论文部分内容阅读
目的:观察过氧化氢(H2O2)对大鼠螺旋神经节细胞(SGCs)的作用,探讨氧自由基损伤SGCs的机制。方法:新生大鼠SGCs原代培养,取培养第4天细胞加入H2O2,浓度分别为0、100、200、500μmol/L,作用2、4、6 h,光镜下观察细胞形态改变,hochest33258及PI染色,计数受损伤细胞的百分比。结果:在H2O2的作用下,原代培养的SGCs随着H2O2浓度的增加以及作用时间的延长,受损伤的细胞数目呈增加趋势。同时,低浓度(100及200μmol/L)H2O2作用下,SGCs的损伤主要以凋亡表现为主,PI染色多为阴性;高浓度H2O2(500μmol/L)作用下的SGCs损伤以坏死为主。结论:H2O2可以引起SGCs凋亡,且作用有明显的剂量及时间依赖性。凋亡的发生可能和凋亡相关基因的启动有关,但仍需进一步实验证实。
Objective: To observe the effect of hydrogen peroxide (H2O2) on rat spiral ganglion cells (SGCs) and to explore the mechanism of the injury of SGCs by oxygen free radicals. Methods: Primary cultured neonatal SGCs were cultured in the presence of H2O2 at the concentration of 0, 100, 200 and 500 μmol / L for 4, 6 and 6 h respectively. The morphological changes of cells were observed under light microscope, PI staining, counting the percentage of damaged cells. Results: Under the action of H2O2, the primary cultured SGCs showed an increasing tendency with the increase of H2O2 concentration and the prolongation of action time. At the same time, under the action of low concentrations of H2O2 (100 and 200μmol / L), the main damage of SGCs was apoptosis, while PI staining was mostly negative. The damage of SGCs was mainly caused by high concentration of H2O2 (500μmol / L). Conclusion: H2O2 can induce apoptosis of SGCs, and the effect is obvious dose and time dependent. Apoptosis may be related to the initiation of apoptosis-related genes, but still need further experimental confirmation.