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The background has been confirmed, hypertension and cardiac hypertrophy is an independent risk factors for cardiovascular events. The cardiomyocyte hypertrophy hypertension and cardiac hypertrophy basis of important cellular pathology, clarify its occurrence and regulation mechanism is of great significance for the prevention and treatment of cardiovascular disease. Many studies show that connective tissue growth factor (CTGF) stimulate the heart into fibroblast proliferation, growth factor increased collagen synthesis, but its ability to induce cardiomyocyte hypertrophy and its role in signal transduction mechanism is not very clear . Calcium channel blocker lacidipine is clinically a novel antihypertensive drugs, it with Down significant, lasting effect characteristics, it is important that it is in a stable blood pressure, while also effectively protect the target organ may be significantly reduce high blood pressure due to cardiovascular events and cardiovascular disease mortality. Clinical observation, and lacidipine have a certain effect on reversing left ventricular hypertrophy. However, lacidipine impact of CTGF induced cardiomyocyte hypertrophy is not very clear, experimental cardiac hypertrophy specific mechanism of action remains to be further reveals. Research purposes CTGF in primary culture neonatal SD rat cardiomyocytes hypertrophy role and CTGF induces hypertrophy and intracellular transduction signal the relationship of ERK1 / 2 and lacidipine intervention effects observed on both the cellular and molecular level explore CTGF neonatal SD rat cardiac myocyte hypertrophy induced signal transduction mechanism; lacidipine inhibit the role of neonatal SD rat cardiac myocyte hypertrophy and signal transduction mechanisms, provide a theoretical basis for lacidipine reversal of cardiac hypertrophy and new treatment ideas. Research methods and content of myocardial cells, primary cultures of neonatal SD rat cardiomyocytes experimental model, the surface area of ??the image analysis method for the determination of myocardial cells, myocardial cell protein was measured using [3H] - leucine incorporation. synthesis rate, myocardial cell protein content was measured with Coomassie blue staining and Western blot (western blot) Determination of cardiac myocyte total ERK1 / 2 (t-ERK1 / 2) and phosphorylated ERK1 / 2 (p-ERK1 / 2 ) protein expression levels. Dynamic observation: (1) CTGF cellular surface, the rate of protein synthesis and protein content; (2) of CTGF myocardial cells total ERK1 / 2 and phosphorylated ERK1 / 2 expression; (3) lacidipine CTGF induced myocardial cell surface area, the rate of protein synthesis and protein content; (4) lacidipine CTGF induced cardiac myocyte total ERK1 / 2 and phosphorylated ERK1 / 2 expression. Results (1) With the the CTGF concentration increased, the surface area of ??the myocardial cells showed a dose-dependent increase, wherein 10ug / L of 25ug / L, 50ug / L, of cardiomyocytes the surface area 100ug / L CTGF groups, were 902.76 ± 127.83um2 , 1378.44 ± 130.65um2, 1729.85 ± 145.24um2, 2002.46 ± 197.78um2, were significantly higher cell surface area (621.28 ± 76.62um2) difference is very significant (P <0.01), a statistically significant; (2) with the forward CTGF increase in the concentration of the protein synthesis rate of myocardial cells in a dose-dependent increased 10ug / L, 25ug / L, 50ug / L, the 100ug / L of CTGF myocardial cells [3H] - leucine incorporation rates were 1329.71 ± 107.19cpm/well, 1573.39 ± 149.27cpm/well, 1993.84 ± 130.43cpm/well, 2247.58 ± 171.35cpm/well, were significantly higher myocardial cells [3H] - leucine incorporation rate (1098.04 ± 132.30 cpm / well), the difference is very significant (P <0.01); (3) With the increase of CTGF concentration, dose-dependent increase in the protein content of the myocardial cells 10ug / L, 25ug / L, 50ug / L, 100ug / L CTGF myocardial cell protein content were 0.805 ± 0.089ng/cell, 1.028 ± 0.087ng/cell, 1.302 ± 0.109ng/cell, 1.540 ± 0.112ng/cell, the myocardial cells were significantly higher protein content (0.649 ± 0.075 ng / cell), the difference was significant (P <0 01); (4) With the increase of CTGF concentration, the myocardial cells p-ERK1 / 2 expression in a dose-dependent increased 10ug / L, 25ug / L, 50ug / L 100ug / L of CTGF myocardial cells of p-ERK1 / 2 expression was significantly higher than that in the control group (P <0.01), and t-ERK1 / 2 in each group expression was not significantly different (P> 0.05); CTGF role In 0min, 5min, 10min, 15min, 30min, 60min, 120min time point, P-ERK1 / 2 expression was time-dependent changes, including 0 ~ 15min P-ERK1 / 2 expression was elevated gradually in 15min when highest expression was decreased gradually thereafter, and t-ERK1 / 2 expression was not significantly different (P> 0.05) at all time points; (5) 50ug/LCTGF group of cell surface area is 1812.52 ± 168.73um2 with the control group (689.31 ± 96.58um2,) relatively significant increase (P <0.01); 5μmol / L, 10 μmol / L, 25 μmol / L, 50 μmol / L of lacidipine intervention group myocardial cell surface area is 1476.52 ± 156.73μm2 1120.39 ± 149.68 μm2, 926.10 ± 101.44μm2, 739.81 ± 91.55μm2, and CTGF group comparison in a concentration-dependent reduction (P <0.01); (6) 50ug / L of CTGF group of myocardial cells [3H] - leucine incorporation rate of 2368.72 ± 122.45 cpm / well, and the control group (950.26 ± 89.43cpm/well), a significant increase (P <0.01); 5μmol / L, 10 μmol / L, 25 μmol / L, 50 μmol / L lacidipine myocardial cells in the intervention group [3H] - leucine incorporation rates were 2023.12 ± 106.15cpm/well, 1629.15 ± 103.46 cpm / well, 1302.19 ± 98.53cpm/well, 1055.72 ± 90.96cpm/well, and CTGF group comparison in a concentration-dependent reduction ( P <0.01); (7) 50ug / L of CTGF group of myocardial cell protein content to 1.692 ± 0.203 ng / Cell, with the control group (0.622 ± 0.068 ng / Cell) Comparative significantly significantly increased (P <0.01); 5μmol / L 10μmol / L, 25 μmol / L, 50 μmol / L lacidipine myocardial cell protein content in the intervention group were the 1.269 ± 0.167ng/cell, the 0.923 ± 0.119ng/cell, the 0.766 ± 0.085ng/cell, 0.682 ± 0.063ng/cell and CTGF in a concentration-dependent reduction (P <0.01); significantly higher expression of p-ERK1 / 2 (8) CTGF myocardial cells 5μmol / L, 10 μmol / L, 25 μmol / L, 50 μmol / L lacidipine intervention cardiomyocytes p-ERK1 / 2 expression of CTGF group in a concentration-dependent reduction (P <0.01); cardiac myocytes t-ERK1 / 2 expression in each group there is no significant difference (P> 0.05). Conclusions (1) of CTGF may be dose-dependent induction of cell surface area increases, the rate of protein synthesis increased myocardial cells, the protein content of the myocardial cells increase, suggesting that CTGF induced cardiomyocyte hypertrophy; (2) CTGF dose-dependent and time dependently induced cardiomyocytes ERK phosphorylation, suggesting that CTGF induced cardiomyocyte hypertrophy mechanism may be achieved through the ERK1 / 2 phosphorylation; (3) lacidipine dose-dependent inhibition of CTGF-induced myocardial cell surface area increased myocardial cell protein synthesis rate increased myocardial cells increase in protein content that has prompted Lacidipine role in inhibition of CTGF induced cardiomyocyte hypertrophy; (4) lacidipine dose-dependent inhibition of of of CTGF induced myocardial cells ERK1 / 2 phosphorylation, to inhibit CTGF induced cardiomyocyte hypertrophy Table Ming Laxi besylate may be achieved by inhibiting the phosphorylation of ERK1 / 2. In summary, it is not difficult to see that CTGF can be induced cardiomyocyte hypertrophy, and thus participate in the development of cardiac remodeling, the mechanism may be closely related with the phosphorylation of ERK1 / 2. Lacidipine inhibits CTGF induced myocardial hypertrophy, thus inhibiting the development of cardiac remodeling, closely related to the mechanism may be related to the mechanism of the role of ERK1 / 2 phosphorylation. ERK1 / 2 phosphorylation and inhibition of CTGF inhibition of CTGF-induced cardiomyocyte hypertrophy induced cardiomyocyte hypertrophy and lacidipine signal transduction mechanism needs further study.
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