目的 探讨β-蜕皮甾酮对1-甲基-4-苯基吡啶离子(MPP+)诱导的人骨髓神经母细胞瘤(SH-SY5Y)细胞损伤的保护作用及其机制。方法 采用体外细胞培养的方法,建立SH-SY5Y细胞MPP+损伤模型,同时给予β-蜕皮甾酮干预。观察细胞形态,测定细胞存活率(噻唑蓝法)、乳酸脱氢酶(LDH)活性,用试剂盒检测超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量,流式细胞仪检测细胞凋亡率。结果 同1-甲基-4-苯基吡啶离子组比较,终浓度为50、100、150 μmol·L-1的β-蜕皮甾酮能减轻1-甲基-4-苯基吡啶离子引起的SH-SY5Y细胞的损伤,且呈剂量依赖性关系,明显提高细胞的存活率,减少乳酸脱氢酶的释放,超氧化物歧化酶升高,丙二醛降低,凋亡率降低。结论 β-蜕皮甾酮对1-甲基-4-苯基吡啶离子诱导的SH-SY5Y细胞有明显的保护作用。其机制可能与抑制氧化反应,减少细胞凋亡有关。
Abstract
To investigate the protective effect and probable mechanism of 20-Hydroxyecdysone on SH-SY5Y cells injured by MPP+. METHODS MPP+ induced SH-SY5Y cells injury model was established. 20-Hydroxyecdysone was added into the culture to test its protective effect. The morphological changes of cells were observed. Cell viability was detected by method of MTT. The contents of LDH、MDA and activity of SOD were inspected by kits. Apoptosis rate of cells was detected by flow cytometry. RESULTS Compared with MPP+ group, 20-Hydroxyecdysone group (50,100,150 μmol·L-1) alleviated the damage of SH-SY5Y cells induced by MPP+, significantly improved cell survival rate, reduced the release of LDH, increased the activity of SOD, decreased the contents of MDA and reduced the apoptosis of cells. CONCLUSION 20-Hydroxyecdysone has a significant protective effect on SH-SY5Y cells injured by MPP+. The probable mechanism may be anti-oxidation and anti-apoptosis.
关键词
β-蜕皮甾酮 /
1-甲基-4-苯基吡啶离子 /
SH-SY5Y细胞 /
脂质过氧化 /
凋亡
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Key words
20-hydroxyecdysone /
MPP+ /
SH-SY5Y cells /
lipid peroxidation /
apoptosis
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中图分类号：
R965
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参考文献
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