龍葵水萃取物對於改善實驗性帕金森氏症機轉之研究

中山醫學大學機構典藏 CSMUIR > 醫學院 > 生化微生物免疫研究所 > 博碩士論文 > Item 310902500/2383

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題名:	龍葵水萃取物對於改善實驗性帕金森氏症機轉之研究 Aqueous Extract From Solanum Nigrum L. Ameliorates Neurodegeneration in Experimental Parkinson's Disease
作者:	郭義明 Yi-Ming,Kuo
貢獻者:	中山醫學大學:醫學院;生化暨生物科技研究所;李彗禎
關鍵詞:	龍葵水萃物 SNWE
日期:	2010
上傳時間:	2010-10-14T04:35:34Z (UTC)
摘要:	帕金森氏症在解剖學上的特徵是腦中的黑質體中的多巴胺分泌細胞大量死亡，雖然在帕金森氏症中細胞死亡的原因還未被充分闡明，但是增加的氧化壓力和不正常的粒線體功能，可能是最主要的傷害起始或是調控者。由於葵成份已有多項抗癌及抗氧化之報告，因此本研究目的在於如何利用龍葵水萃物(SNWE)減少氧化壓力而降低罹患帕金森氏症風險。動物模式以每天腹腔注射30mg/kg的MPTP連續5天，誘導C57BL/6小黑鼠產生類帕金森氏症。由結果發現預處理SNWE能提高腦組織中catalase與GSH的量，也能降低MDA的量，同時也發現餵食SNWE的老鼠能回復由MPTP所減少的tyrosine hydroxylase量，因此，SNWE應能透過調節腦部抗氧化狀態以預防帕金森氏症。在細胞實驗中則是利用H2O2模擬氧化壓力的環境，在MTT實驗中，發現處理SNWE(0.05、0.1、0.2μg/mL)能提高細胞的存活能力(37.5％、41％、37.5％)，且具有統計上的意義。利用Western blot發現處理SNWE能降低由H2O2所誘導的JNK及p38的磷酸化，推測SNWE可能是透過MAPK這條路徑增加細胞的存活能力。綜合以上的結果，我們認為SNWE可能具有減低罹患帕金森氏症風險的潛力。 Parkinson's disease (PD) is a complex neurodegenerative syndrome likely involving contributions from various factors in individuals including genetic susceptibility, exposure to environmental toxins, and aging. Increased oxidative stress appears to be a common causative aspect involved in the preferential loss of dopaminergic neurons in substantia nigra (SN) of the brain prominently affected by the disorder. Previous studies have suggested that water extracts of Solanum Nigrum L.(SNWE) has anti-oxidative ability. This study aimed to detect the effect of SNWE on experimental Parkinson's mice. The results showed that SNWE can increase catalase activity, GSH level, and reduce the lipid peroxidation. Our study also shows that the neuroprotective effect of SNWE against dopaminergic cell damage may be mediated by the elevation of Tyrosine hydroxylase activity on dopaminergic system after MPTP treatment in mice. In ex vivo assay, treatment of SNWE protects PC-12 cells from oxidative stress-inducing cell damage, and the mechanisms might be contributed by regulating the ERK phosphorylation cascade. SNWE also shows the effect in blocking the oxidative stress-inducing phosphorylations of c-Jun N-terminal kinase (JNK) and p38 stress-activated protein kinase. In conclusion, the results show SNWE possesses the potential to reduce the risk of Parkinson’s disease, and one of the possible mechanisms is regulation of MAPK pathway.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/2383
顯示於類別:	[生化微生物免疫研究所] 博碩士論文

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