-3 tau ua kom muaj txiaj ntsig zoo nyob rau hauv tus txha caj qaum dorsal horn ntawm OA tsiaj uas tsim los ntawm kev txhaj tshuaj intra-articular ntawm monosodium iodoacetate rau hauv lub hauv caug pob qij txha [34, 35]. Txawm hais tias lub luag haujlwm pathophysiological ntawm CINC-2 thiab CINC-3 hauv OA pathogenesis tseem tsis tau paub ntau, cov kev tshawb fawb no qhia tau hais tias qhov kev qhia ntawm CINC-2 thiab CINC-3 nyob rau hauv tus txha caj qaum dorsal horn nyob rau hauv OA tej yam kev mob tej zaum yuav ze ze nrog kev loj hlob ntawm kev sib koom mob thaum lub sij hawm OA pathogenesis.
cistanche tshuaj ntsuab
CNTF, uas yog pluripotent neurotropic yam tseem ceeb thiab muaj feem xyuam nrog tsev neeg cytokine uas suav nrog IL-6, IL-11, leu-kemia inhibitory tsev neeg, thiab oncostatin, khi thiab cov cim los tswj cov pob txha homeostasis los ntawm gp130 corecep-tor subunit [36]. Txawm hais tias kev ua haujlwm lom neeg ntawm CNTF tseem tsis paub ntau hauv OA, cov kev tshawb fawb tsis ntev los no tau pom tias CNTF-gp130 teeb liab tuaj yeem cuam tshuam nrog kev kho pob txha pathologic pom tseeb hauv rheumatoid mob caj dab (RA), kab mob periodontal, spondyloarthropathies, thiab OA los ntawm kev tswj hwm qhov sib txawv thiab. Kev ua haujlwm ntawm osteoblast, osteo-oclast, thiab chondrocytes [36]. Tsis tas li ntawd, ib txoj kev tshawb fawb tsis ntev los no tau pom tias -NGF, qhov cuam tshuam rau neurotrophic cuam tshuam nrog kev tswj hwm lub cev ntawm cov hlwb neuronal, tau tswj hwm hauv cov ntshav thiab cov kua dej synovial hauv cov neeg mob OA [37]. Txawm li cas los xij, ntau qhov kev tshawb fawb tau tshaj tawm tias qhov thaiv ntawm NGF txo OA mob [38–40]. Yog li, neurotrophic yam tseem ceeb suav nrog CNTF thiab NGF tsis yog tsuas yog suav tias yog cov kab mob pheej hmoo ntawm OA kev loj hlob tab sis kuj tseem muab cov kev sib txuas ntawm cov paj hlwb ntawm cov pob txha mos ntawm cov pob txha mos thiab kev loj hlob ntawm OA mob. Tsis tas li ntawd, nws tau raug suav hais tias yog kev kho mob lub hom phiaj molecule los txo qhov mob OA mob ntev.
Fractalkine tseem hu ua chemokine CX3CL1 yog exuberantly qhia nyob rau hauv ob leeg neeg laus thiab nas articular chondrocytes kho nrog IL-1 [41, 42]. Cov kev tshawb fawb tsis ntev los no tau tshaj tawm tias fractalkine txhawb kev qhia ntawm MMP- 3 los ntawm CX3CR1, c-Raf, MEK, ERK, thiab NFκB cellular signaling pathways hauv cov ntaub so ntswg synovial tau los ntawm cov neeg mob OA [43]. Tsis tas li ntawd, genomic-wide DNA methylation tsom hauv OA chondrocytes tau qhia tias cov noob fractalkine tsis yog hypomethylated nkaus xwb tab sis kuj tseem cuam tshuam nrog nws cov mRNA qhia [44]. MCP-1, ib tug tswv cuab ntawm tsev neeg chemokine los ntxias cov kab mob, ua rau chemotaxis thiab transendothelial migration ntawm monocyte mus rau inflammatory lesion. Tsis ntev los no, Xu et al., tau tshaj tawm tias MCP-1 thiab chemokine (CC motif) receptor 2 axis koom nrog kev degradation ntawm pob txha pob txha los ntawm kev qhia ntawm MMP-13 thiab nce ntawm OA
chondrocyte apoptosis [45]. Tsis tas li ntawd, MIP-3 kuj hu ua chemokine CCL20 tau nthuav tawm ntau nyob rau hauv cov pob txha pob txha ntawm cov neeg mob uas muaj OA thiab ua rau cov pob txha pob txha loj zuj zus los ntawm kev qhia ntawm pob txha mos-degrading enzymes xws li MMP-1 thiab MMP -3, tus neeg nruab nrab ntawm tus kab mob kis xws li PGE2, thiab proinflammatory cytokine IL-6 [46]. Yog li ntawd, cov tshuaj chemokines xws li fractalkine, MCP-1, thiab MIP{10}} kuj tau raug suav hais tias yog ib qho kev pheej hmoo ntawm pathophysiological los pib qhov kev loj hlob ntawm OA.
Leptin yog peptide cov tshuaj hormones ntawm adipokines, uas yog cytokines secreted los ntawm cov ntaub so ntswg adipose [47]. Cov kev tshawb fawb tsis ntev los no tau tshaj tawm tias qib ntawm leptin tsis yog tsuas yog nce siab hauv tib neeg lub cev nrog kev rog, tab sis kuj nce ntxiv hauv cov ntshav thiab cov kua dej synovial sau los ntawm cov neeg mob OA uas cuam tshuam nrog OA hnyav [48]. Yog li, cov kev tshawb fawb tsis ntev los no tau qhia tias cov lus qhia ntawm leptin thiab nws cov receptor tau raug suav tias yog qhov muaj feem cuam tshuam nrog kev loj hlob ntawm OA [49–51]. [52]
IL-1 tsev neeg, suav nrog IL-1 thiab IL-1, yog suav tias yog qhov tseem ceeb tshaj plaws cytokine cuam tshuam nrog pathogenesis ntawm OA uas ua rau cov txheej txheem catabolic ua ke nrog lwm yam catabolic xws li kev laus, rog rog, thiab raug mob pob qij txha [53]. Feem ntau, theem ntawm IL-1 tsev neeg nyob rau hauv lub synovial uid, synovial membrane, articular pob txha, thiab cov pob txha subchondral yog siab nyob rau hauv lub synovial sib koom ntawm cov neeg mob OA [54]. Tom qab IL-1 tsev neeg khi rau lawv cov receptors, nws tshwm sim qhov kev loj hlob ntawm cov pob txha mos los ntawm kev qhia ntawm lwm cov cytokines, chemokines, adhesion molecules, inflammatory mediators, thiab pob txha-degrading enzymes los ntawm cov xov tooj ntawm tes phosphorylation. transcriptional yam xws li NFκB thiab MAPKs [54]. Raws li pom hauv daim duab 7, acteoside tsis tsuas yog txo cov phosphorylation ntawm ERK1/2, p38, thiab JNK tab sis kuj inhibited phosphorylation ntawm NFκB hauv thawj nas chondrocytes kho nrog IL-1 . Ntxiv mus, Daim duab 8 qhia tau hais tias acteoside inhibited qhov kev hloov ntawm NFκB los ntawm cytosol rau nucleus hauv thawj nas chondrocytes kho nrog IL-1 . Yog li, peb cov txiaj ntsig tsis tu ncua qhia tias acteoside tawm tsam IL-1 -induced catabolic cuam tshuam xws li kev qhia ntawm pob txha mos-degrading enzymes thiab tsim cov proinflammatory cytokines thiab inflammatory mediators los ntawm inactivation ntawm cellular signaling txoj kev thiab xws li NFκB hauv thawj nas chondrocytes. Tsis ntev los no, zoo ib yam li peb txoj kev tshawb fawb, Qiao li al. tau tshaj tawm tias acteoside inhibits inflammatory teb nyob rau hauv OA-induced tsiaj [55]. Lawv tau qhia txog kev tawm tsam ntawm cov kab mob cytokines los ntawm kev tsis ua haujlwm ntawm JAK / STAT teeb liab txoj hauv kev hauv cov ntaub so ntswg synovial ntawm DMM-induced OA tsiaj uas tau txais kev txhaj tshuaj intraperitoneal ntawm acteoside [55]. Txawm li cas los xij, txhawm rau kwv yees qhov ua tau zoo ntawm acteoside raws li kev tiv thaiv OA ntxiv, acteoside tau hais lus rau DMM-induced OA tsiaj hauv txoj kev tshawb no. Tom qab ntawd, qhov kev hloov pauv ntawm cov pob txha mos tau raug soj ntsuam raws li pom hauv daim duab 9. Peb qhov kev ntsuam xyuas histological tau pom tias kev tswj hwm ntawm qhov ncauj ntawm acteoside tsis tu ncua tiv thaiv qhov kev loj hlob ntawm cov pob txha mos los ntawm kev inhibition ntawm proteoglycan poob hauv DMM-induced OA tsiaj.
cistanche acteoside
5. Cov lus xaus
Peb qhov kev tshawb pom qhia tias acteoside muaj peev xwm tswj hwm qhov ncauj thiab tuaj yeem siv los ua cov tshuaj tiv thaiv zoo los tiv thaiv lossis txo qis OA raws li kev nyab xeeb lom neeg thiab cov tshuaj tiv thaiv kab mob tiv thaiv kab mob proinflammatory cytokines.
Cov ntaub ntawv
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