Hydrogen Sulfide Alleviates Lipopolysaccharide-Induced Diaphragm Dysfunction in Rats by Reducing Apoptosis and Inflammation through ROS/MAPK and TLR4/NF-κB Signaling Pathways.
Hydrogen Sulfide Alleviates Lipopolysaccharide-Induced Diaphragm Dysfunction in Rats by Reducing Apoptosis and Inflammation through ROS/MAPK and TLR4/NF-κB Signaling Pathways.
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硫化氢通过 ROS/MAPK 和 TLR4/NF-kappa B 信号通路减少细胞凋亡和炎症，从而减轻脂多糖诱导的大鼠膈肌功能障碍
DOI：
10.1155/2018/9647809
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发表时间：
2018
影响因子：
--
通讯作者：
Ji XY
中科院分区：
文献类型：
--
作者：
Zhang GY;Lu D;Duan SF;Gao YR;Liu SY;Hong Y;Dong PZ;Chen YG;Li T;Wang DY;Cheng XS;He F;Wei JS;Li GY;Zhang QY;Wu DD;Ji XY
膈肌功能障碍是世界范围内的重要临床问题。硫化氢（H2S）参与哺乳动物的许多生理和病理过程。然而，H2S在膈肌功能障碍中的作用和机制尚未完全阐明。在本研究中，我们检测到脂多糖（LPS）处理的L 6细胞中H2S水平降低。用H2S处理增加LPS处理的L 6细胞的增殖和活力。我们发现H2S通过丝裂原活化蛋白激酶（MAPK）信号通路降低了LPS处理的L 6细胞中活性氧（ROS）诱导的凋亡。H2S通过介导L 6细胞中的Toll样受体-4（TLR-4）/核因子-κ B（NF-κB）信号通路减轻LPS诱导的炎症。此外，H2S通过减少脓毒症大鼠膈肌中的炎症和细胞凋亡来改善膈肌功能和结构。总之，这些发现表明H2S通过ROS/MAPK和TLR 4/NF-κB信号通路减少细胞凋亡和炎症来改善LPS诱导的大鼠膈肌功能障碍。新型缓释H2S供体可被设计并应用于治疗膈肌功能障碍。
Diaphragm dysfunction is an important clinical problem worldwide. Hydrogen sulfide (H2S) is involved in many physiological and pathological processes in mammals. However, the effect and mechanism of H2S in diaphragm dysfunction have not been fully elucidated. In this study, we detected that the level of H2S was decreased in lipopolysaccharide- (LPS-) treated L6 cells. Treatment with H2S increased the proliferation and viability of LPS-treated L6 cells. We found that H2S decreased reactive oxygen species- (ROS-) induced apoptosis through the mitogen-activated protein kinase (MAPK) signaling pathway in LPS-treated L6 cells. Administration of H2S alleviated LPS-induced inflammation by mediating the toll-like receptor-4 (TLR-4)/nuclear factor-kappa B (NF-κB) signaling pathway in L6 cells. Furthermore, H2S improved diaphragmatic function and structure through the reduction of inflammation and apoptosis in the diaphragm of septic rats. In conclusion, these findings indicate that H2S ameliorates LPS-induced diaphragm dysfunction in rats by reducing apoptosis and inflammation through ROS/MAPK and TLR4/NF-κB signaling pathways. Novel slow-releasing H2S donors can be designed and applied for the treatment of diaphragm dysfunction.
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