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目的探讨邻苯二甲酸-单-乙基己基酯[mono-(2-ethylhexyl)phthalate,MEHP]对原代培养新生大鼠下丘脑神经元活性的影响及其氧化损伤作用。方法选取24 h内新生清洁级SD大鼠,取下丘脑神经元进行原代培养,分别加入含终浓度0(溶剂对照)、10~(-12)、10~(-9)、10~(-6)、10~(-3)、1.0 mmol/L MEHP的培养液暴露24 h。采用MTT法测定下丘脑神经元的活性,试剂盒测定超氧化物歧化酶(SOD)的活力和丙二醛(MDA)的含量。结果与溶剂对照组比较,仅1.0 mmol/L MEHP暴露组新生大鼠下丘脑神经元的存活率较低,差异有统计学意义(P<0.05);且随着MEHP暴露剂量的升高,新生大鼠下丘脑神经元的存活率呈下降趋势。与溶剂对照组比较,仅1.0 mmol/L MEHP暴露组新生大鼠下丘脑神经元上清液中的MDA含量升高,差异有统计学意义(P<0.05);而各MEHP暴露组新生大鼠下丘脑神经元上清液中的SOD活力均无明显改变。结论MEHP可抑制原代培养新生大鼠下丘脑神经元活性,并具有氧化损伤作用,提示其可能是MEHP神经毒性机制之一。
Objective To investigate the effect of mono- (2-ethylhexyl) phthalate (MEHP) on the activity of hypothalamic neurons in primary cultured neonatal rats and its oxidative damage. Methods Newborn SD rats were selected within 24 h. Primary neurons were removed from the hypothalamus and cultured in culture medium containing final concentration of 0 (solvent control), 10 ~ (-12), 10 ~ (-9), 10 ~ -6), 10 ~ (-3), 1.0 mmol / L MEHP for 24 h. The activity of neurons in the hypothalamus was measured by MTT assay. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were determined by kit. Results Compared with the solvent control group, the survival rate of hypothalamic neurons in the neonatal rats exposed to 1.0 mmol / L MEHP was significantly lower than that in the solvent control group (P <0.05). With the increase of MEHP exposure dose, Rat hypothalamic neuron survival rate showed a downward trend. Compared with the solvent control group, MDA content in hypothalamic neuron supernatant of 1.0 mmol / L MEHP exposure group was significantly increased (P <0.05), while the MEHP exposure group neonatal rats There was no significant change in SOD activity in hypothalamic neuron supernatant. Conclusion MEHP can inhibit primary cultured neonatal rat hypothalamic neurons activity, and has the role of oxidative damage, suggesting that it may be one of the mechanisms of MEHP neurotoxicity.