Study of Neuroprotective Effects for Single CompoundsPurified from Chinese Herb Extract

碩士 === 朝陽科技大學 === 生物技術研究所 === 97 === In this project the effects on astrocytes are investigated for single compounds purified from Chinese Herb Extract medicine including Kaepferol-3,7-o-(α)-L-dirhamnoside, (CO1, from Cinnamomum osmophloeum Kaneh) 、Trimethyl-3,4-dehydrochebulate ( PU3, from Phyllant...

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Bibliographic Details
Main Authors: Yi-Ching Lee, 李怡靜
Other Authors: Meng-Jen Lee
Format: Others
Language:zh-TW
Published: 2009
Online Access:http://ndltd.ncl.edu.tw/handle/84392102552034551653
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Summary:碩士 === 朝陽科技大學 === 生物技術研究所 === 97 === In this project the effects on astrocytes are investigated for single compounds purified from Chinese Herb Extract medicine including Kaepferol-3,7-o-(α)-L-dirhamnoside, (CO1, from Cinnamomum osmophloeum Kaneh) 、Trimethyl-3,4-dehydrochebulate ( PU3, from Phyllanthus urinaria)、Metyhylbrevifolincarboxylate (PU6, from Phyllanthus Urinaria), and andrographolide (AP2)、14-deoxy-11,12-dedihydroandrographolide (AP3), both from Andrographis paniculata (Burm.f.) Nees.. Astrocytes play crucial role in the homeostasis and function of the central nervous system (CNS). They participate in the regulation of extracellular ions, neurotransmitters and growth factors, and in the transport and metabolism of nutrients, vitamins and amino acids. The CNS response to trauma, infection, inflammation, excitotoxicity, degenerative and dementia-type diseases manifests with accompanied reactive gliosis largely attributed to astrocytes. Astrocytes release of proinflammatory mediators include interleukin (IL)-1, interleukin 6 (IL-6), tumor necrosis factor (TNF)-α and reactive oxygen species (ROS). Proinflammatory cytokines can also cause neuronal cell death, both directly and indirectly via the induction of NO and free radicals. In addition, reactive astrogliosis generates increased expression of extracellular matrix (ECM) molecules, including chondroitin sulfate proteoglycans (CSPGs). CSPG overexpression is linked to glial scar formation, which inhibits neurite outgrowth and regeneration. Our results showed that firstly PU3, PU6, and AP2, AP3 inhibited TNF-alpha stimulated astrocytic IL-6 and TNF-alpha. Secondly when effects of AP2 and AP3 were investigated, AP2 and AP3 inhibited CSPG secretion, cellular ROS level, and TNF-alpha stimulated IL-1. AP2 is more effective than AP3. These results suggested the potential beneficial properties for AP compounds for the treatment of inflammation-related CNS disease.