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用不同浓度醋酸镉(0、5、10、20μmol/L)以及细胞内钙离子螯合剂BAPTA-AM(10μmol/L)单独或联合作用于大鼠大脑皮质神经细胞12h,利用流式细胞仪检测细胞凋亡率、细胞内[Ca2+]i、活性氧(ROS)水平以及线粒体膜电位(ΔΨm)。结果显示,与对照组相比,各镉染毒组细胞凋亡率、细胞内[Ca2+]i和ROS水平显著或极显著升高(P<0.05或P<0.01),ΔΨm显著或极显著降低(P<0.05或P<0.01)。BAPTA-AM联合组与相应镉染毒组相比,细胞凋亡率、细胞内[Ca2+]i和ROS水平降低,ΔΨm升高,部分组间差异显著或极显著(P<0.05或P<0.01)。结果表明,镉可诱导大脑皮质神经细胞凋亡,细胞内钙稳态失衡在镉诱导大脑皮质神经细胞凋亡中起着重要作用,凋亡机理可能与细胞内钙超载引起ROS水平升高和ΔΨm下降有关。
Rat cerebral cortical neurons were treated with different concentrations of cadmium acetate (0, 5, 10 and 20 μmol / L) and intracellular calcium chelator BAPTA-AM (10 μmol / L) alone or in combination for 12 h. Flow cytometry Apoptosis rate, intracellular [Ca2 +] i, reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm). The results showed that compared with the control group, the apoptotic rate, intracellular [Ca2 +] i and ROS levels were significantly or extremely significantly increased (P <0.05 or P <0.01), and ΔΨm significantly or extremely significantly decreased (P <0.05 or P <0.01). The apoptotic rate, the level of intracellular [Ca2 +] i and ROS and the ΔΨm in BAPTA-AM group were significantly (P <0.05 or P <0.01) higher than those in the control group ). The results showed that cadmium can induce neuronal apoptosis in the cerebral cortex. Intracellular calcium homeostasis plays an important role in cadmium-induced apoptosis of cerebral cortical neurons. The mechanism of apoptosis may be related to the increase of ROS level and ΔΨm Decline related.