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CJAP ›› 2021, Vol. 37 ›› Issue (6): 589-593.doi: 10.12047/j.cjap.6077.2021.086

• ORIGINAL ARTICLES • Previous Articles     Next Articles

Effects of L-carnitine on autophagy and apoptosis of mouse pulmonary microvascular endothelial cells induced by lipopolysaccharide

XUE Feng, WANG Hui, XU Si-duo, LIU Shou-ting, GONG Yong-sheng, FAN Xiao-fang   

  1. Institute of Hypoxia Medicine, Wenzhou Medical University, Wenzhou 325035, China
  • Received:2020-04-22 Revised:2021-03-03 Online:2021-11-28 Published:2021-11-25

Abstract: Objective: To investigate the protective effects of L-carnitine (LC) on lipopolysaccharide (LPS) - injured mouse pulmonary microvascular endothelial cells (PMVECs) and its effects on autophagy and apoptosis. Methods: Cultured mouse PMVECs were divided into three groups: ① Control group, ② LPS group (10 μg/ml, 3, 6, 12, 24 h), ③ LPS (10 μg/ml, 24 h)+LC (2.5, 5.0, 10 μg/ml) (LPS+LC) group. PMVECs apoptosis was examined by Annexin V-FITC/PI double labeling method. Autophagosome was detected by immunofluorescence staining. Levels of autophagy-related protein LC3 and apoptosis-related protein caspase-3 were detected by Western blot. PMVECs viability was measured by CCK-8. Results: ① Compared with the control group, LPS treatment inhibited the PMVECs viability significantly, whereas the apoptosis rate and the expression of autophagy protein LC3 II were markedly increased after LPS treatment for 6 h, 12 h and 24 h. ② Compared with LPS group (10 μg/ml, 24 h), the PMVECs viability, levels of autophagy protein LC3 II and caspase-3 protein expression as well as apoptosis rate in LPS+LC group were increased significantly. Conclusion: LC can increase the activity of PMVECs injuried by LPS, promote autophagy and inhibit apoptosis of PMVECs.

Key words: L-carnitine, lipopolysaccharide, mouse endothelial cells, autophagy, apoptosis

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