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Войти в исследования Journal of pharmacological sciences · 2026
Ferulic acid activates Nrf2/HO-1 signaling axis to ameliorate neuronal Golgi stress by SKP2.
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Dong Qinghua, Liu Chao, Li Aiguo, Zhao Xinwei, Qin Xiaohui, Xu Wencong, Tang Gangjian
Аннотация
BACKGROUND: Traumatic brain injury (TBI) ranks among the top contributors to neurological impairments worldwide, with Golgi stress implicated in neuronal injury. This study investigated the neuroprotective effects of ferulic acid (FA) in TBI by regulating Golgi stress.
METHODS: HT-22 and NSC34 cells were exposed to H2O2 to induce a neuronal injury model. Protein expression were evaluated via Western blot and immunofluorescence. Cell viability and apoptosis were quantified using CCK-8 assay and TUNEL staining, respectively. The interactions between Src, SKP2, and Nrf2 were detected by Co-IP assay.
RESULTS: FA treatment reduced LDH release, as well as repressed Golgi stress and apoptosis by H2O2-induced in HT-22 and NSC34 cells. Mechanistically, FA inhibited Src-mediated phosphorylation of SKP2 at Y131, preventing SKP2-mediated Nrf2 ubiquitination and degradation. Moreover, FA activated the antioxidative Nrf2/HO-1 pathway, alleviating H2O2-induced Golgi stress and neuronal injury.
CONCLUSION: FA reduced neuronal Golgi stress in H2O2-treated neuronal cells by restoring the Nrf2/HO-1 signaling through inhibiting Src-mediated SKP2 phosphorylation. These findings indicate that FA is a potential neuroprotective agent.
METHODS: HT-22 and NSC34 cells were exposed to H2O2 to induce a neuronal injury model. Protein expression were evaluated via Western blot and immunofluorescence. Cell viability and apoptosis were quantified using CCK-8 assay and TUNEL staining, respectively. The interactions between Src, SKP2, and Nrf2 were detected by Co-IP assay.
RESULTS: FA treatment reduced LDH release, as well as repressed Golgi stress and apoptosis by H2O2-induced in HT-22 and NSC34 cells. Mechanistically, FA inhibited Src-mediated phosphorylation of SKP2 at Y131, preventing SKP2-mediated Nrf2 ubiquitination and degradation. Moreover, FA activated the antioxidative Nrf2/HO-1 pathway, alleviating H2O2-induced Golgi stress and neuronal injury.
CONCLUSION: FA reduced neuronal Golgi stress in H2O2-treated neuronal cells by restoring the Nrf2/HO-1 signaling through inhibiting Src-mediated SKP2 phosphorylation. These findings indicate that FA is a potential neuroprotective agent.