Liu Yiming, Zhang Jin
Department of Anesthesiology, Affiliated Shengjing Hospital, China Medical University, Shenyang, Liaoning 110004, P.R. China.
Exp Ther Med. 2017 Jun;13(6):2609-2615. doi: 10.3892/etm.2017.4353. Epub 2017 Apr 18.
The pathogenesis of acute lung injury (ALI) induced by lipopolysaccharide (LPS) involves excessive pulmonary inflammation and oxidative stress. In turn, autophagy is associated with inflammatory diseases and organ dysfunction, and studies have demonstrated that LPS treatment may trigger autophagy. Thus, excessive autophagy may stimulate the strong inflammatory response observed in the development of LPS-induced ALI. Saturated hydrogen saline may alleviate LPS-induced ALI by inhibiting autophagy, however its underlying mechanisms of action remain unknown. It has been suggested that saturated hydrogen saline may downregulate expression of nuclear factor (NF)-κB, leading to a decrease in Beclin-1 transcription and inhibition of autophagy. Inhibition of autophagy also occurs via the phosphorylation of Unc-51-like autophagy activating kinase 1 and autophagy-related protein-13 by mechanistic target of rapamycin, which in turn may be upregulated by saturated hydrogen saline. In addition, signaling pathways involving heme oxygenase-1 and p38 mitogen-activated protein kinase are associated with the alleviative effects of saturated hydrogen saline on LPS-induced autophagy. The present review focuses on potential molecular mechanisms regarding the effects of saturated hydrogen saline in the reduction of autophagy during LPS-induced ALI.
脂多糖（LPS）诱导的急性肺损伤（ALI）的发病机制涉及过度的肺部炎症和氧化应激。反过来，自噬与炎症性疾病和器官功能障碍有关，并且研究表明LPS处理可能触发自噬。因此，过度的自噬可能会刺激在LPS诱导的ALI发展过程中观察到的强烈炎症反应。饱和氢盐水可能通过抑制自噬来减轻LPS诱导的ALI，但其潜在的作用机制仍然未知。有人提出，饱和氢盐水可能会下调核因子（NF）-κB的表达，导致Beclin-1转录减少并抑制自噬。自噬的抑制也通过雷帕霉素作用靶点对Unc-51样自噬激活激酶1和自噬相关蛋白-13的磷酸化而发生，而这反过来可能被饱和氢盐水上调。此外，涉及血红素加氧酶-1和p38丝裂原活化蛋白激酶的信号通路与饱和氢盐水对LPS诱导的自噬的减轻作用有关。本综述重点关注饱和氢盐水在减轻LPS诱导的ALI过程中减少自噬作用的潜在分子机制。
