厚朴酚於後肢肌肉缺血-再灌流傷害之保護效果研究 (II)

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题名:	厚朴酚於後肢肌肉缺血-再灌流傷害之保護效果研究 (II)
作者:	陳鴻儀(Hung-Yi Chen);(Lee EJ);(Lee MY);謝慶良(Ching-Liang Hsieh)
贡献者:	藥學院藥學系
关键词:	厚朴酚;自由基;缺血-再灌流;硝酸鹽與亞硝酸鹽;乳酸去氫脢;骨髓過氧化脢;還原型穀胱甘脢與氧化型穀胱甘脢;Magnolol;Free radical;Ischemia-reperfusion;Nitrate and nitrite;Lactate dehydrogenase;Myeloperoxidase;GSH/GSSG
日期:	2007-07-31
上传时间:	2009-09-01 16:29:17 (UTC+8)
摘要:	自由基與嗜中性白血球是造成缺血再灌流傷害的重要原因；我們用厚朴酚評估對大鼠後肢肌肉缺血-再灌流傷害抓自由基與抗炎的保護效果。我們將大鼠分成3組: (A)控制組(PEG400)，給藥組:事前給厚朴酚(B)0.3mg╱kg 與(C) 1mg╱kg. 與(A)控制組比較，給藥組(B)、(C)對缺血-再灌流造成傷害都較小;事前給厚朴酚或PEG400, 再將大鼠右後肢大腿用止血帶綁緊，造成缺血2小時。之後，將止血帶鬆綁再灌流，經過22小時取後肢肌肉，做下列實驗評估抗氧化與抗炎效果。厚朴酚對後肢肌肉傷害保護效果以H&E染色，測硝酸鹽與亞硝酸鹽代謝物，乳酸去氫脢活性，骨髓過氧化脢，還原型穀胱甘脢與氧化型穀胱甘脢等。經過22小時再灌流後血中硝酸鹽與亞硝酸鹽代謝物與後肢肌肉乳酸去氫脢活性，骨髓過氧化脢值，在(C)1.0 mg╱kg 厚朴酚組 (硝酸鹽與亞硝酸鹽: 2.9 ± 1.1 ; 乳酸去氫脢：106.2 ± 15.5; 骨髓過氧化脢：2.0 ± 0.5 U╱100μg ) 明顯低於(B) 0.3 mg╱kg厚朴酚組(硝酸鹽與亞硝酸鹽:3.8 ± 0.8 ; 乳酸去氫脢：189.5 ± 14.6; 骨髓過氧化脢：4.2 ± 1.5 U╱100μg )與控制組(硝酸鹽與亞硝酸鹽: 5.9 ± 1.5 ; 乳酸去氫脢：216.8 ± 18.2; 骨髓過氧化脢：8.0 ± 0.8 U╱100μg ).厚朴酚對於經過22小時再灌流後還原型穀胱甘脢與氧化型穀胱甘脢含量與控制組比較:厚朴酚(B)(C)組明顯高於控制組(A)。(C)組1.24 ± 0.51明顯高於(B)組(0.44± 0.16) 與 (A) 組(0.16± 0.06).組織病理切片結果，也支持厚朴酚(B)(C)明顯高於控制組(A)。綜合上述實驗結果，顯示厚朴酚對於缺血-再灌流引發後肢的傷害，其抗氧化與抗炎的效果有顯著劑量相關性。 The protective efficacy of magnolol in hind limb muscular ischemia- reperfusion injury. (II) Free radicals and neutrophils are potent sources of ischemia reperfusion injury. We compared the effect of magnolol, a free radical scavenger, and antiinflammation on the on the reperfusion injury in skeletal muscle, using ischemia reperfusion hind limb model in rats. In our study, male Spraque-Dawley rats were randomizied into 3 groups : (A) a control group, (B) a group pretreated by magnolol 0.3 mg╱kg, (C) a group pretreated by magnolol 1.0 mg╱kg. Both the (B) and (C) groups had limited muscle damage compared to the control group. 2 h of ischemia were introduced in right hind limb by application of a elastic rubber tourniquet to the proximal thigh. After 22h of reperfusion, muscle damage was evaluated. Muscle damage evaluated by H&E stain, measurement of NOx metabolites, LDH activity and myeloperoxidase (MPO), GSH activity were analyzed after 22 h after reperfusion. When compared to the control group, both given magnolol groups had limited muscular damage. The magnolol (1.0 mg╱kg) group attenuated muscular inflammation and edema significantly better than magnolol (0.3 mg╱kg) group and the control group. Furthermore, serum level of NOx and muscular level of LDH, MPO in the 1.0 mg╱kg magnolol group (NO: 2.9 +- 1.1 ; LDH：106.2 +- 15.5; MPO：2.0 +- 0.5 U╱100μg ) were significantly lower than 0.3 mg╱kg magnolol group (NO:3.8 +- 0.8 ; LDH：189.5 +- 14.6; MPO：4.2 +- 1.5 U╱100μg ) and control group (NO: 5.9 +- 1.5 ; LDH：216.8 +- 18.2; MPO：8.0 +- 0.8 U╱100μg ) after 22 h of reperfusion. The GSH╱GSSG in the C group (1.24 +- 0.51) were significantly higher than the B group (0.44+- 0.16) and the A group (0.16+- 0.06) after 22 h of reperfusion. Histopathological examinations of the gastrocnemius muscle also supported these results. These findings suggest that magnolol may provide dose-dependent and significantly protective efficacy in rat hind limb muscle ischemia reperfusion injury.
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