Cimifugin Ameliorates Lipotoxicity-Induced Hepatocyte Damage and Steatosis through TLR4/p38 MAPK- and SIRT1-Involved Pathways.
Wenwen YangLinwensi ZhuShanglei LaiQinchao DingTiantian XuRui GuoXiaobing DouHui ChaiZhiling YuSongtao LiPublished in: Oxidative medicine and cellular longevity (2022)
In brief, we demonstrate the protective effects of Cim against lipotoxicity-induced cell death and steatosis in hepatocytes. TLR4-regulated p38 MAPK and SIRT1 pathways are involved in Cim-protected hepatic lipotoxicity. Cim is a potential candidate for improving hepatic metabolic disorders mediated by lipotoxicity.
Keyphrases
- cell death
- oxidative stress
- diabetic rats
- high glucose
- drug induced
- liver injury
- toll like receptor
- inflammatory response
- insulin resistance
- immune response
- high fat diet
- ischemia reperfusion injury
- transcription factor
- endothelial cells
- type diabetes
- high fat diet induced
- metabolic syndrome
- nuclear factor
- cell proliferation