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蜂毒对谷氨酸诱导的神经元和神经胶质细胞毒性的影响。

Effects of bee venom on glutamate-induced toxicity in neuronal and glial cells.

机构信息

Department of Standard Research, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon, 305-811, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2012;2012:368196. doi: 10.1155/2012/368196. Epub 2011 Aug 28.

DOI:10.1155/2012/368196
PMID:21904562
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3166716/
Abstract

Bee venom (BV), which is extracted from honeybees, is used in traditional Korean medical therapy. Several groups have demonstrated the anti-inflammatory effects of BV in osteoarthritis both in vivo and in vitro. Glutamate is the predominant excitatory neurotransmitter in the central nervous system (CNS). Changes in glutamate release and uptake due to alterations in the activity of glutamate transporters have been reported in many neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis. To assess if BV can prevent glutamate-mediated neurotoxicity, we examined cell viability and signal transduction in glutamate-treated neuronal and microglial cells in the presence and absence of BV. We induced glutamatergic toxicity in neuronal cells and microglial cells and found that BV protected against cell death. Furthermore, BV significantly inhibited the cellular toxicity of glutamate, and pretreatment with BV altered MAP kinase activation (e.g., JNK, ERK, and p38) following exposure to glutamate. These findings suggest that treatment with BV may be helpful in reducing glutamatergic cell toxicity in neurodegenerative diseases.

摘要

蜂毒(BV)是从蜜蜂中提取的,用于传统的韩国医学治疗。有几个小组已经在体内和体外证明了 BV 对骨关节炎的抗炎作用。谷氨酸是中枢神经系统(CNS)中主要的兴奋性神经递质。在许多神经退行性疾病中,包括帕金森病、阿尔茨海默病和肌萎缩侧索硬化症,已经报道了由于谷氨酸转运体活性的改变导致的谷氨酸释放和摄取的变化。为了评估 BV 是否可以预防谷氨酸介导的神经毒性,我们在存在和不存在 BV 的情况下检查了谷氨酸处理的神经元和小胶质细胞中的细胞活力和信号转导。我们诱导神经元细胞和小胶质细胞的谷氨酸毒性,发现 BV 可防止细胞死亡。此外,BV 显著抑制了谷氨酸的细胞毒性,并且在用谷氨酸处理之前用 BV 预处理会改变 MAP 激酶的激活(例如 JNK、ERK 和 p38)。这些发现表明,BV 的治疗可能有助于减少神经退行性疾病中的谷氨酸能细胞毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/6650226e7338/ECAM2012-368196.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/41bf12d127ac/ECAM2012-368196.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/3edd389fd25e/ECAM2012-368196.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/9c518c30f719/ECAM2012-368196.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/6650226e7338/ECAM2012-368196.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/41bf12d127ac/ECAM2012-368196.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/3edd389fd25e/ECAM2012-368196.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/9c518c30f719/ECAM2012-368196.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f0/3166716/6650226e7338/ECAM2012-368196.004.jpg

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