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首页> 外文期刊>Gut and Liver >Downregulation of GNAI3 Promotes the Pathogenesis of Methionine/Choline-Deficient Diet-Induced Nonalcoholic Fatty Liver Disease
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Downregulation of GNAI3 Promotes the Pathogenesis of Methionine/Choline-Deficient Diet-Induced Nonalcoholic Fatty Liver Disease

机译：GNai3的下调促进了蛋氨酸/胆碱缺乏饮食诱导的非酒精性脂肪肝病的发病机制

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Background/Aims The pathogenesis of nonalcoholic fatty liver disease (NAFLD) has not be fully elucidated, and the lack of therapeutic strategies for NAFLD is an urgent health problem. Guanine nucleotide binding protein, alpha inhibiting activity polypeptide 3 (GNAI3) participates in several biological processes, but its relationship with lipid metabolism and NAFLD has not yet been reported. We aimed to determine the function of GNAI3 in the development of NAFLD. Methods Mice were fed a methionine and choline-deficient diet to induce NAFLD. An NAFLD model in HepG2 cells was induced by free fatty acid treatment. GNAI3 levels in HepG2 cells were downregulated by shRNA. Protein levels of related proteins were evaluated by Western blotting, and mRNA levels were determined by quantitative reverse transcription polymerase chain reaction. Hematoxylin and eosin and Oil Red O staining were used to observe histological changes in liver tissue. Results The dysregulated hepatic lipid metabolism in the NAFLD mouse model was enhanced by GNAI3 knockout, which also provoked worse liver damage. In the NAFLD model in HepG2 cells, the downregulation of GNAI3 promoted cellular lipid accumulation and enhanced the changes in lipid metabolic enzyme levels. Conclusions This study demonstrates that GNAI3 participates in the development of NAFLD in both cellular and mouse models. The data indicate that GNAI3 is a potential new target for the treatment of NAFLD in humans.
机译：背景/旨在对非酒精性脂肪肝疾病（NAFLD）的发病机制尚未完全阐明，NAFLD缺乏治疗策略是一种紧迫的健康问题。鸟嘌呤核苷酸结合蛋白，α抑制活性多肽3（GNai3）参与几种生物过程，但尚未报告其与脂质代谢和NAFLD的关系。我们旨在确定GNai3在NAFLD发展中的功能。方法将小鼠喂养甲硫氨酸和胆碱缺乏饮食以诱导NAFLD。通过游离脂肪酸处理诱导HepG2细胞中的NAFLD模型。 HepG2细胞中的GNai3水平由shRNA下调。通过Western印迹评估相关蛋白质的蛋白质水平，通过定量逆转录聚合酶链反应测定mRNA水平。苏木辛和曙红和油红O染色用于观察肝组织中的组织学变化。结果GNAI3敲除增强了NAFLD小鼠模型中的失调肝脂质代谢，这也引发了肝脏损伤。在HepG2细胞的NAFLD模型中，GNAI3的下调促进了细胞脂质积累，增强了脂质代谢酶水平的变化。结论本研究表明，GNai3参与了蜂窝和小鼠模型中NAFLD的发育。数据表明，GNai3是人类治疗NAFLD的潜在新目标。

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