Expression of H3K9ac, H3K9me2, HP1, and BDNF Mediated by NMDAR-ERK Pathway in Hippocampus Tissues of Rats Exposed to Aluminum Chloride

Objective To examine expression levels of N-methyl-D-aspartate receptor(NMDAR), phosphorylatedextracellular signal regulated protein kinase(p-ERK), H3K9ac, H3K9me2, HP1, and BDNF in hippocampus tissue of rats chronically exposed to aluminum.

Methods Twenty-four male SD rats(specific pathogen free) were randomly selected by body weight into four groups, in which drinking water contained 0, 2, 12, and 72mg/kg of aluminum chloride(AlCl₃) for 120d respectively. The protein expression levels of NMDAR, p-ERK, H3K9ac, H3K9me2, HP1, and BDNF were detected by Western blot.

Results Compared with the control group, the expression levels of NMDAR, p-ERK, H3K9ac, and BDNF in hippocampus of the 72 mg/kg aluminum exposed group were significantly lower(P < 0.05 or P < 0.01) in an inverse dose-dependent manner(r_NMDAR=-0.61, r_p-ERK=-0.69, r_H3K9ac=-0.93, and r_BDNF=-0.73, all Ps < 0.05). However, the expression levels of H3K9me2 and HP1 in hippocampus of the 72 mg/kg aluminum exposed group were both significantly higher(P < 0.05) in a dose-dependent manner(r_H3K9me2=0.67 and r_HP1=0.72, both Ps < 0.01).

Conclusion Chronic aluminum exposure may change the expression of H3K9ac, H3K9me2, HP1, and BDNF via NMDAR-ERK pathway.