Tripotolide ameliorates inflammation and apoptosis induced by focal cerebral ischemia/reperfusion in rats
10.3785/j.issn.1008-9292.2016.09.07
- VernacularTitle:雷公藤甲素缓解局灶性脑组织缺血再灌注损伤诱发的炎症及其相关凋亡的研究
- Author:
Shi BAI
1
;
Yayi SUN
;
Lijuan WU
;
Zhongmin WU
;
Marong FANG
Author Information
1. 台州学院医学院
- Keywords:
Triptolide/therapeutic use;
Brain ischemia/drug therapy;
Reperfusion injury/drug therapy;
Neuritis/drug therapy;
NF-kappa B/metabolism;
Cyclooxygenase 2/metabolism;
Nitric oxide synthase/metabolism;
Disease models,animal
- From:
Journal of Zhejiang University. Medical sciences
2016;45(5):492-499
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of triptolide on inflammation and apoptosis induced by focal cerebral ischemia/reperfusion in rats .Methods: The rat model of focal cerebral ischemia/reperfusion injury was established according to Longa's method.A total of 80 SD rats were randomly divided into 5 groups: normal control, sham group , DMSO group , middle cerebral artery occlusion ( MCAO ) group , and MCAO with tripolide treatment group .TTC staining was used to examine the site and volume of cerebral infarction , and Longa score was employed for neurological disorders measurement . Number of astrocytes was measured by fluorescence staining , and neuronal apoptosis was determined by TUNEL staining .The expressions of inducible nitric oxide synthase ( iNOS ) , cyclooxygenase 2 ( COX-2 ) and NF-κB proteins were detected by immunohistochemistry , and the expression of iNOS , COX-2 mRNA was detected by real-time PCR.Results: Compared with DMSO group and MCAO group , brain edema was improved ( 80 .03 ±0 .46 ) % ( P <0 .05 ) , infarct volume was reduced (8.3 ±1.4)%(P<0.01), Longa score was decreased (1.38 ±0.20, P<0 .05 ) in triptolide treatment group .Meanwhile triptolide also dramatically reduced the number of GFAP-positive astrocytes ( P <0.05 ), alleviated protein expression of COX-2 (91.67 ±1.31), iNOS (95.24 ±5.07) and NF-κB (75.03 ±2.06) triggered by MCAO ( all P<0 .05 ) , and induced a down-regulation of cell apoptosis as showed by TUNEL assay (64.15 ±3.52, P<0.05).Conclusion: Triptolide can reduce the cerebral infarction volume , attenuate brain edema and ameliorate the neurological deficits induced by cerebral ischemia-reperfusion injury rats , indicating that it might be used as a potential anti-inflammatory agent .
