miR-128b 通过活性氧介导脂多糖诱导的人肺微血管内皮细胞凋亡。
MicroRNA-128b mediates lipopolysaccharide-induced apoptosis via reactive oxygen species in human pulmonary microvascular endothelial cells.
机构信息
Emergency Department of Internal Medicine, Guizhou Provincial People's Hospital, Guiyang, China.
Emergency Department of Internal Medicine, Guizhou Provincial People's Hospital, Guiyang, China.
出版信息
Clinics (Sao Paulo). 2022 Mar 16;77:100020. doi: 10.1016/j.clinsp.2022.100020. eCollection 2022.
OBJECTIVES
This study aimed to explore the effects of miR-128b in the regulation of Lipopolysaccharide (LPS) induced apoptosis.
METHODS
Human Pulmonary Microvascular Endothelial Cells (HPMECs) were transfected with an miR-128b inhibitor and stimulated with LPS for 24 h. FCM was performed to detect apoptosis and Reactive Oxygen Species (ROS) production. In addition, miRNA and caspase-3 expression levels were determined using real-time quantitative polymerase chain reaction and western blotting.
RESULTS
LPS significantly induced apoptosis and ROS production and upregulated miR-128b and caspase-3 expressions in HPMECs. However, LPS-induced effects were suppressed when an miR-128b inhibitor was used. Preincubation with NAC decreased the LPS-induced apoptosis of HPMECs.
CONCLUSIONS
These effects were mediated by miR-128b via the caspase-3 pathway.
目的
本研究旨在探讨 miR-128b 在调节脂多糖（LPS）诱导的细胞凋亡中的作用。
方法
用 miR-128b 抑制剂转染人肺微血管内皮细胞（HPMEC），并用 LPS 刺激 24 h。FCM 检测细胞凋亡和活性氧（ROS）的产生。此外，采用实时定量聚合酶链反应和 Western blot 检测 miRNA 和 caspase-3 的表达水平。
结果
LPS 显著诱导 HPMEC 细胞凋亡和 ROS 的产生，并上调 miR-128b 和 caspase-3 的表达。然而，当使用 miR-128b 抑制剂时，LPS 诱导的作用被抑制。用 NAC 预处理可减少 LPS 诱导的 HPMEC 细胞凋亡。
结论
这些作用是通过 miR-128b 经 caspase-3 通路介导的。
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