| Objective: To investigate the effect of hyperhomocysteinemia on acutemyocardial infarction rats and the mechanism, and to further study the effect offolic acid and vitamin B12on Hhcy and its relationship with oxidative stress,inflammatory reaction.Methods：Forty SD rats were randomly divided into the blank group(10), thecontrol group (10), the Hhcy model group (10), the folic acid and vitamin B12intervention group (10),♀♂were in equal portions. After12weeks,anesthetized rats and connected to the small animal ventilator. Exposed heartand ligated the left ventricular descending artery for90minutes, recordingECG(II). Five rats were randomly selected and stained the myocardium by HE,Ten rats were sacrificed to take the plasma of arterial blood, and measured thelevel of Hcy, TN-I, CK, sICAM-1, MDA and SOD. While observing the ECGchanges in the whole ischemia and reperfusion process.Results:1.The level of Hcy: The level of Hcy in the Hhcy-model group andintervention group were significantly higher than that of the blank group andthe control group (P <0.01), the intervention group were significantly higherthan that of the control group (P <0.01),while there were no difference betweenthe control group and the bland group(P>0.05).2.The levels of the plasmaTN-I, CK: The levels of the plasma TN-I, CK in the Hhcy-model group weresignificantly increased than the control group (P<0.01), while those in theintervention group were significantly decreased(P<0.01).3.The levels of theplasma sICAM-1: In the Hhcy-model group, the expression of the plasma sICAM-1was significantly increased than the control group(P＜0.01), on thecontrary, the intervention group was significantly decreased than the controlgroup(P＜0.01).4.The levels of the plasma MDA, SOD: The level of theplasma MDA in the Hhcy-model group was significantly increased than thecontrol group and the intervention group(P＜0.01), in the Hhcy-model group,the expression of the plasma SOD was significantly decreased than the controlgroup(P＜0.01), on the contrary, the intervention group was significantlyincreased than the control group(P＜0.01), the normal control group was lowerthan that of the intervention group(P<0.05).5.The myocardial HE dyeing: themyocardial cells of the normal blank group were completely and the nucleusshape was normal,the muscle fibers were arranged neatly.But in the normalcontrol group, there were visible focal necrosis on the myocardial cells,dissolved muscle fibers, and the myocardial interstitial edema, inflammatorycells infiltrated around them.Above changes were more grave in theHhcy-model group but were alleviative in the intervention group.6.Thechanges of ECG:90minutes after the ligation, R-waves decreasedsignificantly in each group(P <0.01), ST-segment were significantly higher (P<0.01), the Hhcy model group compared with normal control group andintervention group are more significantly (P <0.05), there was no statisticallysignificant difference in control group and intervention group (P>0.05).Conclusion:1. Hhcy promote the inflammation reaction of AMI, which maybe one of the causes for the increase of acute myocardial infarction.2. Hhcyinhibit the antioxidant ability of the AM.3.Folic acid combined with VITB12can effectively reduce the Hcy level, so as to play a role in the protection ofmyocardial.4.Folic acid may have antioxidant, anti-inflammatory and improveantioxidant system activity. |
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