Neuro-protection of Chlorogenic acid against Al-induced apoptosis in PC12 cells via modulation of Al metabolism and Akt/GSK-3β pathway

Dietary polyphenols showed good scavenging effects on the neurotoxicity of aluminum (Al). The aim of this study was to explore the mechanism of CGA on AlCl3 in PC12 cells. Based on the protective effect of CGA on the apoptosis of PC12 cells induced by AlCl3, we designed a scheme of intervention with CGA before, during and after AlCl3 treatment. The results showed that the co-treatment of CGA and AlCl3 showed the best protective effect, and CGA interfered with the normal metabolism of Al(III) by stimulating the outflow of Al(III) and inhibiting the entry of Al(III) by chelating with extracellular Al(III), thus reducing the intracellular Al(III) level. CGA significantly inhibited the accumulation of ROS and A beta(1-42) induced by AlCl3, slowed down the G0-G1 phase arrest, and then decreased the apoptotic rate of PC12 cells. In general, CGA plays a neuroprotective role by regulating the Akt/GSK-3 beta signaling pathway in PC12 cells.