Zhang Xiangcheng, Shang Futai, Hui Liangliang, Zang Kui, Sun Gengyun
Anhui Medical University, Hefei 230032, China.
Department of ICU, Huai'an First People's Hospital, Huai'an 223300, China.
Saudi Pharm J. 2017 May;25(4):666-670. doi: 10.1016/j.jsps.2017.05.001. Epub 2017 May 10.
For patients who have sepsis, acute lung injury (ALI) causes most of death. Metformin (Met) is an anti-hyperglycemic agent and it has extensive pharmacological properties. This study aimed to analyze the influence of Met on lipopolysaccharide (LPS) -induced ALI. Met (1, 2, and 4 mg/kg) were injected and LPS was injected 30 min later. The data suggested Met can reduce release of inflammatory cytokines and bronchoalveolar lavage fluid (BALF) protein expression, reduce lung wet/dry ratio, and significantly improve LPS-induced lung destruction during ALI. In addition, Met inhibits LPS-induced neutrophil and macrophage infiltration, reduces MPO activity, and promotes AMPK-α1 expression in lung tissues. Our data suggested that metformin alleviates capillary injury during ALI via AMPK-α1.
对于患有败血症的患者，急性肺损伤（ALI）是导致死亡的主要原因。二甲双胍（Met）是一种抗高血糖药物，具有广泛的药理特性。本研究旨在分析Met对脂多糖（LPS）诱导的ALI的影响。注射Met（1、2和4mg/kg），30分钟后注射LPS。数据表明，Met可减少炎性细胞因子的释放和支气管肺泡灌洗液（BALF）蛋白表达，降低肺湿/干比，并显著改善ALI期间LPS诱导的肺损伤。此外，Met可抑制LPS诱导的中性粒细胞和巨噬细胞浸润，降低MPO活性，并促进肺组织中AMPK-α1的表达。我们的数据表明，二甲双胍通过AMPK-α1减轻ALI期间的毛细血管损伤。
