数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
研究问题
Although separate studies have documented the favorable effects of MET and ATO against MASLD, the therapeutic efficacy of their combination and the underlying mechanisms remain to be systematically explored.
方法
After heating at 60 °C for 30 min, the solution was filter-sterilized (0.22 μm), and the final pH was adjusted to pH 7.4.；To verify AMPK pathway involvement, an additional group was included, in which cells were pretreated with 10 μmol/L Compound C (Selleck, China) for 1 h before drug exposure (17).；Cell viability was calculated relative to the untreated cell control group (cells cultured in complete medium without drug intervention) using the following formula: cell viability (%) = [(A-sample – A-blank)/(A-control – A-blank)] × 100%, where A-sample is the absorbance of drug-treated cells, A-control is the absorbance of untreated cells, and A-blank is the absorbance of wells containing complete medium and CCK-8 reagent without cells.；[Animal experiments and experimental desi] SPF-grade male C57BL/6J mice, aged 6 weeks and purchased from Beijing SPF Biotechnology Co., Ltd., were kept in an environment with 22 ± 2 °C temperature, 55 ± 5% relative humidity, and a 12-hour light/dark photoperiod.
核心结论
All values are presented as mean ± SEM (n = 3). *P < 0.05, P < 0.01, *P < 0.001, **P < 0.0001. ‖ 结论**：In conclusion, this study demonstrates that combined MET and ATO effectively ameliorates hepatic lipid accumulation, metabolic dysfunction, and inflammation in experimental MASH, with superior efficacy over monotherapy.
局限
Because the spleen was not directly assessed in our study, this interpretation remains mechanistic and warrants further validation.；Additional measurements of fibrotic parameters in future work will enable a more complete evaluation of the combined MET and ATO intervention against MASLD-associated fibrosis.
对本项目的价值
★★★★☆ 代谢轴既干预敏感性最高，也是老药新用供给最充足的来源。命中核心 mTOR/AMPK；最大样本量约 24。
全文来源
PMC JATS 全文（正文 37,642 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Metformin and atorvastatin ameliorate MASH via the AMPK/NF-κB pathway.
- 期刊与标识：Front Endocrinol (Lausanne) · PMID 42935801 · DOI 10.3389/fendo.2026.1972846**
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写，依据已获取的期刊全文（方法、样本量与结论已回到原文核对）；未能获取全文的同批条目另行标注「摘要级」，全程未做任何数值推算补全。