4.6 Article

JianPi-QingHua formula attenuates nonalcoholic fatty liver disease by regulating the AMPK/SIRT1/NF-κB pathway in high-fat-diet-fed C57BL/6 mice

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PHARMACEUTICAL BIOLOGY
卷 61, 期 1, 页码 647-656

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TAYLOR & FRANCIS LTD
DOI: 10.1080/13880209.2023.2188549

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NAFLD induced by HFD; hepatic lipid accumulation; hepatic inflammation

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A study on mice with NAFLD induced by a high-fat diet found that JianPi-QingHua formula (JPQH), a Chinese herbal formula, has a significant hepatoprotective effect. It can reduce body weight, adipose mass, blood glucose, and liver weight, as well as decrease the levels of serum triglycerides, cholesterol, and liver injury markers. In addition, JPQH can improve liver histopathological changes, reduce lipid accumulation, and suppress inflammatory responses. The study suggests that JPQH protects against HFD-induced NAFLD by regulating the SIRT1/AMPK/NF-kappa B pathway.
Context: Non-alcoholic fatty liver disease (NAFLD) is a common liver disease, accompanied by liver lipid accumulation and inflammation. JianPi-QingHua formula (JPQH), a Chinese herbal formula, exhibits effects on obesity and T2DM. However, the hepatoprotective effect of JPQH has not been elucidated. Objective: To investigate the hepatoprotective effect of JPQH in NAFLD induced by a high-fat diet (HFD) in mice. Materials and methods: C57BL/6J mice were divided into four groups and fed a normal-fat diet (ND), high-fat diet (HFD), HFDthornJPQH (2.5 g/kg), or HFDthornmetformin (300mg/kg) for 6 weeks, respectively. Furthermore, the body weight, epididymal fat mass, blood glucose, and liver weight were measured. Serum total cholesterol (TC), triglycerides (TG), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were performed. Hematoxylin and eosin staining and Oil Red O staining were observed in hepatic histopathological changes. Western blotting and quantitative real-time polymerase chain reaction were utilized to assess the key protein expression of hepatic lipid metabolism and inflammation. Results: Compared with the HFD group, JPQH could reduce body weight, epididymal fat mass, blood glucose and liver weight (p< 0.05), and markedly decreased the levels of serum TC, TG, ALT, AST (p< 0.05). Additionally, JPQH improved liver pathological changes. Consistent with the hepatic histological analysis, JPQH intervention suppressed lipid accumulation and inflammatory responses. Mechanistically, JPQH boosted SIRT1/AMPK signalling, and attenuated NF-kappa B pathway, which suppressed inflammatory responses. Discussion and conclusions: These findings indicate that JPQH supplementation protected against HFD-induced NAFLD by regulating SIRT1/AMPK/NF-kappa B pathway, which provides a theoretical basis for the clinical treatment of patients with NAFLD.

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