丹参酮ⅡA抗MPP<sup>+</sup>诱导的SH-SY5Y细胞氧化损伤的机制研究

doi:10.3969/j.issn.1671-7171.2018.06.006

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Abstract 【Objective】To investigate the mechanism of Tanshinone ⅡA inhibition of MPP⁺ induced SH-SY5Y cell oxidative stress. 【Methods】Oxidative stress of SH-SY5Y cells was induced by MPP⁺ treatment. Tanshinone ⅡA intervention and Znpp inhibition of HO-1 expression were measured. MTT assay was used to detect the cells viability. Oxidative stress indices including superoxide dismutase (SOD) and malondialdehyde (MDA) in cells were applied via test kit. HO-1 mRNA and protein expressions were detected by real-time PCR and Western Blot. The experimental designs were: the control group (routine culture with vehicle), MPP⁺ group (1 mM MPP⁺), MPP⁺ + Tanshinone IIA group (1 mM MPP⁺ + 5 ug/mL Tanshinone IIA), and Znpp + MPP + Tanshinone IIA group (5 μM Znpp pretreatment +1 mM MPP⁺ + 5 ug/mL Tanshinone IIA).【Results】Compared to the control group, the cells viability and SOD level of MPP⁺ group was lower (P<0.05), and the MDA level was higher (P<0.05). Compared with the MPP⁺ group, the cells viability of MPP⁺ + Tanshinone ⅡA group was higher, the level of SOD increased while the MDA level decreased (P<0.05). The expressions of HO-1 mRNA and protein in the MPP⁺ group were higher than those in the control group (P<0.05),while the expression of HO-1 was further increased after tanshinone ⅡA treatment. The protective effects of tanshinone Ⅱ A on cell viability and oxidative stress were eliminated by HO-1 inhibitor Znpp. 【Conclusion】Tanshinone ⅡA can attenuate oxidative stress damage induced by MPP⁺ in SH-SY5Y cells, which may be related to the induction of HO-1 expression.

Key words： Tanshinone/PD 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/AI Neuroblastoma/UL OxidativeStress

Received: 08 August 2017

PACS:

R730.264.4

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	XIAO Hui-qiong
	YUAN Li-li

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XIAO Hui-qiong,YUAN Li-li. Mechanism of Tanshinone ⅡA Inhibition of MPP⁺-induced SH-SY5Y Cell Oxidative Damage[J]. JOURNAL OF CLINICAL RESEARCH, 2018, 35(6): 1056-1058.

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http://www.jcr.net.cn/EN/10.3969/j.issn.1671-7171.2018.06.006 OR http://www.jcr.net.cn/EN/Y2018/V35/I6/1056

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