| In myocardial diseases, Atherosclerosis, Hyperlipidema and Hypertension had been alreadyknown as the important risks. It is well known that the various factors lead to the changes ofendocrine function of endothelium now. The vascular endothelium plays a key role in the Localregulation of vascular tone by the release of vasodilator substances (i.e. EDRF) and vasoconstrictorsubstances. ET-1 is one of the most potent vasoconstrictors yet found and causes contractions thatdevelop slowly and are powerful and long lasting. ET-1 has potent proliferating properties onvascular smooth muscle cells and therefore ET-1 has been implicated in the progression ofatherosclerosis. NO is one of the vasodilative peptide and reversely associated with ET-1.Thepresent study suggests that chronic exercise cause a decrease in production of ET-1. NO in humans,which may product beneficial effects (i.e vasodilative and antiatherosclerotic) on the cardiovascularsystem.Methods: One hundreds male Wistar ratswere randomly into five groups equally: normalcontrol group(NC), atherogenic diet group (AS), atherogenic diet with 1hour swimming (S1),atherogenic diet with 1.5hour swimming (S1.5), atherogenic diet with 1.5hour swimming (S2). NCgroup were placed on normal food,The rats of AS. S1.0 S1.5 S2.0 group were fed with Vitamin D3 (700000IU/kg) three daysbefore aerobic exercise. S1.0 S1.5. S2.0 group swim five days every week from 10mint/dayincreased by 10mint/day to 60mint/day, .90 mint/day, 120 mint/day. Take blood through aorta killedthe next day when the experiment were finished all mice. Blood lipids(TC.TG.HDL.LDL) weremeasured; Respectively, The levels of serum ET-1,NO,OX-LDL were measured withradioimmunoassay, colorimetry, ELISA method; And the microstructures of thoracic aorta wereobserved through light microscope. Techniques of RT-PCR and western blot were used in the studyof ET-1 and NOS in vascular smooth muscle cells of atherosclerotic rat model.Result: (1) The change of Pre and post training on BL00D-lipid of atherosclerotic rats:Compared with NC group, TG,TC,LDL-C in AS group were increased, but HDL were decreased(P＜0.05). Compared with AS group, TG,LDL-C in S1.0 group were decreased, but HDL-C wasincreased (P＜0.05)and TC wasn't obviously difference between S1 group and AS group; TC,LDL-C in S1.5 group were dramatically decreased (P＜0.01), but TG was decreased and HDL-Cwas increased (P＜0.05); TC, LDL-C in S1.5 group were decreased (P＜0.01), but HDL-C wasincreased (P＜0.05) and TG wasn't obviously difference between S2.0 group and AS group. (2) The microstructures of thoracic aorta were observed through light microscope: In high lipiddiet model group (AS), the intimae were become rough and thicker, many lipid foam cells migratedto the regions of intimae and smooth muscle cells (SMC) which associated injuries with internalelastic lamina.What's more, Light microscope shows that the typical and ripe atheromatous plaqueshave been formed. The microstructures of thoracic aorta in S1.0 S1.5. S2.0 rat group show theintimae were become smooth, furthermore no thrombus and proliferating neointima were found.(3) The change of Pre and post training on OX-LDL in the serum of atherosclerotic rats:Compared with NC group, the level of OX-LDL in AS group was obviously increased (P＜0.05).Compared with AS group, the level OX-LDL of in S1.0. S2.0 rat group decreased, but wasn'tobviously difference between S1.0 S2.0 group and AS group; the level of OX-LDL in S1.5 ratgroup was decreased (P＜0.05).(4) The change of Pre and post training on ET-1 in the serum of atherosclerotic rats:Compared with NC group, the level of ET-1 in AS group was obviously increased (P＜0.05).Compared with AS group, the level of ET-1 in S1.0 rat group decreased, but wasn't obviouslydifference between S1.0 group and AS group; the level of ET-1 in S1.5. S2.0 rat group wasdecreased (P＜0.05).(5) The change of Pre and post training on NO in the serum of atherosclerotic rats:Compared with NC group, the level of NO in AS group was obviously increased (P＜0.05).Compared with AS group, the level of NO in S1 rat group increased, but wasn't obviously differencebetween S1.0 group and AS group; the level of ET-1 in S1.5. S2.0 rat group was increased (P＜0.05).(6) The change of Pre and post training on gene and protein expression of ET-1 invascular smooth muscle cells of atherosclerosis rats: Compared with NC group, ET-1 gene andprotein expression in AS group were increased(P＜0.05). Compared with AS group, ET-1 gene andprotein expression in S1.00.S2.0 rat group were decreased, but wasn't obviously difference betweenS1. 0. S2.0 rat group and AS group;. ET-1 gene and protein expression in S1.5 weredecreased(P＜0.05).(7) The change of Pre and post training on gene and protein expression of NOS in vascularsmooth muscle cells of atherosclerosis rats: Compared with NC group, NOS gene and proteinexpression in AS group were decreased (P＜0.05). Compared with AS group, NOS gene and proteinexpression in S1.0. S2.0 rat group were increased, but wasn't obviously difference between S1.0.S2.0 rat group and AS group; NOS gene and protein expression in S1.5 were increased (P＜0.05).Conclusion: 1. The results suggested that aerobic exercise might effectively reduced the level of lipid andinfluence the metabolism of lipid..especially, Medium exercise in rats with high fat food can causereduction of serum leptin and a series of beneficial biochemical changes, which is a better way forpreventing AS.2. The experimental model of atherosclerosis in rat may be conveniently established by been feelwith vitamin D3 and high fat diet, which can be more fit for aerobic exercise model than otheranimals.3. Aerobic exercise might protest the formation of thrombi and the initial permeability in aorta wallto inhibit the formation of AS.4. Aerobic exercise can inhibit the decreasing No concentration and the increasing ox-LDLconcentration induced by high fat diet significantly and effectively atherosclerosis.5. Aerobic exercise may improve the capability of anti-oxidation and decrease the level of oxidativelow density lipoprotein, resulting in prevention and therapy of atherosclerosis by improving thecapability of anti-per oxidation of lipid.6. After the end of 8 week exercise training, the plasma concentration of ET-1 significantlydecreased and the plasma concentration of NO significantly increased, which may producebeneficial effects on the cardiovascular system.7. Aerobic exercise can rectify the Atherosclerosis regulatory dysfunction of gene and proteinexpression of endothelium-derived relaxing factor NO and vasoconstrictor substance ET-1 onVSMC.
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