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作 者:丁俊丽[1] 贺婕[1] 缴克华[1] 穆斌[1] 肖丽萍[1] 银广悦[1]
机构地区:[1]中国石油天然气集团公司中心医院神经内科,河北廊坊065000
出 处:《标记免疫分析与临床》2014年第6期715-717,共3页Labeled Immunoassays and Clinical Medicine
摘 要:目的探讨一氧化氮(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TNF-α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。Objective To explore the role of L-Arginine (L-Arg) one of NO precursor on early stage of focal cerebral isehemia-reperfusion inflammatory injury in rats. Methods The rat model of focal cerebral ischemia injury were established and divided into sham operation group, isehemia 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.
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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