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决明子,即钝叶决明的种子,对帕金森病模型具有神经保护作用。

Cassiae semen, a seed of Cassia obtusifolia, has neuroprotective effects in Parkinson's disease models.

机构信息

Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, #1 Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.

出版信息

Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2037-44. doi: 10.1016/j.fct.2010.05.002. Epub 2010 May 8.

Abstract

Cassiae semen, a commonly consumed tea and medicinal food, has been shown to have multiple therapeutic actions related to the prevention of dementia and ischemia. In this study, we investigated the effects of extract of Cassiae semen (COE) against neurotoxicities in in vitro and in vivo Parkinson's disease (PD) models. In PC12 cells, COE attenuated the cell damage induced by 100 microM 6-hydroxydopamine (6-OHDA) stress in MTT assay, and it inhibited the overproduction of reactive oxygen species, glutathione depletion, mitochondrial membrane depolarization and caspase-3 activation at 0.1-10 microg/ml. In addition, COE showed radical scavenging activity in the DPPH and ABTS assays. In mesencephalic dopaminergic (DA) culture, COE protected DA cells against 10 microM 6-OHDA- and 10 microM 1-methyl-4-phenylpyridine-induced toxicities at 0.1-1 microg/ml. We also evaluated the effect of COE in a mouse PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In the pole test, COE (50mg/kg, 15 days)+MPTP (30 mg/kg, 5 days)-treated group had decreased T-turn and T-LA which were longer in MPTP group. Moreover, COE significantly protected DA neuronal degeneration induced by MPTP in the substantia nigra and striatum of these mice. These results demonstrate that COE can prevent DA neurons against the toxicities involved in PD.

摘要

决明子,一种常见的茶饮和药食同源品,已被证明具有多种治疗作用,可预防痴呆和缺血。在这项研究中,我们研究了决明子提取物(COE)对体外和体内帕金森病(PD)模型神经毒性的作用。在 PC12 细胞中,COE 在 MTT 测定中减弱了 100 μM 6-羟多巴胺(6-OHDA)应激引起的细胞损伤,并且在 0.1-10μg/ml 时抑制了活性氧的过度产生、谷胱甘肽耗竭、线粒体膜去极化和 caspase-3 激活。此外,COE 在 DPPH 和 ABTS 测定中表现出自由基清除活性。在中脑多巴胺能(DA)培养物中,COE 在 0.1-1μg/ml 时保护 DA 细胞免受 10 μM 6-OHDA 和 10 μM 1-甲基-4-苯基吡啶诱导的毒性。我们还评估了 COE 在 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的小鼠 PD 模型中的作用。在极试验中,COE(50mg/kg,15 天)+MPTP(30mg/kg,5 天)处理组的 T-转弯和 T-LA 比 MPTP 组更长。此外,COE 显著保护这些小鼠黑质和纹状体中由 MPTP 诱导的 DA 神经元变性。这些结果表明 COE 可以预防 DA 神经元对抗 PD 相关毒性。

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