Furthermore, after applying a series of kinase inhibitors, CSA-induced Nrf2 activation was markedly inhibited by BML-275 (an AMPK inhibitor), implying that AMPK was the dominant kinase to regulate the Nrf2 pathway for CSA's neuroprotective effects with enhanced AMPK phosphorylation observed both in vivo and in vitro.



THERM
Furthermore, after applying a series of kinase inhibitors, CSA-induced Nrf2 activation was markedly inhibited by BML-275 (an AMPK inhibitor), implying that AMPK was the dominant kinase to regulate the Nrf2 pathway for CSA's neuroprotective effects with enhanced AMPK phosphorylation observed both in vivo and in vitro.



THERM
Furthermore, after applying a series of kinase inhibitors, CSA-induced Nrf2 activation was markedly inhibited by BML-275 (an AMPK inhibitor), implying that AMPK was the dominant kinase to regulate the Nrf2 pathway for CSA's neuroprotective effects with enhanced AMPK phosphorylation observed both in vivo and in vitro.



THERM
Furthermore, after applying a series of kinase inhibitors, CSA-induced Nrf2 activation was markedly inhibited by BML-275 (an AMPK inhibitor), implying that AMPK was the dominant kinase to regulate the Nrf2 pathway for CSA's neuroprotective effects with enhanced AMPK phosphorylation observed both in vivo and in vitro.



THERM