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香椿叶水提物抑制小胶质细胞介导的神经炎症。

The aqueous extract from Toona sinensis leaves inhibits microglia-mediated neuroinflammation.

机构信息

Department of Anatomy, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

出版信息

Kaohsiung J Med Sci. 2014 Feb;30(2):73-81. doi: 10.1016/j.kjms.2013.09.012. Epub 2013 Nov 1.

DOI:10.1016/j.kjms.2013.09.012
PMID:24444536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7118447/
Abstract

The leaves of Toona sinensis, a well-known traditional oriental medicine, have been prescribed for the treatment of enteritis and infection. Recently, aqueous extracts of Toona sinensis leaves (TSL-1) have demonstrated many biological effects both in vitro and in vivo. In the central nervous system, microglial activation and their proinflammatory responses are considered an important therapeutic strategy for neuroinflammatory disorders such as cerebral ischemia, Alzheimer's disease, and Parkinson's disease. The present study attempted to validate the effect of TSL-1 on microglia-mediated neuroinflammation stimulated by lipopolysaccharide (LPS). As inflammatory parameters, the production of nitric oxide (NO), inducible NO synthase, and tumor necrosis factor-α were evaluated. Our results demonstrate that TSL-1 suppresses LPS-induced NO production, tumor necrosis factor-α secretion, and inducible NO synthase protein expression in a concentration-dependent manner, without causing cytotoxicity. In addition, the inhibitory effects of TSL-1 in LPS-stimulated BV-2 microglia were extended to post-treatment suggesting the therapeutic potential of TSL-1. Therefore, this work provides the future evaluation of the role of TSL-1 in the treatment of neurodegenerative diseases by inhibition of inflammatory mediator production in activated microglia.

摘要

香椿叶,一种著名的传统东方药物,已被用于治疗肠炎和感染。最近,香椿叶的水提物(TSL-1)在体外和体内都表现出许多生物学效应。在中枢神经系统中,小胶质细胞的激活及其促炎反应被认为是治疗脑缺血、阿尔茨海默病和帕金森病等神经炎症性疾病的重要治疗策略。本研究试图验证 TSL-1 对脂多糖(LPS)刺激的小胶质细胞介导的神经炎症的作用。作为炎症参数,评估了一氧化氮(NO)、诱导型一氧化氮合酶和肿瘤坏死因子-α的产生。我们的结果表明,TSL-1 以浓度依赖性方式抑制 LPS 诱导的 NO 产生、肿瘤坏死因子-α分泌和诱导型一氧化氮合酶蛋白表达,而没有引起细胞毒性。此外,TSL-1 在 LPS 刺激的 BV-2 小胶质细胞中的抑制作用延伸至后处理,表明 TSL-1 具有治疗潜力。因此,这项工作通过抑制激活的小胶质细胞中炎症介质的产生,为 TSL-1 在治疗神经退行性疾病中的作用的未来评估提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/553e159d9c2d/KJM2-30-73-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/cd85cc48a611/KJM2-30-73-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/14d05399bc46/KJM2-30-73-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/162196228ecc/KJM2-30-73-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/31ba074ea26a/KJM2-30-73-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/553e159d9c2d/KJM2-30-73-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/cd85cc48a611/KJM2-30-73-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/14d05399bc46/KJM2-30-73-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/162196228ecc/KJM2-30-73-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/31ba074ea26a/KJM2-30-73-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8922/11916394/553e159d9c2d/KJM2-30-73-g001.jpg

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