摘要
目的探讨丹参酮ⅡA(TanⅡA)对脑缺血再灌注损伤大鼠脑组织及血清中一氧化氮(NO)含量、一氧化氮合酶(NOS)及诱导型一氧化氮合酶(iNOS)活性的影响。方法40只Wistar大鼠随机分为假手术组、缺血再灌注组、TanⅡA低剂量治疗组和TanⅡA高剂量治疗组,线栓法建立局灶性脑缺血再灌注模型。TanⅡA高、低剂量治疗组于术前连续灌胃给予高、低剂量TanⅡA3d,每天1次。各组于脑缺血90min再灌注24h进行HE染色观察病理形态学变化,检测脑组织和血清中NO含量和NOS、iNOS活性。结果TanⅡA高、低剂量治疗组脑组织缺血损伤病理学改变轻于缺血再灌注组,TanⅡA高剂量治疗组缺血改变轻于低剂量治疗组。与假手术组比较,缺血再灌注组脑组织和血清中NO含量和NOS、iNOS活性明显升高;与缺血再灌注组比较,TanⅡA高、低剂量治疗组脑组织和血清中NO含量和NOS、iNOS活性均降低,高、低剂量组之间有显著性差异(P<0.05)。结论TanⅡA可减轻神经元损伤程度,对缺血再灌注脑损伤具有保护作用,其机制可能与可降低NOS、iNOS活性,减少NO含量有关。
Objective To study the effect of Tanshinone Ⅱ A (Tan Ⅱ A) on the contents of nitrous oxide (NO) and the activities of nitric oxide synthase (NOS) and immunologic NOS (iNOS) following cerebral ischemia reperfusion (I/R)injury in rats. Methods 40 Wistar rats were randomly divided into 4 groups, which were sham group, I/R group, low dosage Tan Ⅱ A treated group and high dosage "Fan Ⅱ A treated group. The focal middle cerebral artery occlusion (MCAO) model was made. Rats were pretreated with Tan Ⅱ A for 3 d respectively before MCAO, After 90 min MCAO following 24 h of reperfusion, HE staining was investigated, The contents of NO and the activities of NOS and iNOS were also investigated. Results The change of ischemic impairment in low or high dosage Tan Ⅱ A treated group was lighter than that of I/R group, and high dosage Tan Ⅱ A treated group was lighter than that of low dosage Tan Ⅱ A treated group. Compared with the sham group, the contents of NO and the activities of NOS and iNOS increased in the isehemie territory (P〈0. 05) , Compared with I/R group, low and high dose Tan Ⅱ A treated group reduced the contents of NO and the activities of NOS and iNOS dose-dependently (P〈0.05). Conclusion "Fan lI A may reduced cerebral ischemia-reperfusion injure by reducing the contents of NO and the activities of NOS and iNOS dose-dependently.
出处
《中国康复理论与实践》
CSCD
2008年第5期430-432,F0003,共4页
Chinese Journal of Rehabilitation Theory and Practice
基金
广西自然科学基金资助(0542110)