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

藤黄果种子乙醇提取物通过调节氧化应激、炎症和脂质积累,减轻高糖高脂饮食/链脲佐菌素(HGHFD/STZ)诱导的糖尿病大鼠非酒精性脂肪肝。

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Abstract

OBJECTIVES: 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.

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