Anti‐Inflammatory and Neuroprotective Effects of Triptolide via the NF‐κB Signaling Pathway in a Rat MCAO Model. Issue 2 (9th December 2015)

• Record Type: Journal Article
• Authors: Bai, Shi; Hu, Zhiying; Yang, Yang; Yin, Yifei; Li, Weiyun; Wu, Lijuan; Fang, Marong
• Is Part Of: Anatomical record. Volume 299:Issue 2(2016)
• Page Start: 256
• Page End: 266
• Publication Date: 2015-12-09
• Subjects: triptolide -- cerebral ischemia -- neuroinflammation -- COX‐2 -- NF‐κB; Anatomy -- Periodicals; Evolution (Biology) -- Periodicals; Morphology -- Periodicals; 571.3
• DOI: 10.1002/ar.23293
• Languages: English
• ISSNs: 1932-8486

Abstract

ABSTRACT: Stroke is the leading cause of neurological disability in humans. Middle cerebral artery occlusion (MCAO) followed by reperfusion is widely accepted to mimic stroke in basic medical research. Triptolide is one of the major active components of the traditional Chinese herb Tripterygium wilfordii Hook F, and has been reported to have potent anti‐inflammatory and immunosuppressive properties. Since its preclinical effects on stroke were still unclear, we decided to study the effects of Triptolide on focal cerebral ischemia/reperfusion injury in this study. The results showed that Triptolide treatment significantly attenuates brain infarction volume, water content, neurological deficits, and neuronal cell death rate, which were increased in the MCAO model rats. Immunohistochemistry was used to analyze the expression of glial fibrillary acidic protein (GFAP), Cyclooxygenase‐2 (COX‐2), inducible nitric oxide (iNOS), and NF‐κB in the ischemic brains. The administration of Triptolide showed down‐regulation of the iNOS, COX‐2, GFAP, and NF‐κB expression in MCAO rats. It also increased the expression of bcl‐2, and suppressed levels of bax and caspase‐3 compared with the MCAO group. Our findings revealed that Triptolide exerts its neuroprotective effects against inflammation with the involvement of inhibition of NF‐κB activation. Anat Rec, 299:256–266, 2016. © 2015 Wiley Periodicals, Inc.