HUANG Mei-song, LIU Peng, WANG Shi-cai, et al. Ligustilide Inhibits Ang Ⅱ C-induced Cardiac Myocytes Hypertrophy[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(13): 150-155.
DOI:
HUANG Mei-song, LIU Peng, WANG Shi-cai, et al. Ligustilide Inhibits Ang Ⅱ C-induced Cardiac Myocytes Hypertrophy[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(13): 150-155. DOI: 10.13422/j.cnki.syfjx.2016130150.
Ligustilide Inhibits Ang Ⅱ C-induced Cardiac Myocytes Hypertrophy
Objective: To investigate the effect of ligustilide (LIG) on angiotensin Ⅱ (AngⅡ)-induced cardiac myocytes hypertrophy and its mechanism in neonatal rats. Method: Myocardial cells of SD rats were isolated and purified for primary culture. The cultured myocardial cells were induced by AngⅡ (0.5 mg·L-1) and treated with LIG (various concentrations:20
40
80 mg·L-1) for 1 to 3 days. Another blank group was established. Then the cells morphology was observed under inverted microscope and the cells surface area was determined. Total intracellular protein levels were detected by using commercial BCA protein kit and the rate of apoptosis was determined by flow cytometer. The protein expression levels of p53
Bcl-2 and Bax in myocardial cells were determined by Western blot. Result: As compared with the blank group
the cell morphology was obviously changed after exposure to AngⅡ; hypertrophy effect was present in myocardial cells
the cells surface area
total protein levels
and apoptosis rate were increased significantly (P < 0.05). The protein expression levels of p53 and Bax were increased significantly
and the protein expression level of Bcl-2 was decreased significantly (P < 0.05). As compared with AngⅡ alone group
the combination effect of LIG with different concentrations and AngⅡ can ameliorate the AngⅡ-induced hypertrophy of neonatal rat myocardial cells
the cells surface area
total protein levels and apoptosis rate were decreased in a dose-dependent manner (P < 0.05). Conclusion: LIG can inhibit the AngⅡ-induced hypertrophy of cardiomyocytes
and reduce the apoptosis rate maybe by inducing Bcl-2 protein expression and inhibiting p53 and Bax protein expressions.