南方医科大学学报 ›› 2004, Vol. 24 ›› Issue (08): 864-868,891.

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补阳还五汤对脑缺血大鼠nNOS免疫阳性神经元的影响

廖春来, 佟丽, 陈育尧   

  1. 第一军医大学中医系中药新药实验室, 广东, 广州, 510515
  • 出版日期:2004-08-20 发布日期:2004-08-20
  • 基金资助:
    收稿日期:2004-3-18。
    基金项目:国家自然科学基金(39970900);广东省中医药管理局基金(100006)
    作者简介:廖春来(1976-),男,江西宁都人,1999年毕业于江西中医学院,现为第一军医大学中医系中药专业硕士,方向:中药复方药理研究,电话:020-61648265,E-mail:liaochunlai0314@sina.com
    通讯作者:佟丽,研究员,硕士研究生导师,电话:020-61648265,E-mail:tongli56t@hotmail.com

Effect of Buyanghuanwu decoction on neuronal nitric oxide synthase expression after permanent focal cerebral ischemia in rats

LIAO Chun-lai, 0TONG Li, CHEN Yu-yao   

  1. 第一军医大学中医系中药新药实验室, 广东, 广州, 510515
  • Online:2004-08-20 Published:2004-08-20

摘要: 目的 探讨补阳还五汤对大鼠持续性局灶性脑缺血后脑组织内神经元型一氧化氮合酶(nNOS)免疫阳性神经元表达的影响。方法 动物分为正常对照组,模型对照缺血1、4、10h组,补阳还五汤预处理缺血1、4、10h组。局灶性脑缺血模型由线栓法阻塞大鼠大脑中动脉(MCAO)制成,免疫组化SABC法测定大鼠脑缺血后,不同脑区在不同时间段的nNOS免疫阳性神经元表达的变化。结果 缺血侧各脑区内nNOS免疫阳性神经元表达较正常对照组升高(P<0.05),随时间延长而递增,在大脑皮层纹状区与尾壳核表达增加程度最高。补阳还五汤预处理缺血4、10h组大脑皮层纹状区nNOS免疫阳性神经元表达(170.80±21.71、189.20±18.53)比模型组同时段表达(244.60±12.44、363.00±24.82)显著性降低(P<0.05);补阳还五汤预处理缺血1、4、10h组尾壳核nNOS免疫阳性神经元表达(127.33±19.83、215.20±38.80、191.20±22.39)比模型组同时段表达(138.67±13.99、266.40±29.25、373.20±31.55)显著性降低(P<0.05)。早期即起效,并随缺血时间延长而递增。结论 提示补阳还五汤能抑制缺血后脑组织内早期nNOS活性的升高,对缺血后脑组织具有早期保护作用。

Abstract: Objective To observe the effect of Buyanghuanwu decoction (BYHWD) on neuronal nitric oxide synthase (nNOS) immunoreactivity after permanent focal cerebral ischemia in rats. Methods The rats were randomized into normal control group, cerebral ischemia model groups (with ischemia for 1, 4, and 10 h respectively), and corresponding ischemia groups treated with BYHWD. Focal cerebral ischemia was produced by permanent middle cerebral artery occlusion (MCAO) with nylon suture inserted through the internal carotid artery. Brain nNOS in different brain regions was assayed by SABC immunohistochemistry at different time points ranging from 1 to 10 h after occlusion. Results nNOS activity in the cerebral tissues was enhanced in the ischemic hemisphere as the time following ischemia prolonged. Pretreatment with BYHWD group significantly decreased nNOS activity to 170.80γ83, 215.20γthe untreated cerebral ischemia model group (244.60γthe striatum cortex 18a region and 138.67γ55 in the caudate putamen, P<0.05), and this effect began to be observed in the early stage of ischemia and gradually high-lighted as the ischemia time increased. Conclusion BYHWD significantly restrains the up-regulated activity of nNOS after focal cerebral ischemia to protect the cerebral ischemic lesion from the early stage following the onset of ischemia.

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