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目的研究甲基汞致大鼠神经毒性的作用机制,探讨茶多酚对甲基汞致神经毒性作用的影响。方法36只Wistar大鼠随机分成3组,对照组,染汞组(12μmol/kg),茶多酚干预组(1 mmol/kg),连续干预染毒4周,最后1次染毒后24 h,将大鼠麻醉后处死,断头取脑,冰浴下分离大脑皮质,测定Na+-K+-ATP酶、Ca2+-ATP酶活力及细胞内Ca2+、活性氧簇(ROS)含量及细胞凋亡情况。结果与对照组比较,单纯染汞组Na+-K+-ATP酶[(2.72±0.46)μmol/(h.mg)]、Ca2+-ATP酶活力[(1.52±0.26)μmol/(h.mg)]明显降低(P<0.01),细胞内Ca2+含量(239.52±44.84)nmol/L、ROS含量(313.86±35.11)及细胞凋亡率[(40.84±6.26)%]明显升高(P<0.01);与染汞组比较,茶多酚干预组Na+-K+-ATP酶活力[(3.58±0.71)μmol/(h.mg)]、Ca2+-ATP酶活力[(1.98±0.29)μmol/(h.mg)]明显升高(P<0.05或P<0.01),细胞内Ca2+含量(188.39±7.43)nmol/L、ROS含量(238.03±22.99)及细胞凋亡率[(28.31±4.34)%]明显降低(P<0.05或P<0.01)。结论茶多酚对甲基汞致大鼠神经毒性有一定拮抗作用。
Objective To study the mechanism of methylmercury-induced neurotoxicity in rats and explore the effect of tea polyphenols on the neurotoxicity induced by methylmercury. Methods Thirty-six Wistar rats were randomly divided into three groups: control group, 12 μmol / kg group, 1 mmol / kg TCA group, and continuous intervention for 4 weeks. After the last exposure, The rats were killed after anesthesia, the brain was decapitated, and the cerebral cortex was separated by ice bath. The activity of Na + -K + -ATPase, Ca2 + -ATPase and the content of intracellular Ca2 + and reactive oxygen species (ROS) . Results Compared with the control group, the activities of Na + -K + -ATPase (2.72 ± 0.46 μmol / (h · mg)] and Ca2 + -ATPase activity in pure mercury group [(1.52 ± 0.26) μmol / (h · mg) (P <0.01). The content of intracellular Ca2 + (239.52 ± 44.84) nmol / L, the content of ROS (313.86 ± 35.11) and the apoptosis rate [(40.84 ± 6.26)%] were obviously decreased. Compared with the control group, the activity of Na + -K + -ATPase in the tea polyphenols intervention group was significantly higher than that in the control group ([(3.58 ± 0.71) μmol / (h.mg)], Ca2 + -ATPase activity [(1.98 ± 0.29) ) Were significantly increased (P <0.05 or P <0.01). The contents of intracellular Ca2 + (188.39 ± 7.43) nmol / L, ROS content (238.03 ± 22.99) and cell apoptosis rate [(28.31 ± 4.34)%] (P <0.05 or P <0.01). Conclusion Tea polyphenols can antagonize the neurotoxicity induced by methylmercury in rats.