Research Paper Volume 13, Issue 15 pp 19643—19656

The protective effect of allicin on myocardial ischemia-reperfusion by inhibition of Ca2+ overload-induced cardiomyocyte apoptosis via the PI3K/GRK2/PLC-γ/IP3R signaling pathway

Effect of allicin on Ca2+ increase in MI/R injury via PI3K -mediated GRK2/PLC-γ/IP3R pathway. (A) The cardiomyocytes from MI/R, MI/R+ Allicin, and MI/R+ Allicin+ m-3M3FBS were stained with Fura-2AM dye, showing allicin decreased intracellular Ca2+ release during MI/R injury, and the pan-PLC activator m-3M3FBS reversed the decreased intracellular Ca2+ release during MI/R. (B) The western blot and quantitative analysis revealed that p-CaMKII, p-PLC-γ, and p-IP3R were increased in the MI/R group and reduced in the Allicin group m-3M3FBS could reverse the decrease of p-CaMKII, p-PLC-γ, and p-IP3R expression levels. (P

Figure 6. Effect of allicin on Ca2+ increase in MI/R injury via PI3K -mediated GRK2/PLC-γ/IP3R pathway. (A) The cardiomyocytes from MI/R, MI/R+ Allicin, and MI/R+ Allicin+ m-3M3FBS were stained with Fura-2AM dye, showing allicin decreased intracellular Ca2+ release during MI/R injury, and the pan-PLC activator m-3M3FBS reversed the decreased intracellular Ca2+ release during MI/R. (B) The western blot and quantitative analysis revealed that p-CaMKII, p-PLC-γ, and p-IP3R were increased in the MI/R group and reduced in the Allicin group m-3M3FBS could reverse the decrease of p-CaMKII, p-PLC-γ, and p-IP3R expression levels. (P < 0.05, Model vs. Allicin).