中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2010年
4期
236-239
,共4页
韩锋%刘伟丽%任浩%齐文成
韓鋒%劉偉麗%任浩%齊文成
한봉%류위려%임호%제문성
关节炎,类风湿%细胞凋亡%滑膜%三氧化二砷
關節炎,類風濕%細胞凋亡%滑膜%三氧化二砷
관절염,류풍습%세포조망%활막%삼양화이신
Arthritis,rheumatoid%Apoptosis%Synovial membrane%As_2O_3
目的 探讨类风湿关节炎(RA)患者滑膜细胞的凋亡异常,以及三氧化二砷(As_2O_3)对体外培养RA的滑膜细胞凋亡的诱导作用.方法 用光镜、电镜、流式细胞仪检测As_2O_3对体外培养的RA滑膜细胞凋亡的诱导作用,As_2O_3,作用于RA滑膜后酶联免疫吸附试验(ELISA)检测凋亡过程中细胞色素C的变化,反转录-聚合酶链反应(RT-PCR)检测Caspase-3.Bel-2 mRNA表达,采用单因素方差分析和LSD-t检验、Dunnet-t检验进行统计学处理.结果 流式细胞仪检测发现不同浓度的As_2O_3作用后,滑膜细胞的凋亡较空白对照组(NC)增加[NC(0.95±0.87)%,RA(0.21±0.12)%,P<0.05],呈一定的剂量依赖性,尤其以80 μmol/L药物浓度最为明显.凋亡早期(6 h)细胞色素C水平升高80 μmol/L组升高明显[NC(0.34±0.27),80 μmol/L组(32.04±1.62),P<0.05];不同浓度的As_2O_3作用后细胞中Caspase-3 mRNA表达显著增强[NC(0.144±0.022),RA(0.323±0.047),(0.824±0.109),(1.213±0.196),P<0.05],Bcl-2的mRNA表达显著减弱[NC(1.08±0.23),RA(0.94±0.15),(0.46±0.08),(0.22±0.06),P<0.05].结论 RA患者滑膜细胞凋亡较健康埘照减少,As_2O_3通过升高细胞色素c及Caspase-3,抑制Bcl-2诱导RA滑膜细胞凋亡.
目的 探討類風濕關節炎(RA)患者滑膜細胞的凋亡異常,以及三氧化二砷(As_2O_3)對體外培養RA的滑膜細胞凋亡的誘導作用.方法 用光鏡、電鏡、流式細胞儀檢測As_2O_3對體外培養的RA滑膜細胞凋亡的誘導作用,As_2O_3,作用于RA滑膜後酶聯免疫吸附試驗(ELISA)檢測凋亡過程中細胞色素C的變化,反轉錄-聚閤酶鏈反應(RT-PCR)檢測Caspase-3.Bel-2 mRNA錶達,採用單因素方差分析和LSD-t檢驗、Dunnet-t檢驗進行統計學處理.結果 流式細胞儀檢測髮現不同濃度的As_2O_3作用後,滑膜細胞的凋亡較空白對照組(NC)增加[NC(0.95±0.87)%,RA(0.21±0.12)%,P<0.05],呈一定的劑量依賴性,尤其以80 μmol/L藥物濃度最為明顯.凋亡早期(6 h)細胞色素C水平升高80 μmol/L組升高明顯[NC(0.34±0.27),80 μmol/L組(32.04±1.62),P<0.05];不同濃度的As_2O_3作用後細胞中Caspase-3 mRNA錶達顯著增彊[NC(0.144±0.022),RA(0.323±0.047),(0.824±0.109),(1.213±0.196),P<0.05],Bcl-2的mRNA錶達顯著減弱[NC(1.08±0.23),RA(0.94±0.15),(0.46±0.08),(0.22±0.06),P<0.05].結論 RA患者滑膜細胞凋亡較健康塒照減少,As_2O_3通過升高細胞色素c及Caspase-3,抑製Bcl-2誘導RA滑膜細胞凋亡.
목적 탐토류풍습관절염(RA)환자활막세포적조망이상,이급삼양화이신(As_2O_3)대체외배양RA적활막세포조망적유도작용.방법 용광경、전경、류식세포의검측As_2O_3대체외배양적RA활막세포조망적유도작용,As_2O_3,작용우RA활막후매련면역흡부시험(ELISA)검측조망과정중세포색소C적변화,반전록-취합매련반응(RT-PCR)검측Caspase-3.Bel-2 mRNA표체,채용단인소방차분석화LSD-t검험、Dunnet-t검험진행통계학처리.결과 류식세포의검측발현불동농도적As_2O_3작용후,활막세포적조망교공백대조조(NC)증가[NC(0.95±0.87)%,RA(0.21±0.12)%,P<0.05],정일정적제량의뢰성,우기이80 μmol/L약물농도최위명현.조망조기(6 h)세포색소C수평승고80 μmol/L조승고명현[NC(0.34±0.27),80 μmol/L조(32.04±1.62),P<0.05];불동농도적As_2O_3작용후세포중Caspase-3 mRNA표체현저증강[NC(0.144±0.022),RA(0.323±0.047),(0.824±0.109),(1.213±0.196),P<0.05],Bcl-2적mRNA표체현저감약[NC(1.08±0.23),RA(0.94±0.15),(0.46±0.08),(0.22±0.06),P<0.05].결론 RA환자활막세포조망교건강시조감소,As_2O_3통과승고세포색소c급Caspase-3,억제Bcl-2유도RA활막세포조망.
Objective To investigate the effects of As_2O_3 on the apoptosis of synoviocytes in rheumatoid arthritis in vitro and to examine the levels of CtyC, and mRNAs of Caspase-3, Bcl-2 in RA synoviocytes induced by As_2O_3. Methods Cultured synoviocytes were incubated with As_2O_3. The effects of apoptosis were detected by light microscope, electronic microscope and flow cytometry. The level of CtyC was measured by ELJSA and the level of Caspase-3, Bcl-2 mRNAs were detected by RT-PCR. the data were analyzed with ony-way ANOVA, LSD-t test and Dunnet-t test. Results The ratio of the apoptosis cells was increased [NC (0.95±0.87)%, RA (0.21 ±0.12)%, P<0.05], the levels of CtyC [NC (0.34±0.27), RA (32.04±1.62), P< 0.05] and Caspase-3 mRNAs [NC (0.144±0.022), RA (0.323±0.047), (0.824±0.109), (1.213±0.196), P< 0.05] were increased and the level of Bcl-2 mRNA (NC (l.08±0.23), RA (0.94±0.15), (0.46±0.08), (0.22±0.06), P<0.05 )was decreased during the apoptosis of RA synoviocytes induced by As_2O_3 than normal control (NC). Conclusion The apoptosis of synoviocytes could be induced by As_2O_3, and the level of caspase-3 is increased. The mechanisms of As_2O_3 induced synoviocytes apoptosis maybe due to the increased level of CtyC and CtyC, and the decreased level of Bcl-2.
