中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
CHINESE JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY
2011年
9期
815-818
,共4页
蒋廷旺%熊怀民%盛建华%崔映红%张红星%申鹏%仲人前
蔣廷旺%熊懷民%盛建華%崔映紅%張紅星%申鵬%仲人前
장정왕%웅부민%성건화%최영홍%장홍성%신붕%중인전
多发性骨髓瘤%Toll样受体3%增殖%凋亡%PolyI:C
多髮性骨髓瘤%Toll樣受體3%增殖%凋亡%PolyI:C
다발성골수류%Toll양수체3%증식%조망%PolyI:C
Multiple myeloma%Toll like receptor 3%Proliferation%Apoptosis%PolyI : C
目的 研究聚肌苷酸胞苷酸( polyI:C)激活的TLR3通路对多发性骨髓瘤RPMI8226细胞的增殖抑制和凋亡相关的生物学作用及相关机制.方法 RPMI8226细胞培养于RPMI 1640培养基,以不同浓度的polyI:C与该细胞作用不同的时间.收集细胞后,分别利用CCK-8和流式细胞术分析其增殖抑制和凋亡情况,同时抽提总RNA,相对定量PCR测定TLR3通路相关基因表达.结果 PolyI:C对RPMI8226的增殖抑制效应随着作用剂量的增加和时间的延长而增加,24h:12.30％±2.04％、22.50％±2.20％、37.90％±1.30％;48h:17.80％±1.52％、29.60±0.85％、45.80％±1.68％;72 h:25.10％±1.01％、34.60％±1.27％、60.50％±2.08％,差异有统计学意义(P＜0.05).浓度为50、100、200μg/ml的polyl:C与RPMI8226作用48 h后,细胞凋亡率分别为5.60％±1.06％、8.71％±1.06％、13.93％±1.17％,差异具有统计学意义(P＜0.05),而且随着polyI:C作用浓度增加,RPMI8226细胞中TLR3和TRIF mRNA相对于内参β-actin的表达均显著增高,TLR3:1.41±0.10、2.24±0.16、4.08±0.13;TRIF:1.07±0.16、1.97±0.13、3.56±0.19,各组间差异具有统计学意义(P＜0.05).结论 TLR3途径可以有效地抑制多发性骨髓瘤细胞增殖,并且诱导其凋亡,对多发性骨髓瘤的生物治疗具有潜在应用价值.
目的 研究聚肌苷痠胞苷痠( polyI:C)激活的TLR3通路對多髮性骨髓瘤RPMI8226細胞的增殖抑製和凋亡相關的生物學作用及相關機製.方法 RPMI8226細胞培養于RPMI 1640培養基,以不同濃度的polyI:C與該細胞作用不同的時間.收集細胞後,分彆利用CCK-8和流式細胞術分析其增殖抑製和凋亡情況,同時抽提總RNA,相對定量PCR測定TLR3通路相關基因錶達.結果 PolyI:C對RPMI8226的增殖抑製效應隨著作用劑量的增加和時間的延長而增加,24h:12.30％±2.04％、22.50％±2.20％、37.90％±1.30％;48h:17.80％±1.52％、29.60±0.85％、45.80％±1.68％;72 h:25.10％±1.01％、34.60％±1.27％、60.50％±2.08％,差異有統計學意義(P＜0.05).濃度為50、100、200μg/ml的polyl:C與RPMI8226作用48 h後,細胞凋亡率分彆為5.60％±1.06％、8.71％±1.06％、13.93％±1.17％,差異具有統計學意義(P＜0.05),而且隨著polyI:C作用濃度增加,RPMI8226細胞中TLR3和TRIF mRNA相對于內參β-actin的錶達均顯著增高,TLR3:1.41±0.10、2.24±0.16、4.08±0.13;TRIF:1.07±0.16、1.97±0.13、3.56±0.19,各組間差異具有統計學意義(P＜0.05).結論 TLR3途徑可以有效地抑製多髮性骨髓瘤細胞增殖,併且誘導其凋亡,對多髮性骨髓瘤的生物治療具有潛在應用價值.
목적 연구취기감산포감산( polyI:C)격활적TLR3통로대다발성골수류RPMI8226세포적증식억제화조망상관적생물학작용급상관궤제.방법 RPMI8226세포배양우RPMI 1640배양기,이불동농도적polyI:C여해세포작용불동적시간.수집세포후,분별이용CCK-8화류식세포술분석기증식억제화조망정황,동시추제총RNA,상대정량PCR측정TLR3통로상관기인표체.결과 PolyI:C대RPMI8226적증식억제효응수착작용제량적증가화시간적연장이증가,24h:12.30％±2.04％、22.50％±2.20％、37.90％±1.30％;48h:17.80％±1.52％、29.60±0.85％、45.80％±1.68％;72 h:25.10％±1.01％、34.60％±1.27％、60.50％±2.08％,차이유통계학의의(P＜0.05).농도위50、100、200μg/ml적polyl:C여RPMI8226작용48 h후,세포조망솔분별위5.60％±1.06％、8.71％±1.06％、13.93％±1.17％,차이구유통계학의의(P＜0.05),이차수착polyI:C작용농도증가,RPMI8226세포중TLR3화TRIF mRNA상대우내삼β-actin적표체균현저증고,TLR3:1.41±0.10、2.24±0.16、4.08±0.13;TRIF:1.07±0.16、1.97±0.13、3.56±0.19,각조간차이구유통계학의의(P＜0.05).결론 TLR3도경가이유효지억제다발성골수류세포증식,병차유도기조망,대다발성골수류적생물치료구유잠재응용개치.
Objective To investigate the roles of TLR3 pathway activiated by polyI:C in proliferation and apoptosis of multiple myeloma (MM) RPMI8226 cell line.Methods RPMI8226 cells were cultured in RPMI 1640 with different dose of polyl:C.Cells were collected in different time.Proliferation and apoptosis were detected by CCK-8 kit and flow cytometry,separately.Results The proliferation of RPM18226 was inhibited by polyI:C,and it was dose and time dependent,24 h:12.30％ ±2.04％,22.50％±2.20％,37.90％ ±1.30％ ; 48 h:17.80％ ±1.52％,29.60％ ±0.85％,45.80％ ±1.68％ ;72 h:25.10％±1.01％,34.60％±1.27％,60.50％±2.08％,P＜0.05.RPMI8226 cells were incubated with 50 μg/ml,100 μg/ml and 200 μg/ml polyI:C for 48 h.Apoptotic rate were 5.60％ ±1.06％,8.71％ ±1.06％ and 13.93％ ±1.17％,P＜0.05.TLR3 and TRIF mRNA expression increased obviously and dose dependent,TLR3:1.41±0.10,2.24±0.16,4.08±0.13; TRIF:1.07±0.16,1.97±0.13,3.56±0.19,P＜0.05.Conclusion The proliferation of MM cells were inhibited by TLR3 pathway obviously,and apoptosis was induced by polyI:C.
