Paiva L A F, Gurgel L A, De Sousa E T, Silveira E R, Silva R M, Santos F A, Rao V S N
Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará (FM), Rua Cel Nunes de melo 1127, Caixa Postal 3157, Porangabussu, 60430-270 Fortaleza, CE, Brazil.
J Ethnopharmacol. 2004 Jul;93(1):51-6. doi: 10.1016/j.jep.2004.03.028.
The oleo-resin from Copaifera langsdorffii (Leguminosae) was evaluated in rats on acetic acid-induced colitis. Rats were pretreated orally (15 and 2 h) or rectally (2 h) before the induction of colitis with copaiba oleo-resin (200 and 400 mg/kg) or vehicle (1 ml, 2% Tween 80). Colitis was induced by intracolonic instillation of a 2 ml of 4% (v/v) acetic acid solution and 24 h later, the colonic mucosal damage was analyzed for the severity of macroscopic colonic damage, myeloperoxidase (MPO) activity, and malondialdehyde levels. A significant reduction in gross damage score and in wet weight/length ratio of colonic tissue were evident in test substance-pretreated animals as compared to vehicle or oleo-resin alone-treated controls. This effect was confirmed biochemically by a reduction in colonic myeloperoxidase activity, the marker of neutrophilic infiltration, and by a marked decrease in malondialdehyde level, an indicator of lipoperoxidation. Furthermore, microscopical examination revealed the diminution of inflammatory cell infiltration, and submucosal edema in the colon segments of rats treated with copaiba oleo-resin. The data indicate the protective effect of copaiba oleo-resin in the animal model of acute colitis possibly through an antioxidant and or anti-lipoperoxidative mechanism.
对来自兰氏 Copaifera langsdorffii(豆科)的油树脂在大鼠乙酸诱导的结肠炎模型中进行了评估。在用巴伊亚香脂油树脂(200 和 400 mg/kg)或赋形剂(1 ml,2%吐温 80)诱导结肠炎之前,大鼠经口(15 和 2 小时)或直肠(2 小时)预处理。通过向结肠内注入 2 ml 4%(v/v)的乙酸溶液诱导结肠炎,24 小时后,分析结肠黏膜损伤情况,包括宏观结肠损伤的严重程度、髓过氧化物酶(MPO)活性和丙二醛水平。与单独用赋形剂或油树脂处理的对照组相比,经受试物质预处理的动物结肠组织的大体损伤评分和湿重/长度比显著降低。结肠髓过氧化物酶活性(中性粒细胞浸润的标志物)降低以及丙二醛水平(脂质过氧化的指标)显著下降,从生化角度证实了这一效应。此外,显微镜检查显示,用巴伊亚香脂油树脂处理的大鼠结肠段炎症细胞浸润和黏膜下水肿减少。数据表明,巴伊亚香脂油树脂在急性结肠炎动物模型中可能通过抗氧化和/或抗脂质过氧化机制发挥保护作用。