葛根素通过调控USP25信号保护脓毒症诱导的H9c2心肌细胞损伤OA

Objective To investigate the role and mechanism of puerarin(Pue)in lipopolysaccharide(LPS)-induced H9c2 cell in-jury.Methods H9c2 cells were treated with LPS to simulate septic myocardial injury and randomly divided into four groups:control group,LPS group,Pue+LPS group,and Pue+si-USP25+LPS group.Cellular morphology,cell viability,and apoptosis were assessed to evaluate injury severity.RT-PCR was used to measure TNF-α,IL-6,and IL-1β mRNA levels.Intracellular reactive oxygen species(ROS)level was detected by DCFH-DA staining.ELISA were used to detect LDH,CAT,SOD activities,and MDA contents.Western blot was used to analyze cleaved caspase-3,Cytochrome C,USP25,and NF-κB expression.Immunofluorescence staining was per-formed to assess USP25 expression.Results Compared with control group,H9c2 cells exhibited swelling,reduced density,de-creased viability,CAT and SOD activities(P＜0.01),elevated MDA and ROS levels(P＜0.01),upregulated cleaved caspase-3 and Cy-tochrome C expression(P＜0.01),increased TNF-α,IL-6,and IL-1β mRNA levels(P＜0.01),reduced USP25 expression(P＜0.01),and enhanced NF-κB expression in LPS group(P＜0.01).Compared with LPS group,H9c2 cells in Pue+LPS group showed alleviated cell swelling,increased density,elevated viability,CAT and SOD activities(P＜0.01),reduced MDA and ROS levels(P＜0.01),downregulated cleaved caspase-3 and Cytochrome C expression(P＜0.01),decreased pro-inflammatory cytokine mRNA levels(P＜0.01),upregulated USP25 expression(P＜0.01),and suppressed NF-κB expression(P＜0.01).Compared with Pue+LPS group,the above indexes were reversed in Pue+si-USP25+LPS group.Conclusion Pue mitigates LPS-induced H9c2 cell damage by activating USP25 signaling,suppressing inflammatory responses and oxidative stress,and enhancing cellular viability.