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目的:研究I组代谢型谷氨酸受体(mGluRs)反义寡核苷酸对谷氨酸钠(Glu)引起的小鼠大脑皮层神经元损伤的保护作用。方法:以细胞乳酸脱氢酶(LDH)漏出、光镜下细胞形态变化为指标,观察培养液中加入Glu引起的神经元损伤及mGluRl反义寡核苷酸或mGluR5反义寡核苷酸的保护作用;用免疫细胞化学检测神经元mGlulα仪和mGluR5表达。结果:实验显示0.1mmol.L-1的谷氨酸钠可明显造成神经元损伤,使LDH漏出增加(P<0.01),mGluRl反义寡核苷酸或mGluR5反义寡核苷酸6μmol.L-1和8μmol.L-1可明显拮抗Glu引起的神经元损伤,使LDH漏出显著减少(P<0.01);免疫组化实验证实体外培养神经元mGluRlα和mGluR5阳性表达。结论:mGluRl反义寡核苷酸和mGluR5反义寡核苷酸可对抗Glu引起的皮层神经元损伤。
Objective: To study the protective effects of Group I metabotropic glutamate receptor (mGluRs) antisense oligonucleotides on glutamate-induced neuronal damage in mouse cerebral cortex. Methods: Neuronal damage induced by adding Glu into culture medium was observed by the leak of cell lactate dehydrogenase (LDH) and morphological changes of cells under light microscopy. The effect of mGluR1 antisense oligonucleotide or mGluR5 antisense oligonucleotide The neuroprotection of mGlulα and mGluR5 were detected by immunocytochemistry. Results: The results showed that 0.1 mmol.L-1 sodium glutamate could obviously damage the neurons and increase the leakage of LDH (P <0.01). The mGluR1 antisense oligonucleotide or mGluR5 antisense oligonucleotide 6 μmol·L -1 and 8μmol.L-1 could obviously antagonize the neuronal damage induced by Glu and significantly reduce the leakage of LDH (P <0.01). Immunohistochemistry confirmed the positive expression of mGluRα and mGluR5 in neurons. Conclusion: Both mGluRl antisense oligonucleotides and mGluR5 antisense oligonucleotides can antagonize Glu-induced cortical neuron injury.