| Objective Study the mechanism of the rabbit's atherosclerosis caused by hy- perhomocysteinemia.Observe the effect on the reduced glutathione to treatment rabbit's hyperhomocysteinemia lead to atherosclerosis,explore the mechanism and effect of the reduced glutathione anti-atherosclerosis.Methods Forty-four ordinary grade male New Zealand white rabbits were randomly divided into four groups: control group, model group, low dose drug treat- ment group and high dose drug treatment group. The control group feeding by sta- ndard diet, the model group feeding by 1% methionine diet 100g / d, the low dose drug treatment group feeding by 1% methionine diet 100g/ d and GSH15mg/d intr- amuscularly, the high doses drug treatment group feeding by 1% methionine diet 100g/d and GSH 30mg /d intramuscularly. Before the test and after 8 weeks of the experiment , using the rabbit central ear artery blood plasma to examined the hom- ocysteine levels, measured serum of total cholesterol and triglycerides,by immun -eity transmission Turbidimetric method to examined the C-reactive protein, dete- rmined by xanthenes'oxidase and superoxide dismutase. After 8 weeks use ultra- sound examined the rabbit intra-aortic thickness, animals were sacrificed and iso- lated abdominal aorta, the vessel placed in the10% neutral formalin fixed 24 hours after HE staining, light microscopy and image analysis system with intra-aortic thickness.Results After 8-week the plasma homocysteine concentration of the model group were significantly higher the control group, high and low dose drug treatment group, significantly different (P<0.05), high dose treatment group was lower than low-dose drugs Hcy intervention group (P<0.05); made module serum TC, TG higher than the control group were significantly different (P<0.05), high and low dose drug treatment group TC, TG compared with the control group no significant difference (P>0.05); model compared with the control group decreased SOD activity were significantly different (P<0.05), high and low dose drug treatment group and model group were significantly increased SOD were significantly different (P<0.05); model group CRP increased with the control group were significantly different (P<0.05), high and low dose drug group and model group decreased CRP significantly different (P<0.05); ultrasound examination model group, the aortic medial thickness thicker than the control group were significantly different (P<0.05), model group than in the thickness of high and low doses of medication in the intervention were significantly different (P<0.05),low and high intervention group in the film thickness to high levels of drug intervention group were significantly different (P<0.05); aortic pathology measuring medial thickness in model group than in the control group were significantly different in the membrane thickness (P<0.05) and foam cells can be seen, model thickness group was higher than the high and low doses of medication in the intervention group were significantly different (P<0.05), low-dose intervention group than in the thickness of high dose treatment group had statistically significant (P<0.05). Pathological examination revealed that the abdominal aorta: control group, intima smooth and complete, no foam cell; model group, irregular intimal thickening with foam cells; low-dose drug group there is a small foam cell; high dose in the intervention group was no foam cell.Conclusions 1.Hyperhomocysteinemia may cause the atherosclerosis form- ation by the oxidative stress and inflammatory reactions.2.Glutathione as anta- gonists of endogenous homocysteine and reducing agent can reduce plasma ho- mocysteine concentration, inhibition of oxidative stress reduce inflammation and have anti-atherosclerotic effect. |
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