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绿原酸通过抑制内质网应激发挥其在 6-羟多巴胺诱导的神经毒性中的有益作用。

Chlorogenic Acid Exerts Beneficial Effects in 6-Hydroxydopamine-Induced Neurotoxicity by Inhibition of Endoplasmic Reticulum Stress.

机构信息

Department of Neurology, No.1 People's Hospital of Jining City, Jining, Shandong, China (mainland).

出版信息

Med Sci Monit. 2019 Jan 15;25:453-459. doi: 10.12659/MSM.911166.

Abstract

BACKGROUND Chlorogenic acid (CGA), a dietary polyphenol derived from many plants, has been previously reported to exert neuroprotective properties. However, its pharmacological role in Parkinson's disease (PD) and the underlying mechanisms are unclear. MATERIAL AND METHODS In the present study, we investigated the beneficial effects of CGA against the toxicity of 6-hydroxydopamine (6-OHDA) in animal and cellular models. One week after 6-OHDA administration, the behavioral activities of rats were determined by rotarod test and apomorphine-induced rotational test. The viability and apoptosis of SH-SY5Y cells following 6-OHDA exposure were determined by MTT assay and annexin V-FITC/PI double staining, respectively. The activities of antioxidant enzymes in the rat striatal tissues and SH-SY5Y cells were detected by ELISA. RESULTS The results demonstrated that 6-OHDA-induced PD-like behavioral impairments of rats were significantly forestalled by CGA administration. The increased apoptosis and reduced activities of antioxidant enzymes in the striatum of 6-OHDA-lesioned rats were also attenuated by CGA. Moreover, in an in vitro experiment, the impaired viability and enhanced apoptosis of 6-OHDA-injured SH-SY5Y cells were significantly restored by CGA pretreatment. In addition, CGA also obstructed 6-OHDA-induced ROS production and endoplasmic reticulum (ER) stress in SH-SY5Y cells. CONCLUSIONS Taken together, these data show that CGA might be an effective neuroprotective compound that mitigates oxidative stress and ER stress in PD.

摘要

背景

绿原酸(CGA)是一种从许多植物中提取的膳食多酚,先前已有报道称其具有神经保护作用。然而,其在帕金森病(PD)中的药理作用及其潜在机制尚不清楚。

材料和方法

在本研究中,我们研究了 CGA 对 6-羟多巴胺(6-OHDA)在动物和细胞模型中毒性的有益作用。6-OHDA 给药后 1 周,通过转棒试验和阿扑吗啡诱导旋转试验测定大鼠的行为活动。通过 MTT 测定和 Annexin V-FITC/PI 双重染色分别测定 6-OHDA 暴露后 SH-SY5Y 细胞的活力和凋亡。通过 ELISA 测定大鼠纹状体组织和 SH-SY5Y 细胞中抗氧化酶的活性。

结果

结果表明,CGA 给药可显著预防 6-OHDA 诱导的 PD 样大鼠行为损伤。CGA 还减轻了 6-OHDA 损伤大鼠纹状体中凋亡增加和抗氧化酶活性降低。此外,在体外实验中,CGA 预处理可显著恢复 6-OHDA 损伤的 SH-SY5Y 细胞的活力和增强的凋亡。此外,CGA 还阻止了 6-OHDA 在 SH-SY5Y 细胞中诱导的 ROS 产生和内质网(ER)应激。

结论

综上所述,这些数据表明 CGA 可能是一种有效的神经保护化合物,可减轻 PD 中的氧化应激和 ER 应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/736f/6342059/ec13d12db730/medscimonit-25-453-g001.jpg

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