Abstract: In order to explore the role of death receptor Fas in the autophagosomes formation of rat cerebral cortex induced by cadmium (Cd), twenty-four 21-day-old male SD rats were randomly divided into 4 groups:control group, Cd group, Cd and control virus co-treated group, Cd and Fas gene silencing virus co-treated group. During the experiment, the rats in the control group drank purified water freely. Rats in the virus treatment groups were injected with corresponding virus through the tail vein at a dose of 1.4×10¹¹ vg per rat on the first day. Four weeks later, rats in the Cd-exposed groups received drinking water containing 50 mg·L^-1 Cd freely for 90 days. After the experiment, the number of autophagosomes in the cerebral cortex was observed by transmission electron microscope. The protein expression level of extracellular signal-regulated kinase 1/2 (Erk1/2), p-Erk1/2, autophagy-related protein 7 (ATG7), autophagy related gene (Beclin-1), microtubule-associated protein 1 light chain 3 (LC3) in the cerebral cortex were detected by Western blot. The expression level of LC3 was detected by immunofluorescence staining. The results showed that Cd increased the number of autophagosomes in the cerebral cortex, significantly activated Erk1/2 and up-regulated the protein expression levels of ATG7, Beclin-1 and LC3 (P<0.01). Fas gene silencing inhibited Cd-induced increase of autophagosomes, and significantly inhibited Cd-induced activation of Erk1/2 and upregulation of ATG7, Beclin-1, LC3 protein expression levels (P<0.01). The results indicated that Fas participated in Cd-induced autophagosomes formation by activating Erk1/2 in rat cerebral cortex.

Key words: cadmium, Fas, rat, cerebral cortex, autophagy