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基础研究

L-精氨酸对大鼠局灶性脑缺血再灌注早期炎症损伤研究

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  • 丁俊丽,贺 婕,缴克华,穆 斌,肖丽萍,银广悦
丁俊丽(1971—),女,硕士研究生,副主任医师,从事脑与神经临床工作

收稿日期: 2014-06-05

  修回日期: 2014-08-24

  网络出版日期: 2014-12-26

The Influence of L-Arginine on Early Reperfusion Injury of Focal Cerebral Ischemia in Rats

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  • Department of Neurology, The Central Hospital of China Petroleum Corporation, Langfang 065000, China

Received date: 2014-06-05

  Revised date: 2014-08-24

  Online published: 2014-12-26

摘要

探讨一氧化氮( NO)前体L-精氨酸(L-Arg)对大鼠局灶性脑缺血再灌注早期炎症损伤的影响。方法 建立大鼠局灶性脑缺血再灌注模型,设立假手术组、缺血组(ischemia/reperfusion, IS组),L-Arg治疗组(n=10)。L-Arg治疗组于缺血2h再灌注即刻给予L–Arg,缺血组给予生理盐水。将大鼠于缺血再灌注 6 h 后断头取脑,检测脑组织中肿瘤坏死因子(TNF-α)、白细胞介素6(IL-6)和白细胞介素10(IL-10)的活性,测定脑组织含水量和脑梗死体积。结果 局灶性脑缺血再灌注大鼠给予L-Arg治疗组TNFα和IL-6的表达下降,IL-10升高,脑组织含水量及脑梗死面积减少。结论 L-精氨酸可以通过抑制脑组织炎性因子TNF-α和IL-6的表达,上调IL-10的含量来发挥抗炎作用,从而对大鼠局灶性脑缺血再灌注损伤早期产生一定程度的保护作用。

本文引用格式

丁俊丽,贺 婕,缴克华,穆 斌,肖丽萍,银广悦 . L-精氨酸对大鼠局灶性脑缺血再灌注早期炎症损伤研究[J]. 标记免疫分析与临床, 2014 , 21(6) : 715 . DOI: :10.11748/bjmy.issn.1006-1703.2014.06.030

Abstract

 Objectives To explore the role of L-Arginine (L-Arg) one of NO precursor on early stage of focal cerebral ischemia-reperfusion inflammatory injury in rats. Methods The rat model of focal cerebral ischemia injury were established and divided into sham operation group, ischemia reperfusion group and L-Arg treatment group (10 rats in each group). L–Arg was given immediately after 2 hours of cerebral ischemia in L-Arg treatment group, saline solution was given in ischemia group. The

rats of each group were beheaded after 6 hours focal cerebral ischemia-reperfusion. The levels of inflammatory cytokines tumor necrosis factor (TNF-α), interleukin 6 (IL-6) and interleukin 10 (IL-10) in beheaded brain of rats were detected. The brain infarction area and water content in brain tissue were also determined. Results The levels of inflammatory factor TNF-α and IL-6 in L-Arg treatment group rats were reduced and the expression of IL-10 was raised, the brain tissue water content and cerebral infarction area were also reduced. Conclusion L-Arginine play a role of anti-inflammatory by inhibiting the brain tissue inflammatory factor TNF and IL-6 and increasing the content of IL-10, which produces a degree of protection on cerebral ischemia in rats.

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