A novel painkiller nanomedicine triggers the specific delivery of enkephalin neuropeptide into inflamed tissues.

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.