Vitexin ameliorates GCDC-induced hepatocyte injury through SIRT۶ and JAK۲/STAT۳ pathways
- سال انتشار: 1400
- محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 24، شماره: 12
- کد COI اختصاصی: JR_IJBMS-24-12_013
- زبان مقاله: انگلیسی
- تعداد مشاهده: 234
نویسندگان
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
Department of Pediatric Surgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, ۰۵۰۰۰۰, China
چکیده
Objective(s): Vitexin, a natural flavonoid, is commonly found in many foods and traditional herbal medicines and has clear health benefits. However, the role of vitexin in cholestasis is presently unclear. This study investigated whether vitexin mitigated glycochenodeoxycholate (GCDC)-induced hepatocyte injury and further elucidated the underlying mechanisms.Materials and Methods: A cell counting kit-۸ (CCK-۸) assay was conducted to evaluate cell viability. The mitochondrial membrane potential (MMP, Δψm), reactive oxygen species (ROS) levels, and apoptosis rate of hepatocytes exposed to GCDC were detected by flow cytometry (FCM). We then measured the cytoprotective effects of vitexin against oxidative stress. The molecular signaling pathway was further investigated by using Western blotting and signaling pathway inhibitors.Results: Here, we showed that vitexin increased cell viability and reduced cell apoptosis, necroptosis, and oxidative stress in a dose-dependent manner in GCDC-treated hepatocytes. In addition, by using selective inhibitors, we further confirmed that inhibition of the JAK۲/STAT۳ pathway by vitexin was mediated by prolonged activation of Sirtuin ۶ (SIRT۶).Conclusion: Vitexin attenuated GCDC-induced hepatocyte injury via SIRT۶ and the JAK۲/STAT۳ pathways.کلیدواژه ها
Apoptosis, cholestasis, Glycochenodeoxycholic acid, Necroptosis, Oxidative stress, SIRT۶, Vitexinاطلاعات بیشتر در مورد COI
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