Cov teebmeem ntawm ginsenosides ntawm cytokines hauv lub cev fibrosis
TGF- 1 yog ib qho cytokine ntau yam uas muaj cov yam ntxwv ntawm fibrosis thiab yog ib qho tseem ceeb hauv lub cev fibrosis. Nws txhawb nqa lub cev fibrosis los ntawm kev ua kom lub cev tso tawm ntawm ECM thiab txo nws cov degradation. Smad yog ib qho tseem ceeb ntawm cov teeb liab hloov pauv hauv TGF- 1- nyob ntawm kev taw qhia. Tsis tas li ntawd, ECM deposition plays lub luag haujlwm tseem ceeb hauv kev txhim kho pulmonary fibrosis. ECM feem ntau yog degraded los ntawm MMP, thiab qhov degradation efficiency ntawm MMP yog tswj los ntawm MMP inhibitors. Qhov sib npaug ntawm MMP thiab cov ntaub so ntswg inhibitors ntawm metalloproteinase (TIMP) plays lub luag haujlwm tseem ceeb hauv kev tsim cov kab mob hauv nruab nrog cev.
Nyob rau hauv tus qauv ntawm cCL4-induced siab fibrosis, tshuaj lom metabolites ntawm CCl4 qhib Kupffer hlwb kom secrete cytokines, xws li IL-1 thiab TNF-, thiab txhawb zus tau tej cov TGF- . Hou et al. pom tias ginsenoside Rb1 inhibited daim siab fibrosis los ntawm down-regulating qib ntawm TNF- , Prostaglandin E2 (PGE2) thiab TIMP-1 nyob rau hauv daim siab.
Guan et al. pom tias ginsenoside Rg1 tuaj yeem txo qis cov protein thiab mRNA kev nthuav qhia ntawm TGF- 1, Smad 2 thiab Smad 3 hauv nas ntsws fibrosis, thiab txhim khu kev qha ntawm Smad 7. Cov txiaj ntsig no qhia tias ginsenosides tuaj yeem cuam tshuam pulmonary fibrosis los ntawm inhibiting. TGF- 1/Smad signaling pathway, yog li tswj cov fibroblast proliferation thiab txawv txav ECM deposition. Yang et al. pom tias tag nrho cov ginsenosides tuaj yeem txo qhov kev tswj hwm ntawm MMP2, MMP9 thiab TIMP-1 cov protein qhia hauv cov nas pulmonary fibrosis, thiab kev tiv thaiv ntawm bleomycin (BLM) -induced pulmonary fibrosis muaj feem xyuam rau MMP system. Lub luag haujlwm tseem ceeb ntawm TIMP-1 yog los tswj kev zais cia thiab kev ua haujlwm ntawm MMP, thiab nws cov lus qhia nce ntxiv nrog rau kev loj hlob ntawm pulmonary fibrosis. Qhov kev qhia ntawm MMP2 thiab MMP9 yog txhim kho thaum lub sij hawm inflammatory theem ntawm BLM-induced pulmonary fibrosis, uas yuav ua lub luag hauj lwm nyob rau hauv kev puas tsuaj ntawm lub hauv paus membrane, ntxeem tau ntawm alveolar qhov chaw los ntawm fibroblasts, thiab pulmonary fibrosis.
Xu et al. pom tias ginsenoside Rg1 tuaj yeem cuam tshuam rau adriamycin-induced autophagosome tsim thiab endoplasmic reticulum expansion. Piv nrog rau cov pab pawg adriamycin, ginsenoside Rg1 pab pawg tau txais txiaj ntsig transcription factor 6 (ATF6, inositol-requiring enzyme 1 (IRE1), transcriptional intermediary factor1, Phosphorylated Ribosomal protein S6 kinase, phosphorylated Ribosomal protein S6 kinase, p-P70. -terminal kinase 1, JNK1 thiab Beclin1, glucose regulatory protein 78 (GRP78) qhia tau nce. Cov txiaj ntsig no qhia tias ginsenoside Rg1 tuaj yeem txhim kho doxorubicin-induced cardiac dysfunction los ntawm inhibiting endoplasmic reticulum stress thiab autophagy. Zheng et alseno Rb. tswj me me GTP binding protein (GTP binding protein, Rho-txog coil-coil sib sau protein kinase (RHO-txog coil-coil sib sau protein kinase, rho-txog coil-coil sib sau protein kinase, rho-kho coil-coil sib sau protein kinase, rho-related coil-coil forming protein kinase ROCK (ROCK) thiab PI3K / mammalian Lub Hom Phiaj ntawm rapamycin (mTOR) txoj hauv kev inhibit autophagy ntawm nas cardiomyocytes ua si tiv thaiv lub plawv f ailure muaj nuj nqi. Tsis tas li ntawd, ginsenoside Re tuaj yeem txo cov ntshav TGF- 1 qhia thiab txhim kho cov tshuaj pharmacological ntawm isoproterenol-induced myocardial fibrosis thiab plawv tsis ua hauj lwm (tsawg kawg hauv ib feem) los ntawm kev qhia ntawm Smad 3 thiab hom I collagen hauv cov ntaub so ntswg plawv, cuam tshuam. nrog rau txoj cai ntawm TGF- 1/Smad 3 txoj kev.
Li et al. pom tias UUO tuaj yeem txhawb nqa qhov kev qhia ntawm TGF- 1 thiab phosphorylated Smad 3 (P-smad 3) thiab thaiv qhov kev qhia ntawm Klotho (KL) thiab Smad 7, thiab cov kab lus no tau thim rov qab tom qab ginsenoside Rg1 tau tswj hwm. Cov txiaj ntsig tau qhia tias ginsenoside Rg1 ameliorates lub raum tubulointerstitial fibrosis los ntawm kev tsom mus rau Klotho / TGF- 1/Smad txoj kev, thiab cov qauv tiv thaiv no txhawb kev siv ginsenoside Rg1 los kho lub raum fibrosis txuam nrog Klotho deficiency. Zhou et al. tsim kom muaj tus qauv nas ntshav qab zib los ntawm kev noj zaub mov muaj suab thaj thiab rog rog ua ke nrog STREptozotocin IP. Hyperglycemia hloov pauv tuaj yeem ua rau cov hlwb mesangial thiab txhawb kev apoptosis, thaum dysregulation ntawm lipid metabolism thiab txawv txav lipid deposition tuaj yeem ua rau hyperplasia ntawm glomerular cell membrane thiab maj mam nce ntawm ECM. Nws tau pom tias 20(S) -ginsenoside Rg3 txo qis- tswj kev qhia ntawm TGF- 1, NF-κB P65 thiab TNF- hauv ob lub raum. Cov txiaj ntsig tau qhia tias 20(S) -ginsenoside Rg3 tuaj yeem siv rau hauv kev kho mob ntshav qab zib nephropathy hauv kev taw qhia tshiab.
Fibrosis yog ib qho ntawm ntau yam kab mob hauv lub cev, tab sis tam sim no tsis muaj cov tshuaj kho mob txaus siab, thiab kev tshawb pom ntawm cov hmoov txhuas nrog kev ua haujlwm siab, tsis tshua muaj tshuaj lom thiab ntshiab anti-fibrosis mechanism yog qhov xav tau kev kho mob sai. Ginsenosides muaj ntau yam tshuaj, xws li antioxidant, anti-inflammatory, pro-apoptotic thiab kev tiv thaiv kab mob, thiab lwm yam. Nws cov nyhuv anti-fibrosis tau lees paub, tab sis lub hauv paus txheej txheem kev koom tes tseem tsis meej. Cov txheej txheem tshwj xeeb ntawm ginsenoside's anti-fibrosis xav tau kev soj ntsuam ntxiv.
Ginseng saponin tau tshuaj xyuas nyob rau hauv daim ntawv no hais txog kev tiv thaiv fibrosis mechanism, nrog rau EMT inhibiting inflammatory cov tshuaj tiv thaiv thiab inhibiting cell, txhim kho oxidative kev nyuaj siab, inhibiting collagen ntau lawm, regulating cytokine qhia, thiab lwm yam, rau txoj kev kawm ntawm lub mechanism ntawm anti-fibrosis. ntawm kev tshawb pom ntawm cov hmoov txhuas thiab muab cov kev sim hauv paus, rau kev tiv thaiv fibrosis ntawm ginsenosides rau hauv kev tshawb fawb tshuaj muab kev tshawb xav.
