TY - JOUR AB - Traumatic brain injury (TBI) is usually caused by accidental injuries and traffic accidents, with a very high mortality rate. Treatment and management following TBI are essential to reduce patient injury and help improve long‑term prognosis. Wogonin is a flavonoid compound with an antioxidant effect extracted from Scutellaria baicalensis Georgi. However, the function and mechanism of wogonin in protecting brain injury remain to be elucidated. The present study established a TBI model of Sprague‑Dawley rats and treated them with wogonin following trauma. The results showed that wogonin treatment significantly reduced neurobehavioral disorders, brain edema and hippocampal neuron damage caused by TBI. It was found that in TBI rats, administration of wogonin increased the levels of antioxidant factors glutathione, superoxide dismutase and catalase in the CA1 region of the hippocampus and significantly inhibited the production of malondialdehyde and reactive oxygen species. western blotting data showed that wogonin exerted antioxidant activity by downregulating the level of NOX2 protein. In inhibiting cell apoptosis, wogonin upregulated the expression of Bcl‑2 protein in the hippocampal CA1 region of TBI rats and inhibited caspase‑3 and Bax proteins. Additionally, wogonin inhibited the progression of injury following TBI through the PI3K/Akt/nuclear factor‑erythroid factor 2‑related factor 2 (Nrf2)/heme oxygenase‑1 (HO‑1) signaling pathway. Wogonin increased the expression of phosphorylated Akt, Nrf2 and HO‑1 in the hippocampus of TBI rats. Following the administration of PI3K inhibitor LY294002, the upregulation of these proteins by wogonin was partly reversed. In addition, LY294002 partially reversed the regulation of wogonin on NOX2, caspase‑3, Bax and Bcl‑2 proteins. Therefore, wogonin exerts antioxidant and anti‑apoptotic properties to prevent hippocampal damage following TBI, which is accomplished through the PI3K/Akt/Nrf2/HO‑1 pathway. AD - Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China Department of Obstetrics, The Fourth Hospital of Shijiazhuang, Shijiazhuang, Hebei 050011, P.R. China Department of Critical Care Medical, Linxi County People's Hospital, Xingtai, Hebei 054000, P.R. China AU - Feng,Yan AU - Ju,Yaru AU - Yan,Zhongjie AU - Ji,Mingjun AU - Yang,Ming AU - Wu,Qiang AU - Wang,Liqun AU - Sun,Guozhu DA - 2022/04/01 DO - 10.3892/ijmm.2022.5109 IS - 4 JO - Int J Mol Med KW - wogonin traumatic brain injury oxidative stress apoptosis PI3K/Nfr2/HO‑1 PY - 2022 SN - 1107-3756 1791-244X SP - 53 ST - Protective role of wogonin following traumatic brain injury by reducing oxidative stress and apoptosis via the PI3K/Nrf2/HO‑1 pathway T2 - International Journal of Molecular Medicine TI - Protective role of wogonin following traumatic brain injury by reducing oxidative stress and apoptosis via the PI3K/Nrf2/HO‑1 pathway UR - https://doi.org/10.3892/ijmm.2022.5109 VL - 49 ER -