Resveratrol Improves LPS-induced Cardiomyocyte Injury by Upregulating miR-149-5p to Inhibit Ferroptosis
10.11969/j.issn.1673-548X.2024.10.016
- VernacularTitle:白藜芦醇通过上调miR-149-5p抑制铁死亡改善LPS诱导的心肌细胞损伤
- Author:
Jiandong HAO
1
;
Guiping XU
Author Information
1. 830054 乌鲁木齐,新疆医科大学研究生院
- Keywords:
Resveratrol;
miR-149-5p;
Ferroptosis;
Cardiomyocytes
- From:
Journal of Medical Research
2024;53(10):87-92
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of resveratrol(Rsv)on inhibiting miR-149-5p-mediated ferroptosis and impro-ving lipopolysaccharide(LPS)-induced cardiomyocyte(H9C2)injury.Methods Different concentrations of Rsv were used to treat H9C2 cells,followed by LPS stimulation to observe the effect of Rsv on LPS-induced injury in H9C2 cells.The H9C2 cells were divided into different groups,including the Control group,LPS group,LPS+Rsv group,LPS+miRNA-inhibitor-NC group,LPS+miR149-5p-inhibitor group,and LPS+miR149-5p-inhibitor+Rsv group.CCK-8 assay was used to detect cell viability,and a kit was used to measure changes in lactate dehydrogenase(LDH),glutathione(GSH),and malondialdehyde(MDA)release in H9C2 cells.DCFH-DA fluorescent probe was used to determine the level of reactive oxygen species(ROS)in H9C2 cells.Iron ion colorimetry was used to observe changes in Fe2+content in cardiomyocytes,and RT-qPCR was used to detect the expression of miR-149-5p in cells.Results Rsv significantly reduced LPS-induced injury in H9C2 cells.Compared with the LPS group,the Rsv+LPS group showed in-creased cell viability,reduced LDH secretion,increased GSH release,reduced lipid ROS generation,decreased Fe2+content,reduced MDA release,and increased miR-149-5p expression.Compared with the LPS+miR-149-5p-inhibitor group,the LPS+miR-149-5p-inhibitor+Rsv group showed increased cell viability,reduced LDH content,increased GSH,reduced ROS production,re-duced lipid peroxidation and iron accumulation,and increased miR-149-5p expression.Conclusion Rsv may inhibit ferroptosis by upregulating miR-149-5p expression and thus alleviate LPS-induced injury in H9C2 cells.
