氯化铝染毒大鼠海马组织NMDAR-ERK通路调节H3K9ac、H3K9me2、HP1和BDNF蛋白的表达
Expression of H3K9ac, H3K9me2, HP1, and BDNF Mediated by NMDAR-ERK Pathway in Hippocampus Tissues of Rats Exposed to Aluminum Chloride
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摘要:
目的 研究慢性染铝对大鼠海马组织N-甲基-D-天冬氨酸受体（NMDAR）、p-细胞外信号调节蛋白激酶（p-ERK）、H3K9ac、H3K9me2、HP1、BDNF表达量的影响。
方法 雄性SD大鼠，SPF级，共24只，按体重随机分为对照组（自来水）和铝染毒2、12、72 mg/kg组，每组6只。染毒组每天经饮水染毒AlCl3，共持续120 d。染毒结束后，用Western blot法测定各种蛋白表达量。
结果 与对照组相比，72 mg/kg组海马中NMDAR、p-ERK的表达量均降低（
P < 0.05）；72 mg/kg组H3K9ac、BDNF的表达量与对照组比较均下降（均P < 0.01），且随着染毒剂量的增加表达量均呈下降趋势（r NMDAR=-0.61；r p-ERK=-0.69；r H3K9ac=-0.93；r BDNF=-0.73，均P < 0.05）；而72 mg/kg组H3K9me2、HP1的蛋白表达量均高于对照组（P < 0.05，P < 0.01），且随着染毒剂量的增加表达量呈上升趋势（r H3K9me2=0.67；r HP1=0.72，均P < 0.01）。结论 铝可能经NMDAR-ERK通路引起大鼠海马组织H3K9ac、H3K9me2、HP1、BDNF表达量发生改变。
Abstract: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 orP < 0.01) in an inverse dose-dependent manner(r NMDAR=-0.61,r p-ERK=-0.69,r H3K9ac=-0.93, andr BDNF=-0.73, allPs < 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 andr HP1=0.72, bothPs < 0.01).Conclusion Chronic aluminum exposure may change the expression of H3K9ac, H3K9me2, HP1, and BDNF via NMDAR-ERK pathway.
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