Ntu Ⅱ Molecular Mechanisms Thiab Therapeutic Potential Ntawm - Thiab -Asarone hauv Kev Kho Mob Neurological Disorders
Apr 27, 2023
Neuroprotective Effects ntawm - thiab -Asarone
Hauv kev tshawb fawb preclinical, - thiab -asarone qhia muaj zog neuroprotective kev ua ub no. Ntawm qib molecular, qhov kev tiv thaiv neuroprotection no tau raug ntaus nqi rau antioxidant, anti-neuroinflammatory, thiab antiapoptotic teebmeem ntawm - thiab -asarone, nrog rau lawv lub peev xwm los hloov ntau yam neuroprotective signaling pathways, xws li phosphatidylinositol -3-kinase (PI3K/ Akt), camp teb cov ntsiab lus-binding protein (CREB), mitogen-activated protein kinase (MAPK), neurotrophic factor (NTFs), thiab Kelch-zoo li ECH-associating protein 1 (Keap1)/nuclear factor erythroid factor 2- Related factor 2 (Nrf2)/antioxidant responsive element (ARE) axes. Cov teebmeem neuroprotective ntawm - thiab -asarone tau sau tseg hauv Table 1 thiab cov kev sib txawv uas - thiab -asarone siv cov teebmeem no tau tshuaj xyuas hauv qab no.
1. Cov teebmeem ntawm - thiab -Asarone ntawm Oxidative Stress
Kev ntxhov siab oxidative tshwm sim los ntawm qhov tsis sib xws ntawm kev tsim cov ROS thiab reactive nitrogen hom (RNS) thiab kev ua haujlwm ntawm kev tiv thaiv antioxidant. Oxidative stress tau txuam nrog cov kab mob thiab kev loj hlob ntawm ntau yam kab mob neurodegenerative, suav nrog AD thiab PD, thiab ua rau muaj kev puas tsuaj rau lwm yam paj hlwb (xws li, ischemic stroke thiab schizophrenia) [65,66]. Cov tshuaj tiv thaiv antioxidant neutralizes tsim cov dawb radicals ntau dhau los teb rau oxidative kev nyuaj siab, tiv thaiv cellular puas. Ntau yam nroj tsuag theem nrab metabolites nrog cov khoom antioxidant pom pom muaj txiaj ntsig zoo rau lub hlwb kev ua haujlwm thiab kev noj qab haus huv tag nrho hauv tib neeg [22,23]. Ob qho tib si hauv vitro thiab hauv vivo kev sim tau pom tias - thiab -asarone nthuav tawm cov khoom antioxidant. Cov kev ua si dawb-radical scavenging ntawm - thiab -asarone tau pom tias siv ntau yam hauv vitro antioxidant kev soj ntsuam, suav nrog 2, 2-diphenyl-1- picrylhydrazyl (DPPH) dawb radicals scavenging assay thiab txoj kev txo cov poov tshuaj ferricyanide. , thiab los ntawm kev saib xyuas cov qib ntawm hydroxyl radicals, superoxide, thiab lipid peroxidation [67-69]. Interestingly, - thiab -asarone kev kho mob tseem ceeb txhim kho catalase (CAT), superoxide dismutase (SOD), thiab glutathione (GSH) kev ua ub no thiab inhibited ntau dhau ntawm malondialdehyde (MDA), lactate dehydrogenase (LDH), thiab ROS, qhia tias - thiab -asarone tuaj yeem txhim kho enzymatic antioxidant tiv thaiv kab mob [67,70,71]. Ntxiv mus, -asarone pre-kev kho mob kuj tau pom los ua kom Nrf2 signaling txoj kev thiab nws downstream lub hom phiaj heme oxygenase -1 (HO-1), uas yog koom nyob rau hauv lub quenching ntawm ROS kom txo tau oxidative kev nyuaj siab [71 ]. Thaum me me cuam tshuam RNA (siRNA) tau siv los ua ntsiag to Nrf2, kev tiv thaiv ntawm -asarone raug txo, thiab H2O2-induced oxidative stress tau txhim kho hauv PC12 hlwb [71]. Tsis tas li ntawd, siv A-stimulated PC12 cell qauv, Meng li al. pom tias -asarone pretreatment tuaj yeem txhim kho cell viability thiab txo cov cell puas thiab apoptosis. -asarone kuj tseem tuaj yeem txo qis ROS thiab MDA, nce qib ntawm SOD, CAT, thiab GSH-PX, thiab txhawb kev qhia ntawm Nrf2 thiab HO-1 [72] (Daim duab 2).

Tsis ntev los no, Pages et al. [70] and Saki et al. [91] qhia txog kev nce qib ntawm cov lus qhia ntawm endogenous antioxidant enzymes SOD thiab glutathione peroxidase (GPx) nyob rau hauv lub hlwb ntawm nas thiab nas kho nrog - thiab -asarone piv nrog cov tsiaj tsis kho. Tsis tas li ntawd, -asarone kev kho mob txo qis cov lus teb oxidative kev ntxhov siab hauv lub hlwb ntawm tus qauv nas ntawm lub suab nrov vim kev ntxhov siab, ib qho kev cuam tshuam los ntawm kev nthuav tawm ntawm SOD, GPx, thiab CAT, ntxiv rau kev txhawb nqa ntawm lwm yam endogenous non-enzymatic antioxidant. molecules, xws li vitamin C, vitamin E, thiab GSH [92]. Ib yam li ntawd, -asarone kev kho mob nce acetylcholinesterase (AChE) kev ua haujlwm thiab normalized MDA thiab SOD qib hauv hippocampus thiab cerebral cortex ntawm AD-zoo li scopolamine-induced amnesic nas [76]. Lwm txoj kev tshawb fawb tau tshaj tawm tias -asarone kev tswj hwm txo qis lub hlwb thiab lub raum puas tsuaj los ntawm -radiation raug los ntawm kev rov ua kom cov tshuaj tiv thaiv antioxidant, xws li SOD, GPx, CAT, thiab GSH, thiab txo qis lipid peroxidation qib [93]. Yang et al. [83] pom tias -asarone supplementation tseem ceeb rov qab los ntawm GSH, glutathione reductase (GR), CAT, thiab glutathione S transferase (GST) qib thiab txo qis lipid peroxidation qib hauv hippocampus ntawm tus qauv nas ntawm ischemia vim los ntawm nruab nrab cerebral artery occlusion (MCAO ). Wang et al. [94] pom tau tias -asarone kev kho mob tuaj yeem txo qis MDA kev puas tsuaj thiab ua rau CAT thiab SOD cov dej num ntau ntxiv hauv cov qauv nas ntawm AD tsim los ntawm kev txhaj tshuaj intracerebroventricular ntawm A 1-42 ua ke nrog ischemia. Hauv cov qauv nas ntawm MCAO-induced ischemic stroke, -asarone kev kho mob tau qhib Nrf2/ARE cov kab mob ntsig txog cov protein, cov nyhuv uas tau cuam tshuam los ntawm Nrf2 inhibitor [31]. Cov kev tshawb pom no qhia tias cov tshuaj tiv thaiv antioxidant ntawm - thiab -asarone tuaj yeem pab txhawb rau lawv cov txiaj ntsig kho mob hauv kev kho cov kab mob neurological.

Nyem qhov no kom tau txaiscov teebmeem ntawm Cistanche
2. Cov teebmeem ntawm - thiab -Asarone ntawm Neuroprotective Signaling Pathways
Muaj ntau txoj hauv kev rau kev ciaj sia taus, xws li PI3K/Akt thiab extracellular signal-regulated kinase (ERK) 1/2, yog qhib los ntawm - thiab -asarone (Daim duab 2) [72,73]. Cov txheej txheem no ua lub luag haujlwm tseem ceeb hauv kev ua haujlwm ntawm tes, synaptic plasticity, thiab kev nco los ntawm kev hloov cov phosphorylation ntawm cov molecules thiab modulating noob qhia [95-97]. Oxidative stress ua rau MAPK cascades uas ua rau muaj kev ua kom muaj sia nyob p38 MAPKs, c-Jun N-terminal kinase (JNK), thiab ERK signaling pathways. Kev ua haujlwm ntawm ERK signaling suppresses txoj kev tuag-inducing complex tsim thiab boosts cell ciaj sia taus los ntawm upregulating cov anti-apoptotic proteins Bcl-xL thiab Bcl-2 thiab inhibiting Fas-mediated apoptosis [98].
Hauv vitro, cov txiaj ntsig tau sau ntau xyoo tau pom tias - thiab -asarone qhib PI3K / Akt / Nrf2 thiab protein kinase A (PKA) cov cim qhia txoj hauv kev, uas ua lub luag haujlwm tseem ceeb hauv kev tiv thaiv cov hlwb tiv thaiv qib ROS txawv txav thiab kev puas tsuaj rau neuronal, thiab. raws li kev txhim kho cell viability thiab neuroprotective muaj nuj nqi [43,72,73]. Hauv A -kho PC12 hlwb, kev kho ua ntej nrog -asarone nce cell viability thiab txo cell apoptosis [88]. Cov nyhuv tiv thaiv ntawm -asarone tiv thaiv -amyloid-induced neurotoxicity yog ib nrab kho los ntawm inhibition ntawm A -induced JNK ua kom. Tsis tas li ntawd, -asarone tau txo qis A -induced downregulation ntawm Bcl-w thiab Bcl-xL thiab inhibited mitochondrial cytochrome C tso tawm thiab ua kom cov caspase -3 [88]. Nyob rau hauv thawj kab lis kev cai nas astrocytes thiab SH-SY5Y hlwb, - thiab -asarone upregulated Akt signaling thiab tiv thaiv hlwb los ntawm oxidative kev nyuaj siab, ib tug tshwm sim uas tau pom tias yuav tsum tau kho los ntawm scavenging ntawm ROS tsim thiab stimulation ntawm Nrf2- YOG tus kheej tiv thaiv tus kheej, thiab tom qab ua rau kev nthuav tawm ntawm cov enzymes antioxidant, thiab nce qib ntawm anti-apoptotic protein Bcl -2 [73,82]. Lwm txoj kev tshawb fawb tsis ntev los no tau pom tias -asarone tiv thaiv cov hlwb los ntawm A 1–42-induced cytotoxicity thiab attenuates autophagy los ntawm kev ua kom lub Akt-mTOR signaling pathway, uas tej zaum yuav koom nrog hauv neuroprotection ntawm -asarone tiv thaiv A toxicity hauv PC12 hlwb [ 99] ib. - thiab -asarone qhib tsis tau tsuas yog PI3K / Akt tab sis kuj ERK / CREB / BDNF txoj hauv kev hauv vivo thiab hauv vitro, uas pab txhim kho kev nco, tiv thaiv cov neurons, thiab rov qab coj tus cwj pwm hloov pauv nrog rau lub sijhawm tsis muaj zog, kev ua haujlwm hauv locomotor, thiab khiav tawm latency [77 90, 100, 101].

Cistanche ntsiav tshuaj
3. Cov teebmeem ntawm - thiab -Asarone ntawm Proteostasis, ER Stress, thiab Autophagy
Kev sib sau ntawm misfolded intracellular thiab extracellular protein aggregates yog ib qho tseem ceeb ntawm cov kab mob neurodegenerative pathogenesis [102-104]. Nyob rau hauv lub hlwb, ob peb haiv neeg cov proteins (A , tau, thiab -synuclein) tau txais kev hloov pauv vim yog cov caj ces thiab ib puag ncig [104]. Neurodegeneration tau cuam tshuam nrog kev hloov pauv thiab hloov pauv tsis zoo ntawm cov protein monomers, oligomers, thiab insoluble aggregates, tsim los ntawm kev hloov pauv-daim ntawv sib cuam tshuam, uas ua rau tsis ua haujlwm hauv cellular proteolytic txoj kev [105,106]. Pathogenic misfolded protein aggregation exerts cov teebmeem neurotoxic ntawm CNS, ua rau qhov tshwm sim neuronal cell tuag thiab kev loj hlob ntawm cov kab mob neurodegenerative [3,107]. Ntau txoj hauv kev kho mob rau cov kab mob neurodegenerative tau tsom kom txo qis qhov sib xyaw ntawm cov tshuaj lom oligomers, fibril deposits, thiab cov neeg sib sau ua ke [108,109]. Ntau qhov kev tshawb fawb tau qhia tias qee cov tshuaj phytochemicals tuaj yeem cuam tshuam cov amyloidogenic monomer synthesis thiab fibrillar aggregate tsim, txhim kho cov tsim ntawm nontoxic aggregates thiab stimulating lub proteolytic system rau lub hom phiaj neurotoxic pathogenic yam cuam tshuam nrog neuronal poob nyob rau hauv neurodegenerative kab mob [110,111].
Amyloidogenic A 1-42 peptides feem ntau yog tsim los ntawm kev sib cais ntawm amyloid precursor protein (APP) los ntawm - thiab -secretase [112]. Cov kev tshawb fawb tsis ntev los no tau pom tias - thiab -asarone inhibit qhov kev qhia ntawm -secretase BACE1, txhim kho kev txawj ntse thiab kev coj tus cwj pwm hauv cov qauv tsiaj ntawm AD [113,114]. Ib txoj kev tshawb fawb tsis ntev los no tau pom tias -asarone muaj peev xwm ua rau lub hom phiaj ntawm A thiab tau pathology los ntawm inhibiting A 42 aggregation, ntxiv rau inhibiting tau phosphorylation, ua rau kev txhim kho kev kawm kev nco hauv APP/presenilin-1 (PS1) transgenic nas [ 28] (Daim duab 3). Lwm txoj kev tshawb fawb pom tau hais tias kev kho mob nrog -asarone txo tus naj npawb ntawm cov plaques senile thiab txo qis A 40, A 42, thiab APP qhia qib hauv hippocampus ntawm APP / PS1 transgenic nas [85]. Tsis tas li ntawd, -asarone tau nthuav tawm cov txiaj ntsig kho mob tseem ceeb tiv thaiv cov protein ntau ntxiv thiab nce qhov kev qhia ntawm presynaptic protein synapsin 1 (SYN1), uas yuav tsum tshem tawm cov tshuaj lom superoxide anion radicals uas tsim hauv hlwb [114]. thioflavin T (ThT) fluorescence assay ua nyob rau hauv PC12 hlwb kho nrog - thiab -asarone pom ib tug npaum thiab koob-dependant txo nyob rau hauv A aggregation, tiv thaiv PC12 hlwb los ntawm A aggregate-induced toxicity [115] (Daim duab 3).

Presynaptic -synuclein aggregation yog suav tias yog thawj kab mob tshwm sim hauv kev loj hlob ntawm -synucleinopathies, xws li PD [103]. Loj -synuclein aggregates, cuam tshuam nrog qhov muaj qhov tsis zoo ntawm kev hloov pauv hauv -synuclein noob, suav nrog A30P, A53T, thiab E46K, tuaj yeem ua rau muaj kev phom sij los ntawm kev ua kom muaj zog oxidative, mitochondrial tsis ua haujlwm, hloov pauv cov qauv ntawm phosphorylation, thiab kev cuam tshuam nrog phosphoric membrane. 116] ib. Moloney et al. [117] pom tau tias kub poob siab protein 70 (HSP70) tiv thaiv dopaminergic neurons los ntawm protein aggregation thiab inhibits microglial activation, thaum kawg tiv thaiv apoptosis. Lub overexpression ntawm HSP70 exerts ib tug tiv thaiv tawm tsam thaum ntxov-pib -synuclein-induced pathology, raws li pom nyob rau hauv ib tug adeno-koom nrog tus kab mob qauv ntawm -synuclein aggregation [118]. -asarone kev kho mob kuj tau pom los txo cov dopaminergic cell tuag vim yog los ntawm 6-hydroxydopamine (6-OHDA) los ntawm kev tswj hwm ntawm HSP70 mRNA thiab cov qib protein qhia thiab txo qis ntawm -synuclein mRNA thiab cov qib qhia protein [ 29] (Daim duab 4). Tsis tas li ntawd, hauv SH-SY5Y hlwb hloov nrog -synuclein, -asarone kev kho mob tiv thaiv kev tuag ntawm tes los ntawm MPP ntxiv [119]. Hauv tus qauv nas, kev kho -asarone kuj tau siv cov tshuaj tiv thaiv neuroprotective tawm tsam 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD, tiv thaiv Qhov kev txo qis hauv tyrosine hydroxylase (TH)-cov hlwb zoo thiab nce-synuclein qhia ntau ntau, yog li tiv thaiv dopaminergic neurons hauv midbrains [119] (Daim duab 4).

Cov kab mob pathogenic cuam tshuam nrog cov kab mob neurodegenerative ua rau kev ua haujlwm tsis zoo hauv cov cellular proteolytic systems, suav nrog ubiquitin-proteasome system (UPS) thiab txoj hauv kev autophagy-lysosome [120]. Misfolded thiab unfolded proteins raug txheeb xyuas los ntawm ubiquitination thiab tsom rau kev degradation los ntawm proteasome, thiab UPS tsis ua haujlwm tau cuam tshuam nrog kev sib sau ntawm misfolded proteins hauv PD, txawm hais tias lub luag haujlwm tshwj xeeb ua los ntawm UPS hauv PD pathogenesis tseem tsis meej [121]. Kab mob tshwj xeeb cov protein aggregates uas loj dhau rau UPS, suav nrog A , tau, thiab -synuclein aggregates, ntxiv rau cov kab mob puas, xws li mitochondria, feem ntau yog tsom rau kev degradation los ntawm txoj kev autophagy-lysosome [105].

Cistanche ntxiv
Lub endoplasmic reticulum (ER) ua lub luag haujlwm tseem ceeb hauv kev ua kom zoo ntawm daim nyias nyias thiab tsis-cytoplasmic proteins [122–124]. Kev sib sau ntawm misfolded los yog unfolded proteins nyob rau hauv ER ua rau cellular stress thiab ua rau unfolded protein teb (UPR). Kev ua haujlwm ntev lossis ntau dhau UPR tuaj yeem ua rau tuag ntawm tes. UPR activation yog kho los ntawm peb ER stress sensors: protein kinase RNA-zoo li endoplasmic reticulum kinase (PERK), inositol-yuav tsum tau enzyme-1 (IRE1), thiab activating transcription factor 6 (ATF6) [122–124]. Cov piam thaj tswj cov protein GRP78 (tseem hu ua BiP) feem ntau tswj kev pib ntawm UPR los ntawm nws cov kev sib cuam tshuam ncaj qha nrog txhua lub teeb liab-transducing sensor [122,125]. Zoo li ATF6, ATF4 yog ib qho yooj yim leucine zipper (bZIP) cov ntaub ntawv tseem ceeb rau kev tswj hwm cov kab mob hauv lub cev los ntawm kev tswj hwm ntawm UPR-cov hom phiaj koom nrog hauv cov protein ntau folding, cov lus teb antioxidant, thiab amino acid biosynthesis thiab thauj. Ntxiv nrog rau kev txhawb nqa cov lus teb hloov pauv, ATF4 txhawb nqa bZIP cov ntaub ntawv hloov pauv C / EBP homologous protein (CHOP), uas txhawb nqa kev tuag ntawm tes [122,126]. Sib sau ua ke, UPR txoj hauv kev pab cuam kom tsis txhob muaj protein ntau biosynthesis, txhawb nqa cov protein degradation, thiab tsim cov chaperones kom rov ua cov protein tsis zoo.
ER kev ntxhov siab tau raug txheeb xyuas nyob rau hauv ntau qhov kev sim cellular qauv ntawm PD [127], thiab qhov kev nthuav qhia ntau ntxiv ntawm cov tsiaj qus-synuclein txaus los ua rau ER kev nyuaj siab [128]. ER, kev ntxhov siab yog ze ze rau oxidative kev nyuaj siab, uas tuaj yeem ua rau UPR ua kom [129]. Hauv 6- OHDA-induced PD qauv, -asarone kev kho mob txo qis mRNA qib ntawm GRP78 thiab CHOP, uas ua rau muaj kev cuam tshuam ntawm ob ntawm peb txoj kev ua kom UPR [130] (Daim duab 5). GRP78 nyiam khi unfolded los yog misfolded proteins nyob rau hauv ER, tso nws inhibitory tuav ntawm PERK, ATF6, thiab IRE1 [131]. Tsis tas li ntawd, -asarone kev kho mob tau pom tias txo qis kev qhia ntawm GRP78, phosphorylated PERK (p-PERK), thiab CHOP, tswj ER kev ntxhov siab thiab autophagy hauv ib qho 6-OHDA-induced nas qauv ntawm PD [132] (Daim duab 5). Interestingly, kev kho mob -asarone tiv thaiv 7-hydroxycholesterol-triggered macrophage apoptosis los ntawm alleviating ER stress-specific signalings, xws li caspase induction thiab CHOP activation [133]. Tsis tas li ntawd, -asarone kev kho mob txo qis kev mob ntev ntawm kev raug mob los ntawm ER kev ntxhov siab nyob rau hauv tus txha caj qaum, ntxiv rau txo qis microglial activation thiab alleviating neuropathic mob [134]. Hauv kev tshawb fawb hauv vitro tsis ntev los no, kev kho ua ntej nrog -asarone tiv thaiv hippocampal hlwb los ntawm oxidative thiab ER kev ntxhov siab los ntawm kev txo qis ROS ntau lawm thiab suppressing PERK signaling hauv glutamate- thiab tunicamycin-induced hippocampal HT22 hlwb [135].

Autophagy activation tuaj yeem txhim kho qhov kev tshem tawm ntawm cov protein sib sau ua ke, tiv thaiv kev puas tsuaj mitochondrial, tswj axon homeostasis thiab neurogenesis, ua kom lub cev muaj sia nyob, thiab txo qis kev loj hlob tsis txaus thiab ER kev ntxhov siab, nrog rau cov txiaj ntsig kho mob hauv kev ua kom qeeb ntawm cov kab mob pathological ntawm AD, PD, thiab lwm yam neurodegenerative. kab mob [136,137]. Beclin-1, phosphorylated (p)-Akt, thiab mammalian lub hom phiaj ntawm rapamycin (mTOR) yog cov paub txog autophagy regulators, thiab qee cov nroj tsuag muab los ntawm cov metabolites theem nrab tau pom tias siv cov teebmeem neuroprotective los ntawm kev txhawb nqa ntawm autophagy los ntawm ob qho tib si mTOR- kev ywj pheej thiab ywj siab mechanisms [138]. Hauv 6-OHDA-induced PD nas qauv, -asarone kev kho mob tau txo qis ntawm ob qho tib si mRNA thiab protein ntawm Beclin-1 thiab LC3B, thiab nce p62 qhia, qhia txog kev ua kom autophagy [29]. Lwm txoj kev tshawb nrhiav pom tias kev kho mob nrog -asarone txhim kho autophagy hauv macrophages los ntawm kev txhim kho autophagolysosomal tsim [139]. Ib qho kev txheeb xyuas kev sib raug zoo tsis ntev los no tau qhia tias -asarone kev kho mob tuaj yeem cuam tshuam kev sib sau ua ke los ntawm kev txhawb nqa ntawm autophagy hauv PC12 cell qauv ntawm AD [114]. Lwm qhov kev sim tau pom tias -asarone txo qis kev ua kom eIF2 -CHOP los ntawm 7 -hydroxycholesterol, txhim kho autophagy hauv macrophages los ntawm kev txhim kho ntawm autophagolysosomal tsim, nce phosphorylation ntawm Bcl-2, thiab txhawb kev nkag. ntawm Beclin{23}} rau hauv cov txheej txheem autophagic [139]. Cov kev tshawb pom no qhia tias - thiab -asarone tuaj yeem muaj peev xwm txo tau cov protein sib sau ua ke thiab ER kev ntxhov siab los ntawm kev hloov kho autophagy, Antioxidants uas tuaj yeem muaj kev tswj xyuas cov kab mob neurodegenerative.

Standardized Cistanche
Cistanche extract yuav pab txhim kho lub hlwb puas?
Cistanche extract, tseem hu ua Rou Cong Rong hauv cov tshuaj suav tshuaj, yog cov tshuaj ntsuab nrov uas paub txog nws cov txiaj ntsig kev noj qab haus huv. Nws yog muab los ntawm cov nroj tsuag Cistanche, uas feem ntau pom nyob rau hauv Tuam Tshoj thiab lwm qhov chaw ntawm Central Asia. Cov tshuaj ntsuab tau ib txwm siv rau ntau pua xyoo los txhim kho txiv neej kev ua haujlwm ntawm kev sib deev thiab muab kev pab ntawm qee yam mob. Cov kev tshawb fawb tsis ntev los no tau pom tias Cistanche extract plays lub luag haujlwm tseem ceeb hauv kev txhim kho lub hlwb. Kab lus no yuav tham txog yuav ua li cas Cistanche extract tuaj yeem pab txhim kho lub hlwb.
Cistanche extract yog nplua nuj nyob rau hauv antioxidants thiab anti-inflammatory tebchaw uas ua lub luag haujlwm tseem ceeb hauv kev saib xyuas lub hlwb kom zoo. Cov kev tshawb fawb pom tau hais tias ntuj sib xyaws hauv Cistanche extract tuaj yeem pab txo qhov mob hauv lub hlwb, uas yog ib qho tseem ceeb rau kev loj hlob ntawm ntau yam kab mob neurological. Los ntawm kev txo qhov mob hauv lub hlwb, Cistanche extract tuaj yeem pab txhim kho kev nco, kev kawm, thiab kev txawj ntse.
Cov kev tshawb fawb kuj tau pom tias Cistanche extract tuaj yeem pab txhim kho lub hlwb. Qhov no yog qhov tseem ceeb vim tias lub paj hlwb xav tau cov khoom noj tsis tu ncua ntawm oxygen thiab cov as-ham kom ua haujlwm zoo. Kev ua haujlwm tsis zoo hauv lub hlwb tuaj yeem ua rau muaj ntau yam teeb meem kev paub, suav nrog kev nco tsis tau, kev nyuaj siab, thiab tsis nco qab. Los ntawm kev txhim kho lub hlwb ncig, Cistanche extract tuaj yeem pab txhim kho lub hlwb ua haujlwm, nco, thiab kev xav.
Lwm txoj hauv kev uas Cistanche extract tuaj yeem pab txhim kho lub hlwb tsis zoo yog los ntawm kev tsim cov paj hlwb loj hlob. Cov paj hlwb loj hlob ua lub luag haujlwm tseem ceeb hauv kev loj hlob, kev loj hlob, thiab kev saib xyuas cov paj hlwb hauv lub hlwb. Cov kev tshawb fawb tau pom tias cov khoom sib xyaw ntuj hauv Cistanche extract tuaj yeem pab txhawb kev tsim cov paj hlwb, uas tuaj yeem pab txhim kho lub hlwb ua haujlwm thiab txo qhov kev pheej hmoo ntawm ntau yam kab mob neurological.
Kev tshawb fawb kuj tau pom tias Cistanche extract tuaj yeem pab txo qis kev pheej hmoo ntawm cov kab mob neurodegenerative xws li Alzheimer's thiab Parkinson's disease. Lub ntuj tebchaw hauv Cistanche extract tuaj yeem pab tiv thaiv lub hlwb los ntawm kev puas tsuaj los ntawm cov dawb radicals, uas yog ib qho tseem ceeb rau kev loj hlob ntawm cov kab mob no. Los ntawm kev muab lub paj hlwb nrog cov tshuaj tiv thaiv, Cistanche extract tuaj yeem pab txo qis kev pheej hmoo ntawm kev tsim cov kab mob debilitating.
Hauv kev xaus, Cistanche extract yog cov tshuaj ntsuab zoo heev nrog ntau cov txiaj ntsig kev noj qab haus huv, suav nrog nws lub peev xwm los txhim kho lub hlwb. Lub ntuj tebchaw hauv Cistanche extract ua lub luag haujlwm tseem ceeb hauv kev txhim kho lub hlwb kev ua haujlwm, kev nco, thiab kev xav, thiab txo qis kev pheej hmoo ntawm ntau yam kab mob neurological. Nws yog ib qho tseem ceeb uas yuav tau sab laj nrog ib tus kws kho mob ua ntej qhia txog cov tshuaj ntxiv rau kev noj qab haus huv.
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Rengasamy Balakrishnan 1,2, Duk-Yeon Cho 1, In-Su Kim 2, Sang-Ho Seol 3 thiab Dong-Kug Choi 1,2
1. Department of Applied Life Science, Graduate School, BK21 Program, Konkuk University, Chungju 27478, Kauslim; balakonkuk@kku.ac.kr (RB); whejrdus10@kku.ac.kr (D.-YC)
2. Department of Biotechnology, Research Institute of Inflammatory Disease (RID), College of Biomedical and Health Science, Konkuk University, Chungju 27478, Kauslim; kis5497@kku.ac.kr
3. Kev Tshawb Fawb thiab Kev Txhim Kho, Sinil Pharmaceutical Co., Ltd., Seongnam-si 13207, Kauslim; seol@sinilpharm.com






