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目的研究地卓西平对甲基汞致大鼠脑皮质细胞内钙稳态失调的影响。方法 Wistar大鼠32只,按体重随机分成4组,每组8只。第1组为对照组,腹腔注射0.9%氯化钠;第2组为低剂量甲基汞染毒组,腹腔注射4μmol/kg的甲基汞溶液;第3组为高剂量甲基汞染毒组,腹腔注射12μmol/kg的甲基汞溶液;第4组为地卓西平预处理组,隔日皮下注射0.3μmol/kg地卓西平,2 h后腹腔注射12μmol/kg的甲基汞溶液;注射容量均为5 ml/kg,染毒4周,每周5次。观察神经细胞内Ca2+浓度及其凋亡情况,同时测定脑皮质Hg含量和与维持钙稳态相关的酶Na+-K+-ATPase和Ca2+-ATPase活性。结果染毒4周后,随着染毒剂量的增加,脑皮质Hg含量和细胞内Ca2+浓度均明显升高(P<0.01);细胞凋亡率明显高于对照组(P<0.01);脑皮质Na+-K+-ATPase和Ca2+-ATPase活性均不同程度的受到抑制。地卓西平预处理可以明显缓解神经细胞凋亡和细胞内Ca2+超载,对Na+-K+-ATPase和Ca2+-ATPase活性也有一定程度的恢复作用。结论甲基汞通过抑制与维持钙稳态相关的酶Na+-K+-ATPase和Ca2+-ATPase活性,干扰神经细胞内钙稳态,进而造成神经细胞凋亡。地卓西平可以阻断Ca2+通道对钙稳态失调引起的细胞损伤有拮抗作用。
Objective To study the effect of dizocilpine on the imbalance of calcium homeostasis in methylmercury-induced rat cerebral cortical cells. Methods Thirty-two Wistar rats were randomly divided into 4 groups according to body weight, with 8 rats in each group. The first group was control group, intraperitoneal injection of 0.9% sodium chloride; the second group was low dose methylmercury exposure group, intraperitoneal injection of methylmercury solution 4μmol / kg; the third group was high dose methylmercury Group, intraperitoneal injection of 12μmol / kg of methylmercury solution; the fourth group for the diroxipine pretreatment group, subcutaneous injection of 0.3μmol / kgDizoceptive every other day, 2h after intraperitoneal injection of 12μmol / kg methylmercury solution; injection Capacity of 5 ml / kg, 4 weeks, 5 times a week. The concentration of Ca2 + in neurons and their apoptosis were observed. Hg contents in the cerebral cortex and the activities of Na + -K + -ATPase and Ca2 + -ATPase were also determined. Results After 4 weeks of exposure, the contents of Hg and intracellular Ca2 + in cerebral cortex were significantly increased (P <0.01) with the increase of exposure dose. The apoptosis rate was significantly higher than that of control group (P <0.01) Cortical Na + -K + -ATPase and Ca2 + -ATPase activity were inhibited to varying degrees. Dendrolimus preconditioning could relieve nerve cell apoptosis and intracellular Ca2 + overload obviously, and also restored the activity of Na + -K + -ATPase and Ca2 + -ATPase. Conclusion MeHg interferes with intracellular calcium homeostasis by inhibiting the activities of Na + -K + -ATPase and Ca2 + -ATPase, which are related to the maintenance of calcium homeostasis, leading to neuronal apoptosis. Dezococryptine can block the Ca2 + channel antagonism of cell damage caused by calcium homeostasis.