Prostaglandins & other lipid mediators · 2025
Magnoflorine alleviates nonalcoholic fatty liver disease by modulating lipid metabolism, mitophagy and inflammation.
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Wang Liming, Yang Yan, Sun Haibing, Fei Mengxue
Аннотация
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a prevalent liver condition associated with metabolic syndrome, often aggravated by inflammation and mitochondrial dysfunction. This study aims to explore the therapeutic potential of magnoflorine, an alkaloid with known anti-inflammatory properties, in ameliorating NAFLD by modulating mitochondrial autophagy and inhibiting the NLRP3 inflammasome.
METHODS: Male C57BL/6 J mice were fed a high-fat diet (HFD) for 16 weeks to induce NAFLD. Magnoflorine (5 and 10 mg/kg) was administered by gavage daily for 16 weeks. Liver and serum samples were analyzed for lipid profiles, inflammation markers, and autophagy-related proteins, and liver histology was examined to assess changes.
RESULTS: Magnoflorine treatment improved dyslipidemia in NAFLD mice, shown by decreased serum triglycerides, total cholesterol, and LDL-C, and increased HDL-C. Histological analysis showed reduced hepatic steatosis and inflammation, with less lipid droplet accumulation and hepatocyte ballooning. Western blot results indicated upregulation of Parkin and PINK1, and downregulation of NLRP3, ASC, and caspase-1, with lower serum IL-1β levels, reflecting reduced inflammation.
CONCLUSIONS: Magnoflorine offers a promising approach for mitigating NAFLD progression through modulating mitochondrial autophagy and inhibiting inflammation.
METHODS: Male C57BL/6 J mice were fed a high-fat diet (HFD) for 16 weeks to induce NAFLD. Magnoflorine (5 and 10 mg/kg) was administered by gavage daily for 16 weeks. Liver and serum samples were analyzed for lipid profiles, inflammation markers, and autophagy-related proteins, and liver histology was examined to assess changes.
RESULTS: Magnoflorine treatment improved dyslipidemia in NAFLD mice, shown by decreased serum triglycerides, total cholesterol, and LDL-C, and increased HDL-C. Histological analysis showed reduced hepatic steatosis and inflammation, with less lipid droplet accumulation and hepatocyte ballooning. Western blot results indicated upregulation of Parkin and PINK1, and downregulation of NLRP3, ASC, and caspase-1, with lower serum IL-1β levels, reflecting reduced inflammation.
CONCLUSIONS: Magnoflorine offers a promising approach for mitigating NAFLD progression through modulating mitochondrial autophagy and inhibiting inflammation.