Adiponectin attenuates lipopolysaccharide-induced cell injury of H9c2 cells by regulating AMPK pathway
Adiponectin attenuates lipopolysaccharide-induced cell injury of H9c2 cells by regulating AMPK pathway
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DOI：
10.1093/abbs/gmy162
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发表时间：
2019-02-01
影响因子：
3.7
通讯作者：
Su, Guohai
中科院分区：
文献类型：
--
作者：
Hao, Rui;Su, Guoying;Su, Guohai
脂联素是一种主要由脂肪组织合成和分泌的脂肪细胞因子，具有抗炎、抗凋亡等心脏保护作用。脂多糖（LPS）是一种常见的心肌细胞炎症和凋亡诱导剂。然而，脂联素对LPS诱导的H9 c2细胞炎症和凋亡的作用及其可能的机制尚未见报道。在本研究中，我们发现，脂联素显着减轻LPS诱导的细胞毒性，包括活力下降和LDH释放升高，抑制LPS引发的炎症反应，这是通过增加释放TNF-α，IL-1以及IL-6，并减弱由LPS引起的细胞凋亡率的增加以及caspase-3活性的增加。此外，我们的数据表明，脂联素上调AMP激活的蛋白激酶（AMPK）激活的H9 c2细胞与或没有LPS管理。此外，我们发现化合物c阻断AMPK通路减弱了脂联素对LPS引起的H9 c2细胞的细胞毒性、炎症反应和凋亡的保护作用。我们的观察为理解AMPK通路在脂联素对LPS诱导的心脏毒性的保护作用中的介导作用提供了新的见解。
Adiponectin, an adipokine synthesized and secreted majorly by adipose tissue, is reported to exert cardioprotective properties via anti-inflammation and antiapoptosis. Lipopolysaccharide (LPS) is a common inflammation and apoptosis inducer of cardiomyocytes. However, few studies have reported the roles of adiponectin on LPS-induced inflammation as well as apoptosis of H9c2 cells, and the possible mechanisms of these effects. In the present study, we found that adiponectin significantly relieved LPS-induced cytotoxicity including decreased viability and elevated LDH release, inhibited LPS-triggered inflammation, which is evidenced by increases in release of TNF-, IL-1 as well as IL-6, and attenuated the enhanced rates of apoptotic cells as well as increased caspase-3 activity caused by LPS in H9c2 cells. In addition, our data demonstrated that adiponectin upregulated AMP-activated protein kinase (AMPK) activation of H9c2 cells with or without LPS administration. Moreover, we found that blocking AMPK pathway by compound c attenuated the protective effects of adiponectin against the cytotoxicity, inflammatory response, and apoptosis of H9c2 cells resulted from LPS. Our observations bring novel insights for understanding the mediatory role of AMPK pathway implicated in the protective effects of adiponectin against LPS-induced cardiotoxicity.