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Chinese Journal of Biochemical Pharmaceutics ; (6): 63-65, 2017.
Article in Chinese | WPRIM | ID: wpr-510204

ABSTRACT

Objective To observe the influence of Ginkgo laminae on serum lipid, serum level of homocysteine (HCY) and carotid intima-media thickness (IMT) of patients in recovery phase of cerebral infarction. Methods 100 patients in recovery phase of cerebral infarction were randomly divided into treatment group and control group, with 50 cases in each group. The control group were given aspirin enteric coated tablets 0.1g qn po., atorvastatin calcium capsule 20mg qn po.; the treatment group on the basis of the control group were added Ginkgo laminae, 1 tablet per time, three times daily. The blood liqid and HCY levels pre-treatment and 1, 3 and 6 months post-treatment and IMT value pre-treatment and 6 months post-treatment were collected. Results The triglyceride level had no significantly change in two groups. The high density lipoprotein cholesterol 3, 6 months post-treatment in treatment group was significantly higher than control group(P<0.05). The cholesterol and low density lipoprotein cholesterin 1 ,3, 6 months post-treatment in two groups significantly decreased compared with pre-treatment(P<0.05), while there was no significant difference between two groups at each time point. The cholesterol in treatment group had a smooth decreasing, while it had an increasing trend in control group 3 months post-treatment. The HCY 3 months post-treatment in treatment group was significantly lower than pre-treatment and control group 1, 3 and 6 months post-treatment (P<0.05). The IMT 6 months post-treatment in treatment group was significantly lower than control gorup(P<0.05). Conclusion Ginkgo laminae combined with atorvastatin for reducing lipid, which could raise high density lipoprotein cholesterol and reduce cholesterol smoothly and lower IMT, with the effective protection on vessel. The blood homocysteine level decreases after taking Ginkgo laminae for three months, which also could improve impaired endothelial function induced by high level of HCY and slow down the process of atherosclerotic plaque.

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