1. Ukuvimbela umphumela we-ginsenosides ekuphenduleni kokuvuvukala ku-organ fibrosis
Ngemva kokulimala kwesitho, amangqamuzana egazi amhlophe aqoqana endaweni yokulimala futhi ahehe ama-molecule anamathela ahlukahlukene, ama-monocyte nama-macrophages, akhiqize ngokweqile kwe-nitric oxide nama-cytokines avuthayo, futhi ekugcineni enze impendulo yokuvuvukala. Ukusabela kokuvuvukala okuqhubekayo kubangela ukuba i-fibrosis yakheke, iyenze ibe nzima kakhulu. Ngakho-ke, ukunciphisa ukuvuvukala kungenye yezindlela ezibalulekile zokuvimbela i-organ fibrosis.
Isifo sokusha kwesibindi kohlobo oluhlala njalo kanye ne-autoimmune hepatitis yizimbangela ezibalulekile zezifo ezingapheli ezivuvukalayo esibindini. Ucwaningo luye lwabonisa ukuthi ngokuqeda amagciwane (amagciwane) noma ukuvimbela izimpendulo zokuzivikela komzimba (ukwanda kwe-lymphocyte nokungena), imisebenzi yokuvuvukala ingacindezelwa ngokushesha nangokuqhubekayo, futhi inqubo ye-fibrosis ingamiswa noma ihlehliswe. I-Ginsenosides inomphumela omuhle wokuvimbela ukuvuvukala kwesifo sesibindi. U-Xiao et al. ithole ukuthi i-ginsenoside Rg1 ingadambisa i-steatosis yesibindi, inciphise okuqukethwe kwe-intracellular triacylglycerol, amazinga e-ALT ne-AST, futhi ivimbele ukukhululwa kwama-cytokines avuthayo. Umphumela ungase uhlobane ne-adenosine Monophosphate activated protein kinase (AMPK)/nuclear factor-κB (NF-κB) indlela yokusayina.
Ngemuva kokulimala kwezicubu zamaphaphu, ukusebenza kwama-macrophages kukhipha inani elikhulu lama-cytokines avuthayo, futhi ukwanda kwezici ezivuthayo kuzokwandisa i-pulmonary fibrosis ebangelwa ukuvuvukala kwezicubu zamaphaphu. U-Luo Wenjuan et al. ithole ukuthi i-ginsenoside Rb1 ingavimbela ngokuphawulekayo ukukhululwa kwe-tumor necrosis factor- (TNF-), i-interleukin-6 (IL-6), i-IL-1 nezinye izici ezivuthayo, ngaleyo ndlela kudambise ukuvuvukala kwamaphaphu. Ngaphezu kwalokho, uZhu Zhiyang et al. ithole ukuthi i-ginsenoside Rb1 ingavimbela i-PI3K/PROTEIN kinase B (PROTEIN kinase B, PI3K/PI3K) ngokuvimbela i-PI3K/PI3K. Indlela yokusayina ye-Akt ivikela ukuvuvukala kwe-cardiomyocyte eyenziwe yi-lipopolysaccharid.
Inhlanganisela ehlanzekile ye-CK etholakala ku-ginsenoside iyi-metabolite eyinhloko yamathumbu e-ginsenoside. I-CK ivimbela ukukhiqizwa{{1} kwama-cytokines avuthayo futhi yehlisa izinga lama-pro-ama-cytokine avuthayo ezicutshini zezinso ngokwehlisa-ukulawula indlela yokusayina ye-NF-κB. Ukuhlaziywa kokubonakaliswa kofuzo lwezinso ze-IL-1 , TNF- , Monocyte chemoattractant protein-1 (McP-1) kanye ne-IL-6 kubonise ukuthi i-CK ivimbele ukukhiqizwa kwalawa{19}}ama-cytokine avuthayo ezinsoni ezinesifo. I-oligomerizationdomain ebopha i-Nucleotide{32}}njengeprotheni yomndeni wama-receptor wesizinda se-Pyrin (i-NUCLEOtide ebopha i-oligomerizationDomain-like receptor umndeni we-Pyrin domain protein) iye yavinjelwa kakhulu 3, NLRP3) ukwenziwa kusebenze komzimba ovuvukalayo nokungenwa kwe-monocyte, kanye nokwehla kokulawulwa kokusebenza kwesiginali ye-NL3 ehlobene ne-renal. Hsu et al. ithole ukuthi umzimba ovuthayo we-NLRP3 wawuhlotshaniswa nokuvuvukala kwezinso kanye ne-fibrosis kumagundane ane-unilateral ureteral occlusion. I-CK ivimbele ukusebenza komzimba wokuvuvukala kwe-NLRP3 ngokunciphisa kakhulu umsebenzi we-NLRP3 kanye ne-caspase-1 kanye nezinga le-IL-1 lamaprotheni ezingeni lezinso nomchamo we-IL-1. Ukuvinjelwa kwemizimba evuthayo ye-NLRP3 kuma-macrophages kungase kukhiqizwe ngokuvimbela i-phosphorylated signal transduction erand Activator of transcription 3 (P-STAT3).
2. Imithelela ye-ginsenosides ku-EMT ku-organ fibrosis
I-EMT inqubo lapho amangqamuzana e-epithelial elahlekelwa khona i-cell polarity kanye nokunamathela kwamangqamuzana, athole izindawo zokufuduka kanye nokuhlasela, futhi abe amaseli e-mesenchymal. I-EMT iqala ukubonwa ngesikhathi se-embryogenesis futhi ibalulekile ekuthuthukiseni izicubu nezitho. I-EMT kanye nenqubo yayo ephambene idlala indima ebalulekile ekuqhubekeleni phambili kwesimila, ukuphulukiswa kwesilonda kanye ne-organ fibrosis.
Esibindini, amaseli e-epithelial angathola izakhiwo ze-fibroblast nge-EMT futhi abambe iqhaza ku-fibrogenesis. Lokhu kwenza i-EMT ibe enye yezinto ezingase ziqondiswe kumasu okulwa{1}}nezicubu ze-fibrosis. Ukuvimbela ukuthuthukiswa kwe-EMT kungalawula futhi kuhlehlise i-fibrosis yesibindi. Mayelana nokuthuthukisa i-liver fibrosis, i-ginsenoside Rg1 ingavimbela i-EMT ye-HSC-T6 cells in vitro, futhi imiphumela efanayo itholwe ku-vivo.
I-EMT futhi iyisinyathelo esibalulekile ku-pathogenesis ye-pulmonary fibrosis. I-TGF- 1 indlela yokusayina, njengeswishi eyinhloko ye-EMT, ilawula-i-emT-i-mediated pulmonary fibrosis nge-PI3K/Akt, Notch kanye nezindlela zokusayina ze-Wnt. UZhou Ping et al. ithole ukuthi ama-saponins aphelele e-Panax notoginseng anganciphisa okuqukethwe kwe-hydroxyproline acid kanye nokubonakaliswa kwe-TGF- 1 kumathishu amaphaphu, futhi abambe iqhaza ekwelapheni i-pulmonary fibrosis ngokuvimbela i-EMT. Kutholwe ukuthi i-ginsenoside Rg3 inganciphisa ukuhlasela komdlavuza wamaphaphu ngokuvimbela i-EMT, futhi i-20(R) -i-ginsenoside Rg3 ingathinta i-EMT yamaseli omdlavuza we-colorectal, ngaleyo ndlela iguqule izici zayo zomdlavuza.
I-Cardiac fibroblasts ngokwesiko kukholakala ukuthi isuselwa ekuhlukaniseni okuqondile kwamaseli e-embryonic mesenchymal. Kodwa-ke, ucwaningo lwakamuva luthole ukuthi ama-fibroblasts nawo angakhiqizwa ngesikhathi sokuguqulwa kusuka kumaseli e-endothelial kuya kumaseli e-stromal. Amaseli e-Endothelial abonisa ukuxhumana okuncishisiwe kwe-intercellular kanye nokuvezwa okuncishisiwe kwe-platelet endothelial cell-i-adhesion molecule-1 (PECAM-1/ CD31) ngaphansi kwezimo ze-pathological, nama-stem cells aphinde athole ikhono lokusabalala kanye ne-metastasized. Futhi omaka beseli be-mesenchymal baveze -njenge-actin yemisipha ebushelelezi (-}SMA). I-Ginsenoside Rb3 inganciphisa ukucindezeleka kwe-oxidative, ilungise umonakalo we-endothelial futhi ivikele umsebenzi we-myocardial. Yang et al. ithole ukuthi i-ginsenoside Rb3 ithinte i-EMT yamaseli e-cardiac microvascular endothelial ngemva kokutheleleka kwe-coxsackievirus B3 (CVB3). Amaleveli e-Proline-e-rich protein Tyrosine kinase 2 protein (Pyk2), PI3K, Akt ne-CD31 eqenjini le-ginsenoside Rb3 ayephezulu kunalawo akuqembu le-CVB3, kuyilapho izinga -SMA laliphansi. Imiphumela yabonisa ukuthi i-ginsenoside Rb3 ivimbele i-EMT yamaseli e-CMV epithelial ngemva kokutheleleka kwe-CVB3 ngokusebenzisa indlela yokusayina ye-Pyk2-PI3K-Akt.
Shi et al. ithole ukuthi i-ginsenoside Rg1 ivimbela i-EMT ku-nephropathy yesifo sikashukela i-rat podocyte ngokusebenzisa i-Glycogen Synthase kinase 3 beta (GSK3) / -indlela ye-catenin. I-autophagy ekhubazekile iholela ekulimaleni kwe-podocyte kanye ne-proteinuria, kuyilapho i-autophagy iqala ukulungisa ama-podocyte awonakele. I-Ginsenoside Rg1 ihlehlisa i-podocyte epithelial-inguquko ye-interstitial ngokusebenzisa i-autophagy, futhi yehlisa kakhulu i-renal fibrosis kanye ne-podocyte epithelial-inguquko yangaphakathi kumagundane anesifo sikashukela, okuphakamisa amandla ayo okwelapha e-nephropathy yesifo sikashukela nezinye izifo zeglomerular.
