15脱氧前列腺素J_2抑制脂多糖活化的巨噬细胞对胰岛细胞的损伤作用  

15d-PGJ_2 attenuate the injury of pancreatic islets by LPS activated rat macrophages

作　　者：马志敏[1] 曹仁贤[1] 文芳[1] 刘江华[1] 文格波[1] 

机构地区：[1]南华大学附属第一医院内分泌科

出　　处：《中华糖尿病杂志（1006-6187）》2004年第6期446-449,共4页

基　　金：湖南省教委科研课题基金资助项目 (9615 9) ;湖南省科委科研基金资助项目 (ZD0 2 2 1)

摘　　要：目的　探讨脂多糖 (LPS)活化的巨噬细胞对胰岛细胞的损伤作用及 15脱氧前列腺素J2 (15d PGJ2 )的保护作用。　方法　应用ELISA法测定细胞培养上清中白细胞介素 1β(IL 1β)水平。应用放射免疫分析法、硝酸还原酶法分别测定培养上清中胰岛素、一氧化氮 (NO)的浓度 ,bcl 2 /bax在胰岛细胞中的表达应用免疫组化技术和定量分析检测。　结果　巨噬细胞经LPS处理后 ,IL 1β生成明显增多 ,与对照组相比有显著性差异 (P <0 0 1) ;15d PGJ2 +LPS组与 15d PGJ2 组及对照组相比 ,IL 1β亦明显升高 ,而低于LPS组 ,差异均有显著意义 (P <0 0 5 )。体外巨噬细胞和胰岛细胞共同培养加入LPS处理后抑制高糖刺激的胰岛素的释放及促进NO的产生 ,与对照组相比差异有显著意义(P <0 0 5 ) ,第 6天与 15d PGJ2 +LPS组相比有显著性差异 (P <0 0 5 ) ,LPS组bax表达上调 ,bcl 2表达下调 ,而 15d PGJ2 +LPS组无明显改变。　结论　 15d PGJ2 能拮抗LPS活化的巨噬细胞对胰岛细胞的损伤 ,其机制可能与抑制巨噬细胞细胞因子的产生 ,抑制bax/bcl 2的异常表达有关。Objective To explore the damage of islets by LPS activated rat peritoneal macrophage and 15d PGJ 2 attenuation of the damage Methods IL 1β in culture supernatant was determined by ELISA RIA and nitrite reduction test were used to determine insulin concentration and NO content respectively Expressions of bcl 2 and bax in pancreatic islets were evaluated by immunohistochemical method Results Compared with control, the production of IL 1β by macrophages was more markedly induced by LPS ( P <0 01) Addition of 15d PGJ 2 to LPS activated macrophages resulted in a significant attenuation ( P <0 05) in the production of IL 1β which was still higher than that in control ( P <0 05) The significant difference in NO level was observed between the control and 15d PGJ 2 treatment groups Added to the co culturing medium of macrophage and pancreatic islets,LPS inhibited the insulin release from the islets and increased the production of NO, with significant difference compared with the controls ( P <0 05),and also with obvious difference while compared with the LPS+15d PGJ 2 group at the sixth day ( P <0 05) The expression of bax in LPS group was up regulated while the expression of bcl 2 was down regulated, but the 15d PGJ 2 group had not obvious changes Conclusions 15d PGJ 2 attenuates the injury of pancreatic islets by LPS activated rat macrophages through inhibiting IL 1β release from LPS induced macrophages and inhibiting the abnormal expression of bcl 2/bax

关 键 词：LPS 巨噬细胞 胰岛细胞 对照组 IL-1Β 前列腺素 脂多糖 抑制 损伤作用 胰岛素 

分 类 号：R587.1[医药卫生—内分泌] R392[医药卫生—内科学]