摘要
目的:探讨缓释硫化氢缓释供体对小鼠脑缺血再灌注损伤的影响。方法:采用线栓法建立小鼠局灶性脑缺血模型,将雄性ICR小鼠随机分为假手术组(Sham)、溶剂对照组(Veh)和缓释硫化氢缓释供体ADT-OH组。缺血再灌24h取脑组织,利用TTC染色法检测小鼠脑梗死体积;通过实时定量PCR(qPCR)检测组织中炎症因子。结果:TTC染色结果显示,与Veh相比,ADTOH能够显著降低脑缺血再灌注后大脑皮层、内囊以及大脑半球的梗死体积;qPCR结果显示,与Sham组相比,Veh组小鼠的缺血皮层组织中促炎因子iNOS、IL-1β、TNF-α和IL-6的表达水平明显升高;与Veh相比,ADT-OH显著降低促炎因子表达。结论:硫化氢缓释供体对急性期脑缺血损伤具有一定的保护作用,机制可能与抑制脑缺血损伤诱导的炎症反应相关。
Objective：To investigate the effects of the slow-releasing hydrogen sulfide donor ADT-OH in mice cerebral ischemic reperfusion injury.Methods：The mice focal cerebral ischemia model was found through MCAO and the male ICR mice were randomly divided into Sham,Veh,and slow-releasing hydrogen sulfide donor ADT-OH group.After 24hours＇ ischemic reperfusion,the brain tissue was got out and the mice＇s brain infarct volumes were assessed with triphenyltetrazolium chloride（TTC）staining.The expression of inflammatory factors in tissue was detected by qPCR.Results：The TTC manifested that compared to Veh,the ADT-OH could significantly reduce the cerebral infarct volume of the pallium,internal capsule and cerebral hemisphere after the ischemic reperfusion.The qPCR shown that compared to Sham,the expression level of proinflammatory factors like iNOS,IL-1β,TNF-αand IL-6in the ischemic cortex in Veh was significantly increased;while compared to Veh,ADT-OH reduced the expression of proinflammatory factors significantly.Conclusion：ADT-OH exerted protective effects to acute cerebral ischemic reperfusion injury.The underlying mechanism may be related to the inflammatory reaction which induced by the inhibition of cerebral ischemia.
出处
《陕西医学杂志》
CAS
2016年第3期259-262,共4页
Shaanxi Medical Journal
基金
国家自然科学基金资助项目(81371278)
