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目的探讨1,2-二氯乙烷(1,2-DCE)致大鼠急性中毒性脑病模型中细胞内钙离子的作用。方法离体培养新生SD大鼠脑皮质细胞,设对照组和1、2-DCE低、中、高剂量组,尼莫地平拮抗组。1,2-DCE终浓度分别为0.5、1.0、2.0 mmol/L,拮抗组尼莫地平终浓度为5.0 mmol/L。观察各组神经细胞超微结构、活力及细胞内钙离子浓度的变化。结果与对照组相比,高剂量组神经细胞超微结构有不同程度的损伤,各剂量组细胞活力下降(P<0.01);染毒后24 h内,随着染毒剂量的增加各剂量组细胞内钙离子浓度呈上升趋势,与对照组比较,差异有统计学意义(P<0.01);随着染毒时间的延长,低、中剂量组钙离子浓度呈单峰状,高剂量组呈双峰状;拮抗组神经细胞超微结构较高剂量组有明显改善,细胞活力高于高剂量组(P<0.01)。染毒早期和后期细胞内钙离子浓度低于高剂量组(P<0.01)。结论 1,2-DCE及其代谢产物可致神经细胞水肿坏死,随着染毒剂量的增加各染毒组细胞内钙离子浓度升高,神经细胞损伤严重程度呈上升趋势,而钙离子通道拮抗剂尼莫地平可缓解神经细胞受损程度,提示钙离子在1,2-DCE致神经细胞中毒性脑病中起到重要作用。
Objective To investigate the effect of 1, 2-dichloroethane (1,2-DCE) on intracellular calcium in a rat model of acute toxic encephalopathy. Methods Cultured neonatal SD rat cortical cells were divided into control group and low, medium and high dose 1,2-DCE group, nimodipine antagonistic group. The final concentration of 1,2-DCE was 0.5,1.0,2.0 mmol / L, and the final concentration of nimodipine in the antagonistic group was 5.0 mmol / L. The changes of ultrastructure, vitality and intracellular calcium concentration of nerve cells in each group were observed. Results Compared with the control group, the ultrastructure of nerve cells in high-dose group had different degrees of damage, and the viability of cells in each dose group decreased (P <0.01). Within 24 hours after exposure, (P <0.01). With the prolongation of exposure time, the concentration of calcium ion in the low and medium dose groups showed a unimodal peak, while in the high dose group Bimodal; antagonistic group of ultrastructure of nerve cells in the higher dose group significantly improved, cell viability higher than the high dose group (P <0.01). The intracellular calcium concentration in the early and late stages of exposure was lower than that in the high dose group (P <0.01). Conclusions 1,2-DCE and its metabolites can cause necrosis of neuronal cells. With the increase of exposure dose, intracellular Ca2 + concentration increased and the severity of neuronal injury increased, while Ca2 + channel antagonism Nimodipine can relieve the damage of nerve cells, suggesting that calcium plays an important role in 1,2-DCE-induced neurotoxicity.