Storax protected primary cortical neurons from oxygen-glucose deprivation/reoxygenation injury via inhibiting the TLR4/TRAF6/NF-?B signaling pathway

Storax is a traditional Chinese herb that is widely applied in stroke treatment. However, its neuroprotective effects and mechanisms are yet to be fully elucidated. This study aimed to elucidate the neuroprotective effects and underlying mechanisms of storax on oxygen-glucose deprivation/reoxygenation (OGD/R) in injured cortical neurons. The cortical neurons of Wistar rats were primarily cultured in vitro. The TUNEL method and CM-H2DCFDA probe were used to detect cell apoptosis and reactive oxygen species (ROS) expression. Enzyme -linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blot were used to detect the expression of inflammatory cytokines and proteins of the TLR4/TRAF6/NF-kappa B signaling pathway. Immunofluorescence was used to measure NF-kappa B nuclear translocation. Transfection of TLR4 siRNA was used to detect the potential anti-inflammatory mechanisms of storax. The present results have shown that storax pro-tected primary cortical neurons from OGD/R-induced injury by suppressing ROS generation and cell apoptosis; alleviating HMGB-1, TNF-alpha, IL-1 beta, and ICAM-1 expression; and promoting IL-10 expression. In addition, storax inhibited the activation of TLR4, TRAF6, I kappa B alpha, IKK beta, and NF-kappa Bp65 caused by OGD/R. It is suggested that storax prevents OGD/R-induced primary cortical neuron injury by inhibiting the TLR4/TRAF6/NF-kappa B signaling pathway.

Automated summary

This study aimed to investigate the neuroprotective effects and underlying mechanisms of storax on oxygen-glucose deprivation/reoxygenation (OGD/R) in injured cortical neurons. The results showed that storax protected primary cortical neurons by suppressing ROS generation and cell apoptosis, alleviating inflammatory cytokines expression, and inhibiting the TLR4/TRAF6/NF-kappa B signaling pathway.