Storax Protected Primary Cortical Neurons from Oxygen-Glucose Deprivation/Reoxygenation Injury via Inhibiting the TLR4/TRAF6/NF- κB Signaling Pathway

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. TheTUNELmethod 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-κB signaling pathway. Immunofluorescence was used to measure NF-κB nuclear translocation. Transfection of TLR4 siRNA was used to detect the potential anti-inflammatory mechanisms of storax. The present results have shown that storax protected primary cortical neurons from OGD/R-induced injury by suppressing ROS generation and cell apoptosis; alleviating HMGB-1, TNF-α, IL-1β, and ICAM-1 expression; and promoting IL-10 expression. In addition, storax inhibited the activation of TLR4, TRAF6, IκBα, IKKβ, and NF-κBp65 caused by OGD/R. It is suggested that storax prevents OGD/R-induced primary cortical neuron injury by inhibiting the TLR4/TRAF6/NF-κB signaling pathway.PMID:35878660 | DOI:10.1016/j.brainres.2022.148021
Source: Brain Research - Category: Neurology Authors: Source Type: research