摘要
目的探讨NF-κB抑制剂在大鼠缺血性脑损伤中的作用。方法 116只Wistar大鼠,随机选98只采用改良的大脑中动脉栓塞法制作脑缺血模型后,分为实验组(44只,腹腔注射吡咯烷二硫代氨基甲酸盐0.5 ml)、PBS组(24只)和缺血组(30只),未做脑缺血模型的18只为正常组。记录各组大鼠脑组织水分含量,HE染色检测脑梗死程度,Western blot检测NF-κB p65、白细胞介素(IL)6、IL-1b表达。结果与正常组比较,缺血组大鼠脑组织水分含量明显增多,NF-κB p65明显增加(P<0.05)。与缺血组比较,实验组大鼠脑组织水分含量明显降低,NF-κBp65表达明显降低(P<0.05)。与缺血组和PBS组比较,实验组大鼠脑梗死面积明显减少,IL-6、IL-1b表达减少(P<0.05)。结论抑制NF-κB能够减轻缺血后脑损伤,其机制可能通过抑制脑缺血后炎性反应起作用。
Objective To investigate effect of the NF-κB inhibitor on cerebral ischemia and brain damage.Methods 116 Wistar rats were selected at random and 98 of them were used to make brain ischemia model by embolizing the middle cerebral artery.The models were divided into four groups:44 model rats in experimental group were injected intraperitoneally with PDTC(NF-κB inhibitor),24 model rats in PBS group were injected with PBS,30 model rats in ischemia group were not given anything,and the rest 18 rats constituted normal group.Blood brain barrier permeability,cerebral edema and degree of cerebral infarction detected by HE staining were recorded.NF-κB p65 subunit,IL-6,and IL-1b expression in brain tissue were detected by Western blot.Results Compared with normal group,water content of brain tissue and NF-κB p65 significantly increased in ischemia group(P〈0.05).Compared with ischemia group,water content of brain tissue and NF-κB p65 expression significantly decreased in experimental group(P〈0.05).Compared with ischemia group and PBS group,cerebral infarct size and expression of IL-6 and IL-1b significantly decreased in experimental group(P〈0.05).Conclusion NF-κB is activated in cerebral ischemia and causes brain damage.Inhibiting NF-κB can reduce ischemic brain injury,its mechanism may be inhibiting the inflammatory reaction after cerebral ischemia.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2010年第8期748-750,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词
脑缺血
NF-ΚB
白细胞介素6
炎症
血脑屏障
脑梗死
brain ischemia
NF-kappa B;interleukin-6
inflammation
blood brain barrier
brain infarction