Ethanol extract of Garcinia kola seeds alleviates HGHFD/STZ-induced nonalcoholic fatty liver disease in diabetic rats by modulating oxidative stress, inflammation, and lipid accumulation
نویسندگان
1 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
2 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
3 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
4 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
5 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
6 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
7 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
8 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
9 Department of Pharmaceutical Engineering and Pharmaceutical Chemistry, College of Chemical Engineering, Qingdao University of Science and Technology, Qingdao, 266042, China
doi
10.22038/ijbms.2025.82786.17889چکیده
Objective(s): To investigate the ameliorative effects of Garcinia kola ethanol extract (EGK) on type 2 diabetes mellitus (T2DM) combined with nonalcoholic fatty liver disease (NAFLD) and to explore its underlying mechanisms. Materials and Methods: In vivo, a T2DM rat model was established using HGHFD/STZ. In vitro, 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. Results: In vivo, EGK significantly reduced blood glucose levels (P<0.01), restored body weight (P<0.01), and improved liver LA, OS, and inflammatory levels (P<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 (P<0.01). In vitro, EGK markedly improved lipid accumulation, oxidative stress, and inflammation levels in HepG2 cells (P<0.01). Immunofluorescence and WB results showed that EGK significantly reduced the expression of the SREBP-1c pathway (P<0.01). Conclusion: EGK alleviates T2DM combined with NAFLD by reducing lipid accumulation through the inhibition of oxidative stress, inflammatory responses, and the SREBP-1c signaling pathway.
