| It has been proved that Left ventricular hypertrophy (LVH) is an independent dangerous factor which leads to cardiovascular disease besides hypertension. The sufferers with essential hypertension (EH) and LVH die of myocardial infarction and heart failure, and suffer from other cardiovascular disease with 6-8 times more chances. Myocardial fibrosis (MF) and hypertrophy of mycardial cells are the major pathological causes of LVH, while MF, the rebuilding of cardiac extracellular matrix and heart insufficiency result mainly from overproliferation of cardiac fibroblasts (CFs), increased of collagen synthesis and collagen arrangement turbulence. AVP, which is secreted by hypothalamo-neurohypophysial system and proven to be strong mitosis original, can lead to vascular smooth muscle cell (VSMC) proliferation and MC hypertrophy, and contribute to hyperplasia rebuilding of ventricles and blood vessels by being used together with renin-angiotensin-aldosterone (RAAS). Therefore, the updated cures of EH are to subsidise LVH, improve MF and resume cardiac muscle. It is thought that statin can not only lower strikingly serum cholesterin and low-density lipoprotein but also restrain VSMC from proliferation, prevent thrombosis and protect endothelium and its effect is far beyond that of regulate lipidemia. It remains unknown whether MFcan be bettered by HMG-CoA. The aim of study is to observe the effects of Simvastatin on the collagen synthesis and proliferation of CFs induce by AVP, and intervention effect by mevalonate, and what's more, to further its possible operation and principle to provide new theoretical evidence and the approach of the prevention and treatment for LVH.In this study, neonatal Sprague-Dawley (SD) rats were used as experiment model, 3H-TdR incorporation is adopted to determine DNA synthesis, MTT array to determine cell number, FCM determine cell cycle, 3H-proline incorporation to determine collagen synthesis, immunity chemical coloration technique to analyze p21ras protein expression on cell membrane, dynamic observation is made to identify: (1) the effects of AVP on CFs collagen synthesis and proliferation; (2) the effects of Sim on CFs collagen synthesis and proliferation induced by AVP; (3) the intervention of MVA in Sim's effects on CFs collagen synthesis and proliferation; (4) the effects of Sim on p21ras protein membrane integration; (5) the intervention of MVA in Sim's effects on p21ras protein membrane integration.The results of the study are as follows: (1) the incorporation of 3H-proline and A490 value by MTT assay, cell percentage on S stage, cell proliferation index (PI) and are obviously greater than those in blank control, which is practical in statistics (both p<0.05). With the increase of time in the effects on 10-7 mol/L AVP on CFs (6h, 12h, 24h, 36h, 48h), 3H-Proline incorporation and 3H-TdR incorporation of CFs, A490 value of MTT, cell pencentage on S stage, PI increase gradually, which are clearly in proportion to time (both P<0.01). (2) 3H-Proline incorporation of CFs decreases, as Sim density rises, the incorpora tion in 10-7mol/L Sim, 10~6mol/L Sim and 10~5mol/L Sim group are (302± 43.27cpm/2000cells), (259±32.32cpm/2000cells) and (163±17.53cpm/2000 cells), respectively, which are markedly lower than that (368±37.25cpm/2000 cells) in the control(P<0.05, P<0.01 and P<0.01, respectively) 3H-proline incor poration of the 10-8mol/L Sim group is 324±53.68cpm/2000cells, as contrast, there was no obvious difference between control (P>0.05); With the increase of time of the effects of 10-5mol/L Sim on CFs (6h, 12h, 24h, 36h, 48h), 3H-Proline incorporation of CFs decreases, which is negative relevant to time(r=-0.943, P<0.01). (3) As a result of step-up in Sim density, the 3H-TdR incorporation of CFs is gradually declining and 3H-TdR incorporation in 10-8mol/L Sinu 10-7mol/L Siim 10-6mol/L Sim and 10-5mol/L Sim group are (1767 ± 369.71cpm/2000cells), (1480± 351.64cpm/2000cells), (1175 ± 202.66 cpm/2000cells) and (771 ± 164.86cpm/2000cells), respectively,...
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