广东医学
廣東醫學
엄동의학
GUNAGDONG MEDICAL JOURNAL
2014年
17期
2656-2658
,共3页
microRNA-451%辅助性T淋巴细胞17亚群%病毒性心肌炎
microRNA-451%輔助性T淋巴細胞17亞群%病毒性心肌炎
microRNA-451%보조성T림파세포17아군%병독성심기염
microRNA-451%T helper cells 17%viral myocarditis
目的:通过观察microRNA-451(miR-451)及辅助性T淋巴细胞17(Th17)亚群在病毒性心肌炎小鼠中的变化,进一步探讨其在病毒性心肌炎小鼠发病过程中的作用及意义。方法实验组注射柯萨奇病毒B3病毒液0.1 mL建立Balb/c病毒性心肌炎小鼠模型,对照组注射等量磷酸盐缓冲液。在注射后第0、7、14和28天流式细胞法检测小鼠脾脏Th17亚群比例( Th17/CD4+),荧光定量聚合酶链式反应( PCR)检测心肌组织中miR-451的表达量。结果实验组7 d亚组小鼠脾Th17/CD4+高于0 d亚组,28 d亚组最高,与对照组相应时点亚组比较差异均有统计学意义(均P<0.05)。实验组7 d亚组小鼠心肌miR-451的表达量低于0 d亚组,14 d亚组小鼠心肌miR-451的表达量最低,28 d亚组心肌miR-451的表达量较14 d亚组增高。除0 d组外,实验组各亚组miR-451表达水平均较对照组各相应时点明显降低(均P<0.05)。 miR-451的表达与Th17亚群比例无相关(r=-0.26,P>0.05)。结论 miR-451和Th17参与了病毒性心肌炎的发病过程。 miR-451参与病毒性心肌炎小鼠的发病过程并不依赖于Th17的变化。
目的:通過觀察microRNA-451(miR-451)及輔助性T淋巴細胞17(Th17)亞群在病毒性心肌炎小鼠中的變化,進一步探討其在病毒性心肌炎小鼠髮病過程中的作用及意義。方法實驗組註射柯薩奇病毒B3病毒液0.1 mL建立Balb/c病毒性心肌炎小鼠模型,對照組註射等量燐痠鹽緩遲液。在註射後第0、7、14和28天流式細胞法檢測小鼠脾髒Th17亞群比例( Th17/CD4+),熒光定量聚閤酶鏈式反應( PCR)檢測心肌組織中miR-451的錶達量。結果實驗組7 d亞組小鼠脾Th17/CD4+高于0 d亞組,28 d亞組最高,與對照組相應時點亞組比較差異均有統計學意義(均P<0.05)。實驗組7 d亞組小鼠心肌miR-451的錶達量低于0 d亞組,14 d亞組小鼠心肌miR-451的錶達量最低,28 d亞組心肌miR-451的錶達量較14 d亞組增高。除0 d組外,實驗組各亞組miR-451錶達水平均較對照組各相應時點明顯降低(均P<0.05)。 miR-451的錶達與Th17亞群比例無相關(r=-0.26,P>0.05)。結論 miR-451和Th17參與瞭病毒性心肌炎的髮病過程。 miR-451參與病毒性心肌炎小鼠的髮病過程併不依賴于Th17的變化。
목적:통과관찰microRNA-451(miR-451)급보조성T림파세포17(Th17)아군재병독성심기염소서중적변화,진일보탐토기재병독성심기염소서발병과정중적작용급의의。방법실험조주사가살기병독B3병독액0.1 mL건립Balb/c병독성심기염소서모형,대조조주사등량린산염완충액。재주사후제0、7、14화28천류식세포법검측소서비장Th17아군비례( Th17/CD4+),형광정량취합매련식반응( PCR)검측심기조직중miR-451적표체량。결과실험조7 d아조소서비Th17/CD4+고우0 d아조,28 d아조최고,여대조조상응시점아조비교차이균유통계학의의(균P<0.05)。실험조7 d아조소서심기miR-451적표체량저우0 d아조,14 d아조소서심기miR-451적표체량최저,28 d아조심기miR-451적표체량교14 d아조증고。제0 d조외,실험조각아조miR-451표체수평균교대조조각상응시점명현강저(균P<0.05)。 miR-451적표체여Th17아군비례무상관(r=-0.26,P>0.05)。결론 miR-451화Th17삼여료병독성심기염적발병과정。 miR-451삼여병독성심기염소서적발병과정병불의뢰우Th17적변화。
Objective To observe microRNA-451 (miR-451) and T helper cells 17 (Th17) subsets in mice with viral myocarditis induced by coxsackie virus B3 ( CVB3 ) , thus to investigate the roles of miR-451 and Th17 in patho-genesis of viral myocarditis ( VMC) in mice.Methods VMC mouse models were constructed with peritoneally injection of CVB3 in Balb/c male mice, while phosphate buffer was used as control.Flow cytometry analysis was used to evaluate the frequencies of Th17 subsets in CD4 +T cells on Day 0, 7, 14 and 28 after virus injection.The levels of miR-451 in mice myocardial tissues were determined by quantitative polymerase chain reaction.Results Statistical differences in the proportion of Th17 cells were observed between VMC mice and controls at different time points ( P<0.05 ) .In VMC mice, the proportion of spleen Th17 cells was significantly increased on Day 7 than Day 0, and reached the peaked on Day 28.The expression levels of miR-451 in VMC mice were significantly reduced since the Day 7, and reached the lowest point on Day 14.Significant reduction in miR-451 was observed in VMC mice through the study (P<0.05).No signifi-cant correlation was revealed between the expression of miR-451 and Th17 cells.Conclusion miR-451 and Th17 cells may be involved in process of CVB3 -induced VMC in mice.miR-451 may play a role in the autoimmune patho-genesis of mice with VMC but not through Th17 cells.