The effect of esculin on hypoxia/reoxygenation induced myocardial cell injury by regulating HMGB1/RAGE signaling pathway
- VernacularTitle:秦皮甲素调节HMGB1/RAGE信号通路对缺氧/复氧诱导的心肌细胞损伤的影响
- Author:
Yanbo WAN
1
;
Ming LIU
1
;
Yong WANG
1
Author Information
- Publication Type:Journal Article
- Keywords: myocytes,cardiac; aesculi; HMGB1 protein; receptor for advanced glycation end products; apoptosis; hypoxia; reoxygenation
- From: Tianjin Medical Journal 2025;53(8):796-801
- CountryChina
- Language:Chinese
- Abstract: Objective To explore the effect of esculin(ESCL)on hypoxia/reoxygenation(H/R)-induced myocardial cell injury by regulating high mobility group B1(HMGB1)/receptor of advanced glycation endproducts(RAGE)signaling pathway.Methods H9c2 cells were divided into the control group,the H/R group,the ESCL-low group,the ESCL-medium group and the ESCL-high group(ESCL-L,M,H,0.4,0.8,1.6 mmol/L),the ESCL-H+pcDNA-NC group and the ESCL-H+pcDNA-HMGB1 group.The AnnexinV FITC staining method was used to detect the apoptosis rate of H9c2 cells.Enzyme linked immunosorbent assay was used to measure interleukin(IL)-18,IL-1β,tumor necrosis factor(TNF)-α,the malondialdehyde(MDA),lactate dehydrogenase(LDH)contents and the superoxide dismutase(SOD)activity.The DCHF-DA fluorescent probe was performed to detect active oxygen(ROS)fluorescence intensity.Immunoblotting was performed to detect B-cell lymphoma-2(Bcl-2),Bcl-2 associated X protein(Bax),HMGB1 and RAGE proteins.Results Compared with the control group,the H/R group showed conspicuously higher apoptosis rate,IL-18,IL-1β,TNF-α,MDA,LDH,ROS fluorescence intensity,Bax,HMGB1 and RAGE proteins in H9c2 cells,and conspicuously lower Bcl-2 protein and SOD activity(P＜0.05).Compared with the H/R group,the ESCL-L,ESCL-M and ESCL-H groups showed a gradual decrease in cell apoptosis rate,IL-18,IL-1β,TNF-α,MDA,LDH and ROS fluorescence intensity,Bax,HMGB1 and RAGE proteins with increasing ESCL concentration,and a gradual increase in Bcl-2 protein and SOD activity(P＜0.05).Overexpression of HMGB1 reversed the protective effect of ESCL on H/R induced cardiomyocyte injury.Conclusion ESCL may reduce H/R induced cardiomyocyte injury by inhibiting HMGB1/RAGE pathway.
