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目的:研究阿螺旋霉素[17-(dimethylaminoethylamino)-17-demethoxygeldanamycin hydrochloride,17-DMAG]在葡聚糖硫酸钠(dextran sulphate sodium,DSS)诱导的小鼠溃疡性结肠炎治疗中的作用.方法:C57BL/6小鼠随机分为正常对照组、DSS模型组、磷酸盐缓冲液(phosphate buffer,P B S)治疗组以及17-D M A G治疗组.采用3%D S S连续饮入以复制溃疡性结肠炎小鼠模型.对结肠炎模型小鼠每日腹腔注射17-DMAG[10 mg/(kg?d)]或同体积PBS.观察小鼠体质量、疾病活动度、单位长度结肠质量、结肠病理损伤程度及结肠上皮细胞凋亡情况,以评价17-DMAG对小鼠溃疡性结肠炎病程发展的影响.结果:3%DSS连续饮入5 d后,模型组小鼠较正常对照组小鼠体质量减轻,疾病活动度、单位肠道结肠重量、结肠病理评分及结肠上皮细胞凋亡增加.与PBS治疗组相比,17-DMAG治疗5 d后,结肠炎小鼠体质量降低程度(90.9%±7.78%vs 81%±5.44%,P<0.05)及疾病活动度显著改善(1.8±0.84 vs 4.7±1.21,P<0.05),单位长度结肠质量(4.43 mg/mm±0.16 mg/mm vs 5.71 mg/mm±0.56 mg/mm,P<0.01)及结肠病理评分降低(4.6±1.30 vs 7.4±0.30,P<0.01),结肠上皮细胞凋亡数目(33.2±5.50vs 62.6±9.81,P<0.01)显著减少.结论:17-DMAG可减轻DSS诱导的小鼠溃疡性结肠炎,其可能通过抑制结肠上皮细胞的凋亡而发挥作用.
AIM: To investigate the role of dimethylaminoethylamino-17-demethoxygeldanamycin hydrochloride (17-DMAG) in the treatment of mouse ulcerative colitis induced by dextran sulphate sodium (DSS) .Methods : C57BL / 6 mice were randomly divided into normal control group, DSS model group, phosphate buffer (PBS) treatment group and 17-DMAG treatment group.Using 3% DSS continuous drinking to replicate ulcerative colitis Mouse model.After intraperitoneal injection of 17-DMAG [10 mg / (kg? D)] or the same volume of PBS for colitis model mice, the body weight, disease activity, length of colon per unit length, degree of colonic pathological damage And colon epithelial cell apoptosis in order to evaluate the effect of 17-DMAG on the development of ulcerative colitis in mice.Results: Compared with the normal control group, the body weight of mice in the model group decreased , Disease activity, unit colon weight, colon pathological score and apoptosis of colonic epithelial cells.Compared with PBS treatment group, the decrease of body weight of colitis mice (90.9% ± 7.78 % vs 81% ± 5.44%, P <0.05) and disease activity (P <0.05). The colonic mass per unit length (4.43 mg / mm ± 0.16 mg / mm vs 5.71 mg / mm ± 0.56 mg / mm, P <0.01) (4.6 ± 1.30 vs 7.4 ± 0.30, P <0.01), and the number of apoptosis of colorectal epithelial cells was significantly decreased (33.2 ± 5.50 vs 62.6 ± 9.81, P <0.01) .Conclusion: 17-DMAG can reduce the ulceration of mice induced by DSS Colitis, which may play a role by inhibiting the apoptosis of colonic epithelial cells.