锰超氧化物歧化酶过表达对H2O2诱导PC12细胞凋亡的影响

目的 揭示锰超氧化物歧化酶（MnSOD）在H2O2诱导PC12细胞凋亡中的作用及机制。方法 转染人正义和反义MnSOD基因的PC12细胞，用50 mmol H2O2攻击已转染的细胞系，并采用MTT法、流式细胞术和 Hoechst染色方法研究H2O2的细胞毒作用。结果 转染正义MnSOD的细胞比原细胞的MnSOD酶活性提高1.3倍，而转染反义MnSOD细胞的酶活性降低67%。结论 H2O2对PC12细胞毒作用是通过诱发PC12细胞凋亡作用来实现的；MnSOD具有抑制H2O2诱导PC12细胞凋亡作用，涉及线粒体的损伤，导致氧化还原失衡继而诱发细胞凋亡。

Overproduction of manganese superoxide dismutase modulates H2O2-induced apoptosis in transfected human PC12 cells

Objective To explore the effect and mechanism of manganese superoxide dismutase (MnSOD): on H2O2-induced apoptosis of PC12 cells. Methods PC12 cells were transfected with sense and antisense human MnSOD by lipofectin, and exposed to 50 mmol/L H2O2, MTT assay, low cytometry and Hoechst stain were used to study the cytotoxicity. Results MnSOD activity increased by 130% in cells transfected with sense MnSOD cDNA, and was decreased by 67% in cells transfected with antisense MnSOD cDNA as compared with controls. Conclusion Antisense MnSOD can offer protection against H2O2-induced apoptosis in PC12 cells. The damage of the mitochondria may be attributed to the cytotoxicity of H2O2 against PC12 cells, which induces imbalance of cellular redox and apoptosis.