Objective To investigate the effect and underlying mechanism of baicalin on doxorubicin(Dox)-induced H9c2 cell toxicity.Methods H9c2 cells were pretreated with 50 μmol/L baicalin for 24 h,followed by treatment with 1 μmol/L Dox for 24 h to establish an invitro model of Dox-induced myocardial toxicity.Cell viability was assessed using the CCK8 assay.The levels of lactate dehydrogenase(LDH),cardiac troponin Ⅰ(cTnⅠ),creatine kinase isoenzyme(CK-MB),as well as oxidative stress-related indicators such as superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),and malondialdehyde(MDA)were measured in the cell supernatant of each group.Reactive oxygen species(ROS)content was determined using the DHE assay kit.TUNEL staining was employed to assess cell apoptosis levels in each group.Additionally,RT-qPCR and Western blot experiments were conducted to measure the expression levels of oxidative stress and apoptosis-related molecules.Results Baicalin demonstrated the ability to enhance H9c2 cell viability and decrease LDH,cTnⅠ,and CK-MB levels compared to the Dox group.DHE staining indicated that baicalin reduced ROS generation,increased SOD and GSH-Px activity,and decreased MDA content.TUNEL staining results revealed a reduction in the number of positive cells with baicalin treatment.RT-qPCR and Western blot analysis showed that baicalin upregulated the expression of Nrf2,HO-1,SOD2,and Bcl-2,while downregulating the expression of Cleaved-caspase 3 and Bax.However,ML385,a specific inhibitor of Nrf2,reversed the above changes induced by baicalin.Conclusion Baicalin alleviates oxidative stress and apoptosis by upregulating the Nrf2/HO-1 signaling pathway,thereby mitigating Dox-induced H9c2 cell toxicity.
维普
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