下调和上调
CD36
磷酸化
AKT1型
化学
激活剂(遗传学)
兴奋剂
脂质代谢
过氧化物酶体增殖物激活受体
内分泌学
内科学
药理学
生物化学
受体
医学
基因
蛋白激酶B
作者
Xiaotong Cai,Qin Zhang,Jiwei Wang,Yingying Miao,Yuqing Sun,Ziyin Xia,Luyong Zhang,Qinwei Yu,Zhenzhou Jiang
标识
DOI:10.1021/acs.chemrestox.4c00268
摘要
ZLY06 is a dual agonist of peroxisome proliferator-activated receptor (PPAR) δ/γ, showing potential therapeutic effects on metabolic syndrome. However, our research has revealed that ZLY06 exhibits hepatotoxicity in normal C57BL/6J mice, though the precise mechanism remains unclear. This study aims to investigate the manifestations and mechanisms of ZLY06-induced hepatotoxicity. We administered ZLY06 via oral gavage to C57BL/6J mice (once daily for six weeks) and monitored various indicators to preliminarily explore its hepatotoxicity. Additionally, we further investigate the specific mechanisms of ZLY06-induced hepatotoxicity using PPAR inhibitors (GW9662 and GSK0660) and the Protein kinase B (AKT) activator (SC79). Results showed that ZLY06 led to increased serum ALP, ALT and AST, as well as elevated liver index and hepatic lipid levels. There was upregulation in the gene and protein expression of lipid metabolism-related molecules
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