PDF(Pubmed)
Abstract：
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a significant hepatic condition that has gained worldwide attention. Kaempferol (Kae), renowned for its diverse biological activities, including anti-inflammatory, antioxidant, anti-aging, and cardio-protective properties, has emerged as a potential therapeutic candidate for non-alcoholic steatohepatitis (NASH). Despite its promising therapeutic potential, the precise underlying mechanism of Kae\'s beneficial effects in NASH remains unclear. Therefore, this study aims to clarify the mechanism by conducting comprehensive in vivo and in vitro experiments.
RESULTS: In this study, a murine model of non-alcoholic steatohepatitis (NASH) was established by feeding C57BL/6 female mice a high-fat diet for 12 weeks. Kaempferol (Kae) was investigated for its ability to modulate systemic inflammatory responses and lipid metabolism in this model (20 mg/kg per day). Notably, Kae significantly reduced the expression of NLRP3-ASC/TMS1-Caspase 3, a crucial mediator of liver tissue inflammation. Additionally, in a HepG2 cell model induced with palmitic acid/oleic acid (PA/OA) to mimic NASH conditions, Kae demonstrated the capacity to decrease lipid droplet accumulation and downregulate the expression of NLRP3-ASC/TMS1-Caspase 3 (20 µM and the final concentration to 20 nM). These findings suggest that Kae may hold therapeutic potential in the treatment of NASH by targeting inflammatory and metabolic pathways.
CONCLUSIONS: These findings suggest that kaempferol holds potential as a promising therapeutic intervention for ameliorating non-alcoholic fatty liver disease (NAFLD).
RESULTS: In this study, a murine model of non-alcoholic steatohepatitis (NASH) was established by feeding C57BL/6 female mice a high-fat diet for 12 weeks. Kaempferol (Kae) was investigated for its ability to modulate systemic inflammatory responses and lipid metabolism in this model (20 mg/kg per day). Notably, Kae significantly reduced the expression of NLRP3-ASC/TMS1-Caspase 3, a crucial mediator of liver tissue inflammation. Additionally, in a HepG2 cell model induced with palmitic acid/oleic acid (PA/OA) to mimic NASH conditions, Kae demonstrated the capacity to decrease lipid droplet accumulation and downregulate the expression of NLRP3-ASC/TMS1-Caspase 3 (20 µM and the final concentration to 20 nM). These findings suggest that Kae may hold therapeutic potential in the treatment of NASH by targeting inflammatory and metabolic pathways.
CONCLUSIONS: These findings suggest that kaempferol holds potential as a promising therapeutic intervention for ameliorating non-alcoholic fatty liver disease (NAFLD).
摘要：
背景：非酒精性脂肪性肝病（NAFLD）是一种重要的肝病，已引起全世界的关注。山奈酚（Kae），以其多样化的生物活动而闻名，包括消炎药,抗氧化剂，抗衰老,和心脏保护特性，已成为非酒精性脂肪性肝炎（NASH）的潜在治疗候选药物。尽管它有很好的治疗潜力，Kae对NASH有益作用的确切潜在机制尚不清楚。因此,本研究旨在通过进行全面的体内外实验来阐明其机制。
结果：在这项研究中，通过高脂饮食喂养C57BL/6雌性小鼠12周，建立了非酒精性脂肪性肝炎（NASH）的小鼠模型。研究山奈酚(Kae)在该模型中调节全身炎症反应和脂质代谢的能力(20mg/kg/天)。值得注意的是,Kae显着降低了NLRP3-ASC/TMS1-Caspase3的表达，后者是肝组织炎症的关键介质。此外,在用棕榈酸/油酸（PA/OA）诱导的HepG2细胞模型中模拟NASH条件，Kae表现出减少脂滴积累和下调NLRP3-ASC/TMS1-Caspase3表达的能力（20μM，终浓度为20nM）。这些发现表明Kae可能通过靶向炎症和代谢途径在NASH的治疗中具有治疗潜力。
结论：这些研究结果表明，山奈酚作为改善非酒精性脂肪性肝病（NAFLD）的一种有希望的治疗干预措施具有潜力。
结果：在这项研究中，通过高脂饮食喂养C57BL/6雌性小鼠12周，建立了非酒精性脂肪性肝炎（NASH）的小鼠模型。研究山奈酚(Kae)在该模型中调节全身炎症反应和脂质代谢的能力(20mg/kg/天)。值得注意的是,Kae显着降低了NLRP3-ASC/TMS1-Caspase3的表达，后者是肝组织炎症的关键介质。此外,在用棕榈酸/油酸（PA/OA）诱导的HepG2细胞模型中模拟NASH条件，Kae表现出减少脂滴积累和下调NLRP3-ASC/TMS1-Caspase3表达的能力（20μM，终浓度为20nM）。这些发现表明Kae可能通过靶向炎症和代谢途径在NASH的治疗中具有治疗潜力。
结论：这些研究结果表明，山奈酚作为改善非酒精性脂肪性肝病（NAFLD）的一种有希望的治疗干预措施具有潜力。
