Sun Xiaojing, Yuan Yanxiang, Xin Xianhao, Sun Ping, Sun Yunqi, Xie Mi, Wang Yuefei, Huang Shan, Li Bin
Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China.
National Key Laboratory of Chinese Medicine Modernization, State Key Laboratory of Component-based Chinese Medicine, Tianjin Key Laboratory of TCM Chemistry and Analysis, Tianjin University of Traditional Chinese Medicine, Tianjin, 301617, China.
Iran J Basic Med Sci. 2025;28(5):662-670. doi: 10.22038/ijbms.2025.82786.17889.
To investigate the ameliorative effects of ethanol extract (EGK) on type 2 diabetes mellitus (T2DM) combined with nonalcoholic fatty liver disease (NAFLD) and to explore its underlying mechanisms.
, a T2DM rat model was established using HGHFD/STZ. , HepG2 cells were induced with FFA to create a model of lipid accumulation. Lipid accumulation (LA), oxidative stress (OS) levels, and inflammatory markers were measured using kit methods. Additionally, the expression of the SREBP-1c pathway was detected by immunohistochemistry and western blot (WB) to further understand the potential mechanism of EGK's protective effect on diabetic liver injury.
, EGK significantly reduced blood glucose levels (<0.01), restored body weight (<0.01), and improved liver LA, OS, and inflammatory levels (<0.01) in diabetic rats. Histopathological results indicated that EGK effectively ameliorated diabetes-induced liver injury. Immunohistochemistry and WB results revealed that EGK significantly down-regulated the expression of the SREBP-1c pathway (<0.01). , EGK markedly improved lipid accumulation, oxidative stress, and inflammation levels in HepG2 cells (<0.01). Immunofluorescence and WB results showed that EGK significantly reduced the expression of the SREBP-1c pathway (<0.01).
EGK alleviates T2DM combined with NAFLD by reducing lipid accumulation through the inhibition of oxidative stress, inflammatory responses, and the SREBP-1c signaling pathway.
研究乙醇提取物(EGK)对2型糖尿病(T2DM)合并非酒精性脂肪性肝病(NAFLD)的改善作用,并探讨其潜在机制。
使用HGHFD/STZ建立T2DM大鼠模型。用游离脂肪酸(FFA)诱导HepG2细胞以建立脂质蓄积模型。采用试剂盒方法测量脂质蓄积(LA)、氧化应激(OS)水平和炎症标志物。此外,通过免疫组织化学和蛋白质印迹法(WB)检测固醇调节元件结合蛋白-1c(SREBP-1c)信号通路的表达,以进一步了解EGK对糖尿病性肝损伤保护作用的潜在机制。
EGK显著降低糖尿病大鼠的血糖水平(<0.01),恢复体重(<0.01),并改善肝脏的LA、OS和炎症水平(<0.01)。组织病理学结果表明,EGK有效改善了糖尿病引起的肝损伤。免疫组织化学和WB结果显示,EGK显著下调SREBP-1c信号通路的表达(<0.01)。EGK显著改善HepG2细胞中的脂质蓄积、氧化应激和炎症水平(<0.01)。免疫荧光和WB结果表明,EGK显著降低SREBP-1c信号通路的表达(<0.01)。
EGK通过抑制氧化应激、炎症反应和SREBP-1c信号通路来减少脂质蓄积,从而减轻T2DM合并NAFLD。