Liensinine alleviates LPS-induced acute lung injury by blocking autophagic flux via PI3K/AKT/mTOR signaling pathway

被引:9
作者
Wang, Cheng [1 ,4 ]
Zou, Kang [2 ]
Diao, Yunlian [3 ,4 ]
Zhou, Chaoqi [1 ]
Zhou, Jia [1 ,4 ]
Yang, Yuting [1 ]
Zeng, Zhenguo [1 ]
机构
[1] Nanchang Univ, Affiliated Hosp 1, Med Ctr Anesthesiol & Pain, Dept Crit Care Med, Nanchang 330006, Peoples R China
[2] Gannan Med Coll, Affiliated Hosp 1, Dept Crit Care Med, Ganzhou 341000, Peoples R China
[3] Nanchang Univ, Affiliated Hosp 1, Dept Resp & Crit Care Med, Nanchang 330006, Peoples R China
[4] Jiangxi Inst Resp Dis, Nanchang 330052, Peoples R China
基金
中国国家自然科学基金;
关键词
Acute lung injury; Autophagic flux; Liensinine; PI3K/AKT/mTOR pathway; EXTRACELLULAR VESICLES; PATHOGENESIS; INFLAMMATION; MECHANISMS; BARRIER;
D O I
10.1016/j.biopha.2023.115813
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Acute lung injury (ALI) is a major pathological problem characterized by severe inflammatory reactions and is a critical disease with high clinical morbidity and mortality. Liensinine, a major isoquinoline alkaloid, is extracted from the green embryos of mature Nelumbonaceae seeds. It has been reported to have an inhibitory effect on tumors. However, the effects of liensinine on ALI have not been reported to-date. The aim of this study was to explore the inhibitory effects of liensinine on lipopolysaccharide (LPS)-induced ALI and its possible mechanism. We found that liensinine significantly reduced LPS-induced ALI and reduced the production of inflammatory factors IL-6, IL-8, and TNF-alpha. In addition, liensinine blocked autophagic flux and increased the number of autophagosomes by upregulating LC3-II/I and p62 protein levels. More importantly, pretreatment with the early stages autophagy inhibitor 3-Methyladenine (3-MA) can reverse the inhibitory effects of liensinine on the secretion of inflammatory factors in ALI. The PI3K/AKT/mTOR pathway is involved in LPS-induced autophagy regulated by liensinine in ALI. In summary, this study suggests that liensinine inhibits the production of in-flammatory factors in LPS-induced ALI by regulating autophagy via the PI3K/AKT/mTOR pathway, which may provide a new therapeutic strategy to alleviate ALI.
引用
收藏
页数:11
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