赤芍801通过抑制NF-κB抗脑缺血-再灌注损伤的机制  

Mechanism of the reduction of cerebral ischemic-reperfusion injury through inhibiting the activity of NF-κB by propyl gallate

作　　者：郑建明[1,2] 陈晓春[1] 林敏 张静 林智颖[1] 郑关毅 李康增 

机构地区：[1]福建医科大学附属协和医院神经内科,福建福州350001 [2]福建省宁德市闽东医院神经内科,福建宁德355000 [3]猖建省老年医学研究所,福建福州350001

出　　处：《药学学报》2011年第2期158-164,共7页Acta Pharmaceutica Sinica

基　　金：福建省重大科技基金资助项目(2003F009)

摘　　要：探讨赤芍801减轻在体大鼠脑缺血-再灌注损伤的可能机制。采用线栓模型制作大鼠局灶性脑缺血-再灌注损伤模型,在缺血后给予赤芍801,用Western blotting方法检测脑缺血周边区的NF-κB活性、COX-2和HSP70的表达量,用ELISA方法测定TNF-α的表达量,用RT-PCR方法和免疫荧光染色法检测TLR-4的转录和蛋白表达。结果显示:赤芍801能抑制脑缺血周边区NF-κB活性,减少COX-2和TNF-α的表达,同时抑制NF-κB的上游TLR-4的转录和蛋白表达,对TLR-4的内源性配体HSP70的蛋白表达也有抑制作用。赤芍801作为一种抗氧化剂,有可能通过抑制脑缺血周边区的NF-κB活性,减少局部的COX-2和TNF-α的表达,达到减轻脑缺血-再灌注损伤的目的,同时对NF-κB的上游HSP70和TLR-4产生影响。The probable mechanism of the reduction of rat cerebral ischemic-reperfusion injury by propyl gallate was studied.Intraluminal suture middle cerebral artery occlusion model of rat was employed.Propyl gallate was injected immediately after the ischemia was happened.The activity of NF-κB,and the expression of COX-2 and HSP70 on the peripheral ischemia were determined by Western blotting.The expression of TNF-α was determined by ELISA assay.RT-PCR and immunofluorescence staining were employed to detect the transcription and expression of TLR-4.Results showed that propyl gallate could inhibit the activity of NF-κB in the peripheral ischemia,and reduce the expression of COX-2 and TNF-α.As the upstream of NF-κB,the transcription and expression of TLR-4 decreased,as well as HSP70,the endogenic ligand of TLR-4.As an antioxidant,propyl gallate could reduce the cerebral ischemic-reperfusion injury through inhibiting the activity of NF-κB and decreasing the COX-2 and TNF-α in the peripheral ischemia.It also could influence HSP70 and TLR-4.

关 键 词：赤芍801 NF-ΚB 脑缺血-再灌注损伤 

分 类 号：R963[医药卫生—微生物与生化药学]