[Jianpi Qinghua Formula improves metabolic-associated fatty liver disease by modulating PGC1α/PPARα/CPT1A pathway].

Q3 Pharmacology, Toxicology and Pharmaceutics
Yan-Yan Xiao, Xu Han, Qing-Guang Chen, Jun-Fei Xu, Chi Chen, Fan Gong, Hao Lu
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引用次数: 0

Abstract

Based on the regulation of mitochondrial fatty acid β-oxidation through the PGC1α/PPARα/CPT1A pathway, this study investigated the effect of Jianpi Qinghua Formula on the mitochondrial fatty acid β-oxidation pathway in the livers of mice with metabolic-associated fatty liver disease(MAFLD) induced by a high-fat diet. MAFLD mice were fed a high-fat diet to establish the model, and after successful modeling, the mice were divided into the model group, the Jianpi Qinghua Formula group, and the metformin group, with an additional control group. Each group was treated with the corresponding drug or an equivalent volume of saline via gavage. Body mass and food intake were measured regularly during the experiment. At the end of the experiment, blood lipid levels and liver function-related indices were measured, liver pathological changes were observed, and protein expression levels of PGC1α, PPARα, PPARγ, and CPT1A were detected by Western blot. The results showed that, with no difference in food intake, compared to the model group, the body mass of the Jianpi Qinghua Formula group and the metformin group was reduced, liver weight and liver index decreased, and levels of cholesterol, triglycerides, and low-density lipoprotein cholesterol(LDL-C) were lowered. Additionally, a decrease in alanine aminotransferase(ALT) and aspartate aminotransferase(AST) was observed. Hematoxylin and eosin(HE) staining revealed reduced pathological damage to hepatocytes, while oil red O staining showed improvement in fatty infiltration. The liver disease activity score decreased, and transmission electron microscopy revealed improvement in mitochondrial swelling and restoration of internal cristae. Western blot analysis indicated that Jianpi Qinghua Formula significantly increased the expression of PGC1α, PPARα, and CPT1A proteins in the liver and reduced the expression of PPARγ. These results suggest that the Jianpi Qinghua Formula improves mitochondrial function, promotes fatty acid oxidation, and alleviates the pathological changes of MAFLD. In conclusion, Jianpi Qinghua Formula can improve MAFLD by mediating mitochondrial fatty acid β-oxidation through the PGC1α/PPARα/CPT1A pathway.

[健脾清华方通过调节PGC1α/PPARα/CPT1A通路改善代谢相关脂肪肝]。
本研究通过PGC1α/PPARα/CPT1A通路调控线粒体脂肪酸β-氧化,探讨健脾清化方对高脂饮食诱导代谢相关脂肪肝(MAFLD)小鼠肝脏线粒体脂肪酸β-氧化通路的影响。饲喂高脂饲料建立模型,造模成功后将小鼠分为模型组、健脾清化方组、二甲双胍组,另设对照组。各组给予相应药物或等量生理盐水灌胃。在实验期间定期测量体重和食物摄入量。实验结束时,检测大鼠血脂水平和肝功能相关指标,观察肝脏病理变化,Western blot检测PGC1α、PPARα、PPARγ、CPT1A蛋白表达水平。结果显示,在摄取量无差异的情况下,与模型组相比,健脾清化方组和二甲双胍组大鼠体重减轻,肝脏重量和肝脏指数降低,胆固醇、甘油三酯、低密度脂蛋白胆固醇(LDL-C)水平降低。此外,谷丙转氨酶(ALT)和天冬氨酸转氨酶(AST)降低。苏木精和伊红(HE)染色显示肝细胞病理损伤减轻,油红O染色显示脂肪浸润改善。肝脏疾病活动度评分下降,透射电镜显示线粒体肿胀改善,内嵴恢复。Western blot分析显示,健脾清化方显著提高肝脏PGC1α、PPARα和CPT1A蛋白的表达,降低PPARγ的表达。提示健脾清化方可改善线粒体功能,促进脂肪酸氧化,减轻MAFLD的病理改变。综上所述,健脾清华方可能通过PGC1α/PPARα/CPT1A途径介导线粒体脂肪酸β-氧化,从而改善mald。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Zhongguo Zhongyao Zazhi
Zhongguo Zhongyao Zazhi Pharmacology, Toxicology and Pharmaceutics-Pharmacology, Toxicology and Pharmaceutics (all)
CiteScore
1.50
自引率
0.00%
发文量
581
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