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PD-1 对 MPTP 诱导的小鼠多巴胺耗竭的预防作用。

Preventive role of PD-1 on MPTP-induced dopamine depletion in mice.

机构信息

Oriental Medicine R&D Center, Dongguk University, Gyeongju, South Korea.

出版信息

Cell Biochem Funct. 2010 Apr;28(3):217-23. doi: 10.1002/cbf.1642.

Abstract

Many current studies of Parkinson's disease (PD) suggest that inflammation is involved in the neurodegenerative process. PD-1, a traditional Korean medicine, used to treat various brain diseases in Korea. This study was designed to investigate the effect of PD-1 extract in the Parkinson's model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) lesioned mice. The MPTP administration caused the dopamine neuron loss in the striatum and substantia nigra pars compacta (SNpc), which was demonstrated by a depletion of tyrosine hydroxylase (TH). In addition, a reduction of bcl-2 expression with elevation of bax expression, caspase-3 activation, and release of cytochrome c into cytosol in dopaminergic neurons of SNpc were noted. Oral administration of PD-1 extract (50 and 100 mg kg(-1)) attenuated the MPTP-induced depletion of TH proteins in the striatum and SNpc and prevented the apoptotic effects. These results indicate that PD-1 extract is able to protect dopaminergic neurons from MPTP-induced neuronal death, with important implications for the treatment of PD.

摘要

许多当前的帕金森病(PD)研究表明,炎症参与了神经退行性过程。PD-1 是一种传统的韩国药物,用于治疗韩国的各种脑部疾病。本研究旨在探讨 PD-1 提取物对 1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)损伤的帕金森病模型小鼠的影响。MPTP 给药导致纹状体和黑质致密部(SNpc)中的多巴胺神经元丢失,这表现为酪氨酸羟化酶(TH)的耗竭。此外,还观察到 SNpc 中的多巴胺能神经元中 bcl-2 表达减少、bax 表达升高、caspase-3 激活以及细胞色素 c 释放到细胞质中。PD-1 提取物(50 和 100mg/kg)的口服给药减轻了 MPTP 诱导的纹状体和 SNpc 中 TH 蛋白的耗竭,并防止了细胞凋亡的影响。这些结果表明,PD-1 提取物能够保护多巴胺能神经元免受 MPTP 诱导的神经元死亡,这对 PD 的治疗具有重要意义。

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