177.
Cadmium is a toxic metal that can damage the brain and other organs. This study aimed to explore the protective effects of Potentilla
anserine L. polysaccharide (PAP) against CdCl
2-induced neurotoxicity in N2a and SH-SY5Y cells and in the cerebral cortex of BALB/c mice. In addition, we aimed to identify the potential mechanisms underlying these protective effects. Relative to CdCl
2 treatment alone, pretreatment with PAP prevented the reduction in cell viability evoked by CdCl
2, decreased rates of apoptosis, promoted calcium homeostasis, decreased ROS accumulation, increased mitochondrial membrane potential, inhibited cytochrome C and AIF release, and prevented the cleavage of caspase-3 and PARP. In addition, PAP significantly decreased the CdCl
2-induced phosphorylation of CaMKII, Akt, and mTOR. In conclusion, PAP represents a potential therapeutic agent for the treatment of Cd-induced neurotoxicity, functioning in part via attenuating the activation of the mitochondrial apoptosis pathway and the Ca
2+-CaMKII-dependent Akt/mTOR pathway.
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