丹酚酸A对脂多糖诱导人肺微血管内皮细胞线粒体自噬和细胞损伤的影响

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Abstract Objective: To investigate the effect of salvianolic acid A (Sal A) on mitochondrial autophagy and cell injury in human pulmonary microvascular endothelial cells (HPMVECs) injury induced by lipopolysaccharide (LPS). Methods: LPS 10 μg/mL was used to establish cell injury in vitro. The cells were divided into four groups: control group, Sal A group, LPS group, LPS+Sal A group. MTT was used to analyze cell proliferation. The reactive oxygen species (ROS) content and mitochondrial membrane potential were detected by flow cytometry. Western blot was used to analyze the expression of microtubules associated protein light chain 3 (LC3)-II/I, Beclin1, PTEN mediated putative kinase protein 1 (PINK1) and Parkin. Results: LPS decreased the cell viability in time-dependent manner. The viability in LPS+Sal A group was higher than the LPS group, but lower than the control group (P<0.05). Compared with the control group (100%), the ROS content (283.96%±10.88%) increased and the level of membrane (38.25%±5.69%) potential decreased in LPS group (P<0.05). Compared with LPS group, ROS content (138.76%±11.82%) decreased, and the mitochondrial membrane potential (76.56%±6.22%) increased in LPS+Sal A group (P<0.05). The expression of LC-3II/I, Beclin1, PINK1 and Parkin in LPS group was higher than the control group. The expression of LC-3II/I, Beclin1, PINK1 and Parkin in LPS+Sal A group was lower than LPS group. Conclusion: Sal A alleviates the proliferation inhibition by LPS, which may be related with decreased intracellular ROS content, stabilization of mitochondrial membrane potential and mitochondrial autophagy.

Key words： salvianolic acid A mitochondrial autophagy lipopolysaccharide human pulmonary microvascular endothelial cells cell injury

Received: 21 November 2017

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	LI Weiwen
	LAN Xiu
	LI Yuan
	SUN Lei
	LYU Zhuqing.

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https://xb.wmu.edu.cn/EN/ OR https://xb.wmu.edu.cn/EN/Y2018/V48/I4/267

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