Inhibitory effect of atorvastatin on AGE-induced HCAEC apoptosis by upregulating HSF-1 protein

This study evaluates effect and mechanism of atorvastatin on human coronary artery endothelial cells (HCAEC) apoptosis. Results have shown that HCAEC apoptosis had increased with increasing concentration of AGEs. Atorvastatin may decrease HCAEC apoptosis, but the effect can be attenuated by PI3K inhibitor. Secretion of PI3K and P-Akt in HCAEC increased with increasing concentration of AGEs. Secretion of PI3K in HCAEC may be decreased by atorvastatin. The effect may be attenuated by PI3K inhibitor. HSF-1, HSP-70 mRNA expression level decreased with increasing concentration of AGEs. Atorvastatin may attenuate AGEs-induced HSF-1, HSP-70 mRNA expression in HCAEC, but the effect can be attenuated by PI3K inhibitor. It can be concluded that AGE can dose-dependently promote HCAEC apoptosis by the PI3K/AKT pathway. Atorvastatin may attenuate the effect possibly by upregulating HSF-1.