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

Allicin repressed the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R during MI/R injury. (A) The western blot analysis revealed that MI/R injury could enhance the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R, whereas the pretreatment with allicin can reduce the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R. (B) The quantitative analysis revealed that MI/R injury could enhance the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R, whereas the pretreatment with allicin can reduce the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R. (P

Figure 5. Allicin repressed the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R during MI/R injury. (A) The western blot analysis revealed that MI/R injury could enhance the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R, whereas the pretreatment with allicin can reduce the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R. (B) The quantitative analysis revealed that MI/R injury could enhance the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R, whereas the pretreatment with allicin can reduce the expression of p-GRK2, p-CaMKII, p-PLC-γ, and p-IP3R. (P < 0.05, Model vs. Allicin).