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目的研究铝对大鼠大脑皮层细胞中Ryanodine受体2(ryanodine receptor,Ryr2)和L-型钙通道α1C亚基(α1Csubunit of L-type calcium channels,L-Ca2+α1C)基因表达的影响,探讨铝对细胞内钙浓度改变的机制。方法健康Wistar大鼠随机分为4组,分别按照大鼠氯化铝经口LD50的1/15 LD50(248.7 mg/kg)、1/50 LD50(74.7 mg/kg)、1/100 LD50(37.3mg/kg)给予灌胃染毒,同时设立阴性对照组(蒸馏水)。连续灌胃120 d,分别在染毒45、75和120 d和染毒结束后30 d处死4只实验动物,取大脑皮层。应用荧光定量链式反应(RT-PCR)方法,检测各组动物皮层中Ryr2和L-Ca2+α1c基因表达情况。结果染毒大鼠大脑皮层中Ryr2mRNA表达显著高于对照组;各组动物大脑皮层中Ryr2mRNA表达均随时间延长而增高;染毒大鼠大脑皮层细胞中L-Ca2+α1c mRNA表达在不同染毒时期均高于对照组;各组动物大脑皮层中L-Ca2+α1c mRNA表达均随时间延长而降低。结论铝可引起大脑皮层中Ryr2和L-Ca2+α1c基因表达的增加,而增加细胞内游离钙浓度,从而发挥神经毒性作用。
Objective To investigate the effect of aluminum on gene expression of Ryanodine receptor 2 (Ryr2) and L-type calcium channel α1C subunit (L-Ca2 + α1C) in rat cerebral cortex Mechanism of Aluminum Alteration in Intracellular Calcium Concentration. Methods Healthy Wistar rats were randomly divided into 4 groups according to 1/15 LD50 (248.7 mg / kg), 1/50 LD50 (74.7 mg / kg), 1/100 LD50 (37.3 mg / kg) given intragastric administration, while setting up a negative control group (distilled water). The rats were sacrificed for 120 days. Four experimental animals were sacrificed at 45, 75, and 120 days after exposure and 30 days after the exposure, respectively. The cerebral cortex was removed. The expression of Ryr2 and L-Ca2 + α1c in the cortex of each group were detected by real-time fluorescence quantitative polymerase chain reaction (RT-PCR). Results The expression of Ryr2mRNA in the cerebral cortex of the treated rats was significantly higher than that of the control group. The expression of Ryr2mRNA in the cerebral cortex of rats in each group increased with time. The expression of L-Ca2 + The expression of L-Ca2 + α1c mRNA in cerebral cortex decreased with time. Conclusion Aluminum can induce the increase of Ryr2 and L-Ca2 + α1c gene expression in the cerebral cortex, and increase the intracellular free calcium concentration, which leads to neurotoxic effect.