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GLP-1类似物对小鼠实验性结肠炎治疗作用的研究
Therapeutic effect of GLP-1 analog on dextran sulfate sodium induced experimental colitis in mice
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DOI:
作者:
刘红霞,李晓雯,罗 登,林紫薇,慕开达,赵 简,王 琛,贾伟平
LIU Hongxia1, LI Xiaowen1, LUO Deng1, LIN Ziwei1,Mu Kaida1, Zhao Jie2, WANG Chen 1, JIA Weiping1
作者单位:
上海交通大学附属第六人民医院内分泌与代谢科,上海市糖尿病研究所,上海市糖尿病重点实验室;中国科学院,上海生物科学研究所,细胞分子生物学实验室,生物化学和细胞生物学研究所
1Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital; Diabetes Institute, Shanghai Jiao Tong University; Shanghai Key Laboratory of Diabetes Mellitus, Shanghai 200233, P.R. China 2 Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
关键词:
GLP-1;结肠炎;细胞因子
GLP-1 ; Colitis; Cytokine
摘要:
目的 明确GLP-1类似物对小鼠实验性结肠炎是否有治疗作用,并探讨其可能的作用机制。方法 将C57BL/6J小鼠随机分为3组(n=7):正常对照组、结肠炎模型组和利拉鲁肽治疗组。用葡聚糖硫酸钠(dextran sodium sulfate, DSS)制备小鼠实验性结肠炎模型,给8-12周龄小鼠饮用2%(w/v)的DSS溶液,连续饮用7天。用GLP-1长效类似物-利拉鲁肽进行腹腔注射(2次/天,1mg/kg)治疗,从造模前3天开始,连续给药10天。通过监测小鼠粪便性状和粪隐血获得临床模拟评分;通过评估结肠病理切片的组织损伤和炎性细胞浸润获得组织评分;以实时定量PCR方法检测结肠组织细胞因子的表达水平。统计学处理采用t检验。结果 给予DSS后小鼠出现典型的结肠炎变化。与结肠炎模型组比较,利拉鲁肽治疗组小鼠临床模拟评分(2.86±0.32 vs 3.79±0.18,P <0.05)和组织评分(2.33±0.21 vs 5.43±0.57,P <0.05)下降。同时,利拉鲁肽治疗组结肠炎导致的结肠缩短(4.46±0.12 vs 4.80±0.08,P <0.05)及结肠组织的破坏和炎症细胞的浸润明显缓解。实时-定量PCR结果显示,治疗组结肠组织抗炎因子TGF-β水平的表达增加,是结肠炎模型组的2.74(±0.98)倍(P=0.07)。结论 GLP-1类似物可减轻DSS诱导的小鼠实验性结肠炎,此作用可能与调节细胞因子有关。
Objective To investigate the effect of GLP-1 analog on experimental colitis in mice and the underlying potential mechanism. Menthods C57BL/6J mice were averagely randomized into three groups:Normal control group(n=7), DSS group(n=7) and Treatment(DSS + liraglutide) group(n=7). Colitis was induced by feeding 8-12 weeks mice with 2% (w/v) dextran sodium sulfate (DSS) in the distilled drinking water for 7 days. Mice were treated with a long-acting GLP-1 analog, liraglutide, injected twice daily (1 mg/kg) starting 3 days before the administration of DSS and lasting for 10 day. Clinical score was determined by quantifying stool consistency and hemoccult positivity (or gross bleeding). Tissue score was determined by evaluating tissue lesion and inflammatory cell infiltration. Real-time PCR was conducted to analyse gene expression in colon tissue. Results After DSS treatment, all mice had typical clinical and microscopic manifestation of colitis. Compared with DSS group, liraglutide treatment decreased both the clinical scores (DSS group vs. Treatment group: 3.79±0.18 vs 2.86±0.32, P<0.05), and tissue scores (DSS group vs. Treatment group: 5.43±0.57 vs 2.33±0.21, P<0.05). Moreover, liraglutide treatment reversed the colon length shortening (DSS group vs. Treatment group: 4.46±0.12 vs 4.80±0.08, P<0.05) and historical lesions in the colons of the mice. Real-time PCR reviewed that the level of anti-inflammatory cytokine-TGF-β gene expression tended to increase in liraglutide treatment (P=0.07). Conclusion GLP-1 analog can reduce DSS-induced experimental colitis in mice and the effect of GLP-1 on colitis may through meditating the expression of cytokines.
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