瘦素对小鼠胸腺细胞凋亡的保护机制  

Protection of leptin on LPS-induced apoptosis of thymocytes

作　　者：任晓娟[1] 颜光涛[1] 王桂琴[2] 郝秀华[1] 林季[1] 邓子辉[1] 薛辉[1] 张凯[1] 

机构地区：[1]中国人民解放军总医院基础所生化室,北京100853 [2]山西医科大学微生物免疫学教研室,太原030000

出　　处：《免疫学杂志》2008年第5期491-494,499,共5页Immunological Journal

基　　金：国家自然科学基金资助课题(30670821)

摘　　要：目的观察瘦素对小鼠胸腺细胞凋亡的保护机制,探讨磷酸肌醇3位羟基激酶/AKT(PI3-K/AKT)和胞桨型磷脂酶A2(cPLA2)信号转导通路是否参与瘦素保护机制。方法以LPS诱导小鼠胸腺细胞凋亡为模型,采用Annexin V-FITC/PI双染色法流式细胞仪检测PI3-K/AKT特异性抑制剂LY294002和cPLA2抑制剂AACOCF3对细胞凋亡的影响,以RT-PCR检测cPLA2 mRNA和caspase3 mRNA的表达,用cPLA2活性试剂盒检测cPLA2的活性。结果瘦素可以保护LPS诱导的小鼠胸腺细胞凋亡,使胸腺细胞存活率由58%上升到65%,LY294002(10μmol/L)和AACOCF3(10μmol/L)可以明显抑制瘦素的保护作用,使胸腺细胞的存活率分别降至60%(P<0.05)和62%(P<0.05)。RT-PCR表明加入瘦素后cPLA2 mRNA和caspase3 mRNA的表达下降。cPLA2活性试剂盒表明leptin可抑制cPLA2的活性。结论瘦素抑制LPS诱导的胸腺细胞凋亡同时依赖IP3K/AKT和cPLA2途径。Objective To observe the effects of leptin on apoptosis of thymocytcs and explore whether phosphatidylinositol 3-kinase/ AKT （PI3-K/AKT） signal pathway and cPLA2 signal pathway are involved in anti-apeptotic action. Methods Apeptosis was induced by lipopelysaccharide （LPS） in mice. The effects of a specific inhibitor （LY294002） of PI3-K and an inhibitor （AACOCF3） of cPLA2 on apeptosis of thymocytes was detected using Annexin V-FTTC/PI double staining flow cytometry, cPLA2 mRNA and caspase3 mRNA were measured by RT- PCR. cPLA2 activity was detected by cPLA2 assay kit. Results Leptin protected LPS-induced apeptosis of thymocytes in mice, and elevated the thymocytes viability from 58% to 65%. LY294002 （ 10μmol/L） and AACOCF3 （ 10μmol/L） reversed the protection of leptin the thymocytes viability decreased from 65 % to 62 % （ P 〈 0.05 ） and 60 % （ P 〈 0.05 ）, respectively. The expressions of cPLA2 mRNA and caspase3 mRNA were inhibited by leptin, while cPLA2 activity was inhibited by leptin. Conclusion Leptin inhibits apeptosis in thymus through PI-3K/AKT and cPLA2 signal pathway.

关 键 词：瘦素 胸腺细胞 CPLA2 MRNA CASPASE3 MRNA 

分 类 号：R392.12[医药卫生—免疫学]