Imiphumela ye-ginsenosides kuma-cytokines ku-organ fibrosis
I-TGF- 1 iyi-cytokine esebenza ngezinto eziningi enezici ze-fibrosis futhi iyisici esibalulekile ku-organ fibrosis. Ikhuthaza i-organ fibrosis ngokusheshisa ukufakwa kwe-ECM nokunciphisa ukuwohloka kwayo. I-Smad iyisici esikhulu sokudlulisa isignali ku-TGF- 1-encike ekusayineni. Ngaphezu kwalokho, ukufakwa kwe-ECM kudlala indima ebalulekile ekuthuthukisweni kwe-pulmonary fibrosis. I-ECM yehliswa kakhulu yi-MMP, kanti ukusebenza kahle kokucekelwa phansi kwe-MMP kwakulawulwa ikakhulukazi ama-MMP inhibitors. Ibhalansi phakathi kwe-MMP nama-tissue inhibitors e-metalloproteinase (TIMP) idlala indima ebalulekile ekwakhekeni kwe-organ fibrosis.
Kumodeli ye-cCL4-i-liver fibrosis eyenziwe, ama-metabolites anobuthi e-CCl4 enza amaseli e-Kupffer asebenze ukuze akhiphe ama-cytokines, afana ne-IL-1 ne-TNF- , futhi akhuthaze ukukhiqizwa kwe-TGF- . Hou et al. ithole ukuthi i-ginsenoside Rb1 inhibited liver fibrosis ngokwehlisa-ukulawula amazinga e-TNF- , Prostaglandin E2 (PGE2) kanye ne-TIMP-1 esibindi.
UGuan et al. ithole ukuthi i-ginsenoside Rg1 inganciphisa kakhulu amaprotheni kanye nezinkulumo ze-mRNA ze-TGF- 1, i-Smad 2 ne-Smad 3 ku-mouse lung fibrosis, futhi ithuthukise ngokuphawulekayo ukubonakaliswa kwe-Smad 7. Le miphumela iphakamisa ukuthi i-ginsenosides ingase ivimbele i-pulmonary fibrosis ngokuvimbela i-TGF{6}i-prolifegulating indlela futhi i-prolifeway i-prolife. ukufakwa kwe-ECM okungavamile. Yang et al. ithole ukuthi isamba se-ginsenosides singanciphisa kakhulu-ukulawulwa kwe-MMP2, MMP9 kanye ne-TIMP-1 isisho sephrotheni kumagundane e-pulmonary fibrosis, kanye nomphumela wokuvikela ku-bleomycin (BLM) -i-pulmonary fibrosis ebangelwa ihlobene nesistimu ye-MMP. Umsebenzi oyinhloko we-TIMP-1 ukulawula ukugcinwa kanye nomsebenzi we-MMP, futhi inkulumo yayo ikhula kakhulu ngokuqhubeka kwe-pulmonary fibrosis. Ukubonakaliswa kwe-MMP2 ne-MMP9 kuyathuthukiswa ngesikhathi sesigaba sokuvuvukala se-BLM-induced pulmonary fibrosis, okungase kube neqhaza ekubhujisweni kolwelwesi olungaphansi, ukuhlasela kwesikhala se-alveolar ngama-fibroblasts, kanye ne-pulmonary fibrosis.
Xu et al. ithole ukuthi i-ginsenoside Rg1 ingavimbela ngokuphawulekayo i-adriamycin{2}}ukwakheka kwe-autophagosome kanye nokunwetshwa kwe-endoplasmic reticulum. Uma kuqhathaniswa neqembu le-adriamycin, iqembu le-ginsenoside Rg1 lenziwe lasebenza i-transcription factor 6 (ATF6, inositol{7}}edinga i-enzyme 1 (IRE1), transcriptional intermediary factor1, Phosphorylated Ribosomal protein S6 kinase, phosphorylated Ribosomal protein S6{1SK, P3} c-U-Jun N{17}}i-terminal kinase 1, i-JNK1 ne-Beclin1, isisho se-glucose esilawulayo se-protein 78 (GRP78) sinyusiwe I-Rb1 ingalawula iphrotheni ebophezelayo ye-GTP (i-GTP ebopha iphrotheni, i-Rho{29}}ikhoyili ehlobene{30}}ikhoyili eyenza i-protein kinase (RHO{31}}ikhoyili ehlobene{32}}i-coil eyenza i-protein kinase, i-rho{33}}ikhoyili ehlobene{34}}ikhoyili eyenza i-protein{34}}i-coil eyenza i-protein kinase{3} ukwakha i-protein kinase, i-rho-ikhoyili ehlobene{38}}ikhoyili eyenza i-protein kinase ROCK (ROCK) kanye ne-PI3K/ mammalian Ithagethi ye-rapamycin (mTOR) ivimbela i-autophagy ye-rat cardiomyocyte ukuze idlale{40}}isenzo senhliziyo esiphikisayo{4}kunganciphisa ukuhluleka kwenhliziyo futhi{4}kungathuthukisa i-serum. imiphumela ye-isoproterenol{43}}eyenziwe i-myocardial fibrosis kanye nokwehluleka kwenhliziyo (okungenani ingxenye) ngokuvezwa kwe-Smad 3 kanye nohlobo lwe-collagen ye-I kuzicubu zenhliziyo, okuhlotshaniswa nokulawulwa kwendlela ye-TGF- 1/Smad 3.
Li et al. ithole ukuthi i-UUO ingaphromotha ukuvezwa kwe-TGF- 1 kanye ne-phosphorylated Smad 3 (P-smad 3) futhi ivimbe isisho se-Klotho (KL) ne-Smad 7, futhi lezi zinkulumo zibuyiselwe emuva ngemva kokusetshenziswa kwe-ginsenoside Rg1. Imiphumela iphakamisa ukuthi i-ginsenoside Rg1 ithuthukisa i-renal tubulointerstitial fibrosis ngokukhomba indlela ye-Klotho/TGF- 1/Smad, futhi le phethini yokuvikela isekela ukuthi kungenzeka ukusebenzisa i-ginsenoside Rg1 ukwelapha i-renal fibrosis ehambisana nokushoda kwe-Klotho. UZhou et al. usungule imodeli yegundane elinesifo sikashukela ngokuphakela-ushukela omningi kanye{14}}nokudla okunamafutha aphezulu okuhlanganiswe ne-STREptozotocin IP. Ukushintshashintsha kwe-hyperglycemia kungalimaza amangqamuzana e-mesangial futhi kuthuthukise i-apoptosis, kuyilapho ukungasebenzi kahle kwe-lipid metabolism kanye nokufakwa kwe-lipid okungavamile kungase kubangele i-hyperplasia ye-glomerular cell membrane kanye nokunqwabelana kancane kwe-ECM. Kutholakale ukuthi i-20(S) -i-ginsenoside Rg3 iphansi kakhulu{20}}ilawula ukubonakaliswa kwe-TGF- 1, NF-κB P65 ne-TNF{24}} ezinso. Imiphumela iphakamisa ukuthi i-20(S) -ginsenoside Rg3 ingase isetshenziswe ekwelapheni isifo sikashukela ngendlela entsha.
I-Fibrosis iyisici esivamile sezitho eziningi-zezifo okuhloswe ngazo, kodwa awukho umuthi owenelisayo wokwelapha okwamanje, futhi ukutholakala kwezinhlanganisela zomthofu ezisebenza kahle kakhulu, ubuthi obuphansi kanye nendlela ecacile yokulwa{1}}ne-fibrosis kube yisidingo esiphuthumayo somtholampilo. I-Ginsenosides inemiphumela ehlukahlukene yesayensi yemithi, efana ne-antioxidant, -eqeda ukuvuvukala,{4}}i-apoptotic ne-immune stimulation, njll. Umphumela wayo wokulwa{6}}ne-fibrosis uqinisekisiwe, kodwa indlela eyinhloko ehilelekile ayikacaci. Indlela ethile ye-ginsenoside's anti{8}}fibrosis idinga ukuhlolwa okwengeziwe.
I-Ginseng saponin yabuyekezwa kuleli phepha ngokwemibandela ye-anti-i-fibrosis mechanism, okuhlanganisa i-EMT evimbela ukusabela kokuvuvukala kanye neseli evimbelayo, ukuthuthukisa ukucindezelwa kwe-oxidative, ukuvimbela ukukhiqizwa kwe-collagen, ukulawula ukusho kwe-cytokine, njll., ukuze kuhlolwe indlela ye-anti{2}}fibrosis yokutholwa{3} kwesisekelo sokuhlolwa kwe-lead, kanye nokuhlinzeka{3} i-ginsenosides ocwaningweni lwezokwelapha inikeza isisekelo sethiyori.
