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題名 | Control of Redox Signaling by NAC in Renal Tissue as an Alternative for Attenuating Diabetes Induction of Renal Dysfunction=N-乙醯基半胱氨酸(NAC)減緩糖尿病所引發氧化及硝化壓力所導致的腎臟傷害 |
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作者 | 李佩賢; 張洵浩; 董淳武; 張弘育; 徐永建; 雷震宙; 林俊良; Lee, Pei-hsien; Chang, Hsun-hao; Tung, Chun-wu; Chang, Hung-yu; Hsu, Yung-chien; Lei, Chen-chou; Lin, Chun-liang; |
期刊 | 臺灣腎臟醫學會雜誌 |
出版日期 | 20100300 |
卷期 | 24:1 2010.03[民99.03] |
頁次 | 頁16-23 |
分類號 | 415.74 |
語文 | eng |
關鍵詞 | 氧化壓力; 硝酸化壓力; N-乙酰半胱氨酸; 腎臟纖維化; 細胞凋亡; Oxidative stress; Nitrosative stress; N-acetylcysteine; Renal fibrosis; Apoptosis; |
中文摘要 | 目標:已知糖尿病腎病變與氧化壓力相關,本研究主要評估在糖尿病腎病變動物模型,投予N-乙醯基半胱氨酸(NAC)抗氧化物的藥理治療效果。評估內容包括抗氧化劑介入對於氧化壓力(oxidative stress)、硝化壓力(nitrosative stress)、纖維化(fibrosis)和細胞凋亡(apoptosis)的影響。方法:接受Streptozotocin誘導的糖尿病老鼠,隨機分配成兩組:接受NAC治療和賦形劑治療。測量血液中超氧化物(O2(上标 -))、一氧化氮(NO)、白介素1β(IL-1β)、和腫瘤壞死因子β1(TGF-β1)。另外以免疫組織化學及免疫染色法對腎臟組織加以分析。結果:本研究顯示,糖尿病老鼠除了尿液中白蛋白的排出顯著地增加,血液中O2、IL-1β以及TGF-1也上升。接受抗氧化物NAC的治療,則可以明顯地降低早期糖尿病腎病變的進展。在糖尿病的動物模型中,NAC的治療,有效地降低了8-hydroxy-guandine在糖尿病老鼠腎臟的表現,且同時減低TUNEL染色。進階的免疫染色研究顯示,peroxynitrite(OONO(上标 -))在糖尿病腎臟的表現增加,但是藉由抗氧化物NAC的給予,可以成功地減輕peroxynitrite的表現。免疫組織化學分析則顯示,抗氧化物NAC的治療,不僅可減輕TGF-β1和纖維蛋白(fibronectin)的表現,也降低phospho-ERK和phospho-p38在糖尿病腎絲球的表現。免疫染色則顯示,nitrotyrosine、8-hydroxy-guandine和fibronectin在糖尿病老鼠腎臟中的表現也降低。結論:藉由調節氧化壓力,抗氧化物NAC或許可提供我們一個有效的方法,以降低因糖尿病誘發nitrosative和oxidative傷害所造成的早期腎臟細胞凋亡以及纖維化。 |
英文摘要 | Aims/hypothesis: Increased fibrotic matrix expression in glomerular mesangial and tubular epithelial cells by generating intracellular reactive oxygen species (ROS) contributes to diabetic nephropathy. This study investigated whether antioxidant intervention by NAC could successfully alleviate indices of oxidative stress, nitrosative stress, fibrosis and apoptosis in diabetic animal kidney. Methods: Streptozotocin-induced diabetic rats were randomly assigned to two groups: diabetes treated by NAC (50 mg/kg body weight, day 1-5 per week for consecutive weeks) and diabetes treated by vehicle. Levels of superoxide, nitrate oxide, and TGF-β1 were measured. Kidneys were harvested for immunohistochemical analysis. Results: Urinary albumin excretion and systemic serum superoxide and TGF-β1 production increased significant/v in diabetic animal kidney. Histomorphometric analyses showed that mesangial cells in the diabetes groups displayed strong fibronectin, and TGF-β1 expression immunoreactivity. The same is also true for MAPK activation (phospho-ERK and phospho-p38 activation), oxidative stress (8-hydroxvguanidine expression) and nitrostative stress (ONOO-expression) in diabetic kidney. Importantly, exogenous NAC treatment attenuated diabetes-induced promotion of serum superoxide and TGF-β1 abundance and urinary protein excretion. Furthermore, NAC treatment also attenuated effectively oxidative stress and nitrostative stress of diabetic renal injury. Blockade of redox signaling via NAC treatment attenuated renal-deleterious factor (TGF-β1), which accelerates renal cell apoptosis (TUNEL staining) and fibrosis (fibronectin expression) coincided with decreased phospho-ERK and phospho-p38 expression levels in diabetic renal glomeruli. Conclusion: By manipulating oxidative stress levels, NAC may provide an alternative for the treatment of renal apoptosis and fibrosis associated with nitrosative and oxidative damage in the early diabetic kidney. |
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