Abstract
Inflammatory response plays an important role in the pathogenesis of ischemic stroke and anti-inflammatory agents may provide a choice of treatment. Triptolide is reported to be anti-inflammatory. In this study, we investigated the effects of triptolide on cultured neuronal cell line in vitro and experimental ischemic stroke in vivo. Oxygen–glucose deprivation (OGD) and tumor necrosis factor-α (TNF-α) stimulated SH-SY5Y cells were incubated with triptolide. In vivo, rats were subjected to middle cerebral artery occlusion (MCAO) for 1 h, followed by reperfusion for 23 h. Results of this study showed that triptolide treatment reduced the OGD-induced cytotoxicity and apoptosis and blocked TNF-α-induced activation of NF-κB and p38MAPK in SH-SY5Y cells. Intraperitoneal injection of triptolide showed significant neuroprotective actions in stroke rats. Triptolide attenuated neurological deficit, brain infarct volume, and brain water content, and inhibited activation of NF-κB and p38MAPK. These data show that triptolide protects rats against ischemic cerebral injury via inhibiting NF-κB and p38MAPK signaling pathways.





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Hao, M., Li, X., Feng, J. et al. Triptolide Protects Against Ischemic Stroke in Rats. Inflammation 38, 1617–1623 (2015). https://doi.org/10.1007/s10753-015-0137-x
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DOI: https://doi.org/10.1007/s10753-015-0137-x