The Effects Of GLycyrrhetinic Acid On H₂O₂-Induced Oxidative Stress And Apoptosis In H9c2 Cardiomyocytes

BackgroundCoronary heart disease is the main threat to human Life and heaLth.RecanaLization after coronary artery obstruction is the main treatment,but reperfusion after infarction can trigger infLammation,oxidative stress,apoptosis and other harmfuL reactions.Modern pharmacoLogicaL studies have shown that many herbaL extracts protect Cardiomyocytes by reducing oxidative stress,infLammation and apoptosis.GLycyrrhizin acid is one of the monomers of traditionaL Chinese medicine.However,the scientific evidence on the antioxidant stress potentiaL and its mechanism of gLycyrrhizin acid is stiLL insufficient.ObjectiveTo investigate the efficacy of GLycyrrhetinic acid（GA）in aLLeviating H₂O₂-induced Oxidative Stress and Apoptosis the underLying mechanisms.MethodsThe H₂O₂-induced Oxidative stress and Apoptosis injury modeL of cardiomyocytes was estabLished with rat H9c2.CCK8 ceLL viabiLity assay was performed to ensure the safety dose,Lowest effective dose and cytotoxicity of gLycyrrhizic acid.ROS LeveLs were determined using DCFDA fLuorescent probe in cardiomyocytes with H₂O₂-induced-induced and gLycyrrhizic acid preconditioned cardiomyocytes oxidative stress.ROS LeveLs were to evaLuate the degree of oxidative stress injury.TUNEL staining was used to detect the apoptosis of cardiacmyocytes under oxidative stress.Western bLoting was used to detect the expression of mitochondriaL apoptosis-reLated proteins BCL-2,Bax,cLeaved-Caspase-9,cLeaved-Caspase-3,cLeaved-PARP and the phosphoryLation of p38,JNK-1/2,and ERK-1/2.ResuLtsH₂O₂-induced treatment Led to significant activation of oxidative stress,ceLL apoptosis and production of reactive oxygen species（ROS）in H9c2 cardiomyocytes.GLycyrrhidic acid pretreatment at 10 mol/L improved ceLL viabiLity And significantLy reduced reactive oxygen species（ROS）LeveLs.GA aLso significantLy attenuated H₂O₂-induced apoptosis of H9c2 ceLLs by decrease in expression of both Bax,cLeaved caspase-9,cLeaved caspase-3 and cLeaved PARP and increase in BCL-2expression and the ratio of BCL-2/Bax.Moreover,it inhibited the phosphoryLation LeveLs of p38,JNK-1/2、和ERK-1/2ConcLusionGA has protective effects in the ceLL modeLs and potentiaLLy mitigated H₂O₂-induced ROS generation and antagonized apoptosis in H9c2 Cardiomyocytes by inhibiting p38,JNK,and ERK signaLing pathways...