自噬
PI3K/AKT/mTOR通路
急性呼吸窘迫
蛋白激酶B
败血症
细胞凋亡
呼吸窘迫
医学
癌症研究
细胞生物学
化学
生物
内科学
肺
麻醉
生物化学
作者
Juan Chen,Weichao Ding,Zhe Zhang,Quan Li,Mengmeng Wang,Jing Feng,Wei Zhang,Liping Cao,Xiaohang Ji,Shinan Nie,Zhaorui Sun
出处
期刊:Phytomedicine
[Elsevier]
日期:2024-04-01
卷期号:: 155627-155627
被引量:1
标识
DOI:10.1016/j.phymed.2024.155627
摘要
Sepsis is a life-threatening organ dysfunction caused by an exaggerated response to infection. In the lungs, one of the most susceptible organs, this can manifest as acute respiratory distress syndrome (ARDS). Shenfu (SF) injection is a prominent traditional Chinese medicine used to treat sepsis. However, the exact mechanism of its action has rarely been reported in the literature. In the present study, we detected the protective effect of SF injection on sepsis-induced ARDS and explored its underlying mechanism. We investigated the potential targets and regulatory mechanisms of SF injections using a combination of network pharmacology and RNA sequencing. This study was conducted both in vivo and in vitro using a mouse model of ARDS and lipopolysaccharide (LPS)-stimulated MLE-12 cells, respectively. The results showed that SF injection could effectively inhibit inflammation, oxidative stress, and apoptosis to alleviate LPS-induced ARDS. SF inhibited the PI3K-AKT pathway, which controls autophagy and apoptosis. Subsequently, MLE-12 cells were treated with 3-methyladenine to assess its effects on autophagy and apoptosis. Additional experiments were conducted by adding rapamycin, an mTOR antagonist, or SC79, an AKT agonist, to investigate the effects of SF injection on autophagy, apoptosis, and the PI3K-AKT pathway. Overall, we found that SF administration could enhance autophagic activity, reduce apoptosis, suppress inflammatory responses and oxidative stress, and inhibit the PI3K-AKT pathway, thus ameliorating sepsis-induced ARDS.
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