The role of Nrf2/HO-1 signal pathway in regulating aluminum-induced apoptosis of PC12 cells

Abstract

BackgroundAluminum has definite neurotoxicity and can lead to apoptosis of nerve cells, but the specific mechanism remains to be further explored. The aim of this study was to investigate the role of Nrf2/HO-1 signaling pathway in neural cell apoptosis induced by aluminum exposure. MethodsIn this study, PC12 cells were used as the research object, aluminum maltol [Al(mal)3] was used as the exposure agent, and tert-butyl hydroquinone (TBHQ), an agonist of Nrf2, was used as the intervention agent to construct an in vitro cell model. Cell viability was detected by CCK-8 method, cell morphology was observed by light microscope, cell apoptosis was measured by flow cytometry, and expression of Bax and Bcl-2 proteins and Nrf2/HO-1 signaling pathway proteins were investigated by western blotting. ResultsWith the increase of Al(mal)3 concentration, PC12 cell viability decreased, the early apoptosis rate and total apoptosis rate increased, the ratio of Bcl-2 and Bax protein expression decreased, and Nrf2/HO-1 pathway protein expression decreased. The use of TBHQ could activate the Nrf2/HO-1 pathway and reverse the apoptosis of PC12 cells induced by aluminum exposure. ConclusionNrf2/HO-1 signaling pathway plays a neuroprotective role in the apoptosis of PC12 cells caused by Al(mal)3, which provides a possible target for the intervention of aluminum induced neurotoxicity.