摘要
目的观察雌激素对大鼠局灶性脑缺血再灌注损伤后核转录因子-κB(NF-κB)和肿瘤坏死因子(TNF-α)表达的影响,探讨雌激素对大鼠局灶性脑缺血再灌注损伤的神经保护机制。方法49只雌性Wistar大鼠随机分为4组:脑缺血再灌注组(A组)、卵巢切除组(B组)、雌激素给药组(C组)、假手术组(D组),A、B、C组每组14只,假手术组7只。除假手术组外其余大鼠均采用大脑中动脉线栓法建立局灶性脑缺血再灌注模型,采用免疫组织化学方法检测脑组织NF-κB和TNF-α的表达,HE染色显微镜下观察脑组织病理学变化。结果HE染色:B组与A组和C组比较,脑组织损害较重;免疫组织化学检测:B组NF-κB和TNF-α表达的阳性细胞率在同一时间点明显高于A组及C组(P<0.05),各组不同时间点NF-κB和TNF-α表达的阳性细胞率不同,随时间的延长表达增强(P<0.05)。结论雌激素能抑制脑缺血再灌注损伤后炎症反应,减轻切除卵巢大鼠局灶性脑缺血引起的脑损伤,具有缺血性神经保护作用。
Abstract： Objective To investigate the effects of 17β-estradiol （ 17β-E2 ） on the expression of nuclear factor kappaB （ NF-κB ） and tumor necrosis factor-α （TNF-α） after focal cerebral ischemia reperfusion. To study cerebral protection of mechanism 17β-E2. Methods Forty-nine female Wistar rats were randomly divided into 4 groups： group A ischemia/reperfusion （ I/R ） sham-operated ; group B ovariectomy （OVX） ;group C：OVX ＋ 17β-E2; group D： sham-operated. Focal cerebral I/R was produced by right middle cerebral artery occlusion except for Group D. Group C rats were treated with 17β-E2 （1 mg/kg） intraperitoneal injection for 7 days. NF-κBp65 and TNF-α were detected by immunohistochemistry. Brain tissues were stained with HE staining for observing the brain histopathological change. Results HE staining： compared with group A and group C, the damage of the brain tissue in group B was much heavier. Immunohistochemistry ：in group B, the expressions of NF-κBp65 and TNF-α increased significantly after ischemia and reperfusion at the same time（ P 〈0.05 ）. The expressions of NF-κBp65 and TNF-α at 24 h of all groups increased significantly compared with 2 h （P 〈 0.05 ）. Conclusion Focal cerebral I/R induces significant increase in NF-κBp65 and TNF-α expression. 17β-E2 can inhibit inflammatory reaction after cerebral ischemia by inhibiting the expressions of NF-κB and TNF-α.
出处
《哈尔滨医科大学学报》
CAS
北大核心
2008年第4期354-357,共4页
Journal of Harbin Medical University
