Nicotine induces H9C2 apoptosis by Akt degradation

AIM To determine the effect of nicotine on cardiomyocytes and the mechanism underlying it. METHODS Cultured H9C2 cells were randomly divided into 4 groups: control group, nicotine group(10 μmol/L), control+Akt overexpression group and nicotine (10 μmol/L)+Akt overexpression group. Forty-eight hours after culture, cell viability was detected by CCK-8, apoptosis was detected by Caspase-3 colorimetric activity assay kit and the protein level of Akt was detected by Western blot. RESULTS Compared with the control group, the cell viability of the nicotine group was obviously decreased（P<0.05）, the cell apoptosis was remarkably improved（P<0.01） and the protein level of Akt was decreased（P<0.01）. These changes were all reversed by Akt overexpression（P<0.01）. CONCLUSION Nicotine down-regulates the protein level of Akt, which can induce the apoptosis of H9C2 cells.