Effect of lacidipine on cardiac myocyte hypertrophy induced by CTGF and its relationship with ERK1/2[J]. Chinese Heart Journal, 2009, 21(1): 29-32.
    Citation: Effect of lacidipine on cardiac myocyte hypertrophy induced by CTGF and its relationship with ERK1/2[J]. Chinese Heart Journal, 2009, 21(1): 29-32.

    Effect of lacidipine on cardiac myocyte hypertrophy induced by CTGF and its relationship with ERK1/2

    • AIM To study the effect of lacidipine on cardiac myocytes hypertrophy induced by connective tissue growth factor(CTGF) and its relationship with ERK1/2. METHODS Neonatal cardiomyocytes were obtained from Sprague-Dawley (SD) rats. Image analysis system, 3H-leucine incorporation technique, Coomassie Brilliant blue staining and Western-blot were used to investigate the inhibitory effect of lacidipine on cardiac myocytes hypertrophy induced by CTGF and its relationship with ERK1/2. RESULTS ①50ng/L CTGF significantly increased cardiomyocyte surface area [(1812.52±168.73)μm2] in comparison with that in control group [(689.31±96.58)μm2, P<0.01)]. Lacidipine in the range of 5-50 μmol/L (5, 10, 25 and 50 μmol/L respectively) attenuated the cardiomyocyte surface area in a concentration dependent manner [(1 476.52±156.73), (1 120.39±149.68), (926.10±101.44) and (739.81±91.55)μm2, P<0.01]. ②Compared with that in control group [(950.26±89.43)cpm/well)], the 3H-leucine incorporation rate was markedly increased by 50 ng/L CTGF [(2 368.72±122.45)cpm/well, P<0.01]. Lacidipine in the range of 5-50 μmol/L attenuated the 3H-leucine incorporation rate in a concentration dependent manner[(2 023.12±106.15), (1 629.15±103.46), (1302.19±98.53) and (1055.72±90.96)cpm/well, P<0.01]. ③The cardiomyocyte protein content in 50 ng/L CTGF group [(1.692±0.203)ng/cell] was significantly higher than that in control group [(0.622±0.068)ng/cell, P<0.01]. Lacidipine in the range of 5-50 μmol/L attenuated the cardiomyocyte protein content in a concentration dependent manner [(1.269±0.167, 0.923±0.119), (0.766±0.085) and (0.682±0.063)ng/cell, P<0.01]. ④The protein level of p-ERK1/2 was markedly increased by 50 ng/L CTGF than that in control group. Lacidipine in the range of 5-50 μmol/L attenuated the protein level of p-ERK1/2 in a concentration dependent manner compared with that of the control group. But thers is no significant distinction among the different lacidipine intervention groups. CONCLUSION Lacidipine can inhibit cardiac myocytes hypertrophy induced by CTGF and the mechanism of this effect may be related to the phosphorylation of ERK1/2.
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