论文部分内容阅读
目的 :探讨辛伐他汀对缺氧缺血性脑损伤 (HIBD)保护作用的机制。方法 :选用 7日龄Sprague -Dawley大鼠 72只 ,随机分成假手术组、生理盐水对照组和辛伐他汀治疗组。制成缺氧缺血性脑病 (HIE)模型后于 0、12、2 4、48、72h及 7天处死大鼠 ,测定脑组织一氧化氮合酶 (NOS)各型活性 ,并与假手术组及生理盐水对照组测定结果比较。结果 :0小时HIE组结构型一氧化氮合酶(cNOS)活性明显高于正常对照组 ,辛伐他汀组 2 4、48、72h诱生型一氧化氮合酶 (iNOS)及 72hcNOS活性显著低于对照组。结论 :辛伐他汀对缺氧缺血性脑病的保护作用可能与调节NOS的活性有一定关系。
Objective: To investigate the protective effect of simvastatin on hypoxic-ischemic brain damage (HIBD). Methods: Seventy-two 7-day-old Sprague-Dawley rats were randomly divided into sham operation group, saline control group and simvastatin treatment group. After hypoxia-ischemic encephalopathy (HIE) model was established, rats were sacrificed at 0, 12, 2, 48, 72 and 7 days, and the activity of nitric oxide synthase (NOS) Group and saline control group measured results comparison. Results: At 0 hour, the activity of cNOS in HIE group was significantly higher than that in normal control group, and the activities of iNOS and 72hcNOS at 2, 48, 72 hours in simvastatin group were significantly lower In the control group. Conclusion: The protective effect of simvastatin on hypoxic-ischemic encephalopathy may be related to the regulation of NOS activity.