Anti-inflammatory Effect Of Triptolide On Focal Cerebral Ischemia/reperfusion In Injury In Rats

Objective:To investigate the effect of triptolide on the inflammatory reaction after focal cerebral ischemia/reperfusion injury in rats. Methods:Ischemic brain injury was induced by middle cerebral arterial occlusion (MCAO). A total of80SD rats were included and randomly divided into5groups:normal control, sham group, DMSO group, MCAO group and triptolide-treated group. After24h of reperfusion, brain injury parameters such as infarction volume, water content, neurological deficits were determined. TUNEL staining was used to identify the neuronal cell death rate in rat. Immunohistochemistry was used to analyse the expression of glial fibrillary acidic protein (GFAP), Cyclooxygenase-2(COX-2), inducible nitric oxide (iNOS) and NF-κB in ischemic brain. We also used RT-PCR to detect the level of COX-2and iNOS mRNA. Results:Triptolide treatment significantly decrease brain infarction volume, water content, neurological deficits and neuronal cell death rate, which were increased in the MCAO model rats. Triptolide reduced the number of TUNEL positive cells in the brain. The administration of Triptolide could significantly downregulate the expression of iNOS, COX-2, GFAP and NF-κB in MCAO rats. Conclusion:The outcomes suggest that Triptolide could be an anti-inflammatory and potential neuroprotective agent for cerebral ischemia/reperfusion injury.