首页 | 本学科首页   官方微博 | 高级检索  
     

地塞米松对溃疡性结肠炎鼠外周血及肠黏膜固有层淋巴细胞凋亡的影响
引用本文:李志晋,詹丽英,胡俊,郑闽,徐燕琴,马春曦. 地塞米松对溃疡性结肠炎鼠外周血及肠黏膜固有层淋巴细胞凋亡的影响[J]. 江西医药, 2013, 48(5): 386-387,396
作者姓名:李志晋  詹丽英  胡俊  郑闽  徐燕琴  马春曦
作者单位:李志晋(江西解放军第184医院消化科,鹰潭,335000);詹丽英(江西解放军第184医院消化科,鹰潭,335000);胡俊(江西解放军第184医院消化科,鹰潭,335000);郑闽(江西解放军第184医院消化科,鹰潭,335000);徐燕琴(江西解放军第184医院消化科,鹰潭,335000);马春曦(江西解放军第184医院消化科,鹰潭,335000);
基金项目:南京军区青年学者项目(项目编号:07056)
摘    要:目的观察溃疡性结肠炎(UC)大鼠外周血淋巴细胞(PBL)及肠黏膜固有层淋巴细胞(LPL)凋亡状态,并探讨地塞米松(Dex)对其的影响。方法将45只大鼠随机分为正常组、模型组、实验组3组,各15只,模型组及实验组用三硝基苯磺酸(TNBS)/乙醇灌肠制作实验性溃疡性结肠炎的动物模型,正常组以生理盐水灌肠作为对照,分离各组大鼠PBL及LPL,植物血凝素(PHA)刺激培养72h,流式细胞仪检测其凋亡率,实验组的PBL及LPL再经Dex作用后检测上述指标。结果模型组大鼠LPL在PHA刺激培养72h后凋亡率(5.89±0.65)%较正常组(17.14±1.95)%明显降低,PBL凋亡率(5.28±0.43)%较正常组(6.34±0.71)%两组间无明显差异,实验组PBL(10.85±1.04)%及LPL(15.89±0.65)%凋亡率较模型组增高。结论 UC鼠LPL凋亡减少,而PBL无明显凋亡异常,LPL凋亡减少可能同溃疡性结肠炎发病机制有关,地塞米松通过促进LPL凋亡从而达到治疗作用。

关 键 词:溃疡性结肠炎  凋亡  肠黏膜固有层淋巴细胞  外周血淋巴细胞  地塞米松

Effects of Dexamethason on apoptosis of peripheral blood lymphocytes and lamina propria lymphocytes in ulcerative colitis rats
Affiliation:LI ZhiJin,ZHAN Liying,HU Jun,et al.Department of Gastroenterology,184 Hospital of PLA,Yingtan 335000,China
Abstract:Objective To observe the apoptosis in peripheral blood lymphocytes(PBLs) and lamina propria lymphocytes(LPLs) from ulcerative colitis rats and investigate effects of Dexamethason(Dex) on them.Methods Forty-five healthy cats were randomly divided into three groups:the normal group,the model group,the experimental group.The rat model of UC was established by using Trinitrophenylmethylnitramine(TNBS)and alcohol.PBLs and LPLs were isolated from each group.Apoptosis were detected by flow cytometry after stimuilated by phytohemagglutinin for 72 hours.PBLs and LPLs from experimental group were cultured with Dex and the same indexs were got after culture.Results The apoptosis of LPLs from the model group cultured in vitro was significantly lower than that from the nomal group [(5.89±0.65)%vs(17.14±1.95%)].There was no marked difference in apoptosis of PBLs between the model group and the nomal group [(5.28±0.43)%vs(6.34±0.71%)].The apoptosis of PBLs and LPLs from the experimental group was increased compared with the model group.Conclusion The apoptosis of LPLs from UC rats was delayed,but that of PBLs wasnot obvious.The apoptosis delay of LPLs may the one of mechanism of UC,and Dex could cure UC by accelerating the apoptosis of LPLs.
Keywords:Ulcerative colitis  Apoptosis  Lamina propria lymphocytes  Peripheral blood lymphocytes  Dexamethason
本文献已被 维普 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号