CD38在缺血/再灌注诱导的局灶性脑缺血再灌注大鼠脑损伤及在炎症反应中的可能作用  

Investigation of the possible role of CD38 in focal cerebral ischemia-reperfusion induced brain injury and inflammatory response in rats

作　　者：吴岳[1] 刘皎如 顾存林[1] 唐延军[1] 赵洪乾 高如阳 吴穹[1] WU Yue;LIU Jiaoru;GU Cunlin;TANG Yanjun;ZHAO Hongqian;GAO Ruyang;WU Qiong(Qinghai University Medical College,Xining,Qinghai,China 810001;Qinghai Criminal Police Corps,Xining,Qinghai,China 810000;Department of Aviation Health Support and Flight Safety,Air Force Characteristic Medical Center,Beijing,100089,China)

机构地区：[1]青海大学医学院,青海西宁810001 [2]青海省刑警总队,青海西宁810000 [3]空军特色医学中心研究部航空卫生保障与飞行安全研究室,北京100089

出　　处：《中国高原医学与生物学杂志》2022年第1期24-32,共9页Journal of Chinese High Altitude Medicine & Biology

基　　金：青海省科技计划基金(No.2018-ZJ-720)。

摘　　要：目的探讨CD38在缺血/再灌注诱导的局灶性脑缺血再灌注大鼠脑损伤及在炎症反应中的可能作用。方法建立SD大鼠局灶性脑缺血模型,给大鼠脑海马注射Ad-siCD38腺病毒,评估大鼠神经功能;用Elisa法检测大鼠血清中TNF-α、IL-1β、IL-6水平;用HE染色法观察大鼠脑海马组织形态学变化;用尼氏染色法观察大鼠神经元形态变化,用高尔基体染色法观察脑神经元及树突棘变化;用免疫组化法检测GFAP阳性细胞表达水平、RT-PCR和Western blot法检测大鼠脑组织中NF-kB、TNF-α、IL-1β、IL-6和CD38 mRNA及蛋白表达水平。结果与模型组比较,Ad-si CD38腺病毒干预能通过增加脑组织中尼氏小体、树突棘数量及神经元树突分支复杂性改善大鼠脑损伤情况,降低大鼠血清中TNF-α、IL-1β、IL-6含量,显著下调大鼠脑组织NF-κB p65、TNF-α、IL-1β、IL-6和CD38 mRNA及蛋白表达水平,并能减少大鼠脑组织中GFAP的阳性表达水平。结怡通过CD38基因下调调节炎症反应来延缓局灶性脑缺血再灌注大鼠的脑损伤。Objective To investigate the possible role of CD38 in focal cerebral ischemia-reperfusion induced brain injury and inflammatory response in rats.Methods The model of focal cerebral ischemia in SD rats was estab・lished.The rats were injected with AD-SI CD38 adenovirus into the hippocampus to evaluate the neurological function of the rats.Serum levels of TNF-α,IL-1 and IL-6 were detected by ELISA.Morphological changes of rat hipp-ocampal brain were observed by HE staining.Morphological changes of rat neurons were observed by Nissl staining,and changes of brain neurons and dendritic spines were observed by Golgi body staining.Immunohistochemistry was used to detect the expression of GFAP positive cells.Results compared with model group,the Ad-si CD38 adenovirus can be intervented by increasing the number of brain tissue Nepal's body,the complexity of neuron dendritic branches and number of dendritic spines could improve the injury of rats,decrease the rats'serum TNF-α lpha,-beta and the contents of IL-6,IL-1 and NF-κB.Moreover,p65,TNF alpha,beta,IL-6 and IL-1 CD38 mRNA and protein expression level were significantly downregulated and could reduce the organization GFAP positive expression in rats.Conclusion CD38 gene downdegulation can delay the brain injury in focal cerebral ischemia-reperfusion rats by regulating inflammatory response.

关 键 词：局灶性脑缺血再灌注 CD38 RNA 干扰 炎症 反应 

分 类 号：R34[医药卫生—基础医学]