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莫诺苷抑制培养神经细胞中过氧化氢诱导的细胞凋亡

[Morroniside inhibits H2O2-induced apoptosis in cultured nerve cells].

作者信息

Ai Hou-Xi, Wang Wen, Sun Fang-Lin, Huang Wen-Ting, An Yi, Li Lin

机构信息

Department of Pharmacology, Xuan-wu Hospital of Capital Medical University, Key Laboratory for Neurodegenerative Diseases of Ministry of Education, Beijing 100053, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2008 Sep;33(18):2109-12.

Abstract

OBJECTIVE

To investigate the effects of morroniside on H2O2-induced apoptosis in nerve cells.

METHOD

Human neuroblastoma cell line SH-SY5Y cells were pre-incubaed with morroniside (1, 10, and 100 micromol x L(-1)) for 24 h prior to exposure to H2O2 (500 micromol x L(-1)) for 18 h. The activity of reactive SOD was measured by a biochemical assay. The expression of caspase-3, caspase-9, Bcl-2 and Bax was determined by Wastern blotting method.

RESULT

Pretreatment of the cells with morroniside (10 and 100 micromol x L(-1)) increasd SOD activity by 14% (P<0.01) and 11% (P<0.05) in comparison with cells exposed only to H2O2. Morroniside (1, 10, 100 micromol x L(-1)) lowered caspase-3 level by 31% (P<0.01), 103% (P<0.001) and 95% (P<0.001), decreased caspase-9 content by 71% (P<0.001), 132% (P<0.001) and 37% (P<0.05), and increasd Bcl-1 level by 88% (P<0.01), 121% (P<0.001) and 60% (P<0.01) respectively but no significant change occurred in Bax level in comparison with cells exposed only to H2O2.

CONCLUSION

Morroniside has neuroprotection effect against H2O2-induced oxidation injury in nerve cell.

摘要

目的

探讨莫诺苷对过氧化氢诱导的神经细胞凋亡的影响。

方法

人神经母细胞瘤细胞系SH-SY5Y细胞在暴露于过氧化氢(500 μmol/L)18小时之前,先用莫诺苷(1、10和100 μmol/L)预孵育24小时。通过生化测定法测量活性超氧化物歧化酶(SOD)的活性。采用蛋白质免疫印迹法检测半胱天冬酶-3(caspase-3)、半胱天冬酶-9(caspase-9)、Bcl-2和Bax的表达。

结果

与仅暴露于过氧化氢的细胞相比,用莫诺苷(10和100 μmol/L)预处理细胞可使SOD活性分别提高14%(P<0.01)和11%(P<0.05)。莫诺苷(1、10、100 μmol/L)使caspase-3水平分别降低31%(P<0.01)、103%(P<0.001)和95%(P<0.001),使caspase-9含量分别降低71%(P<0.001)、132%(P<0.001)和37%(P<0.05),并使Bcl-2水平分别提高88%(P<0.01)、1二百二十一%(P<0.001)和60%(P<0.01),但与仅暴露于过氧化氢的细胞相比,Bax水平无显著变化。

结论

莫诺苷对过氧化氢诱导的神经细胞氧化损伤具有神经保护作用。

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