论文部分内容阅读
为观察烟碱对胶原诱导关节炎模型小鼠的作用,并初步探讨其免疫学和分子机制,建立胶原诱导关节炎模型,以PBS溶液喂饲模型小鼠为对照,采用半定量评分系统和病理切片评价关节炎模型小鼠对照组和烟碱实验组的病情进展。并采用流式细胞术分别测定对照组和烟碱实验组小鼠脾脏CD4+细胞表型;RT-PCR方法检测对照组和烟碱实验组脾细胞Th1/Th17相关细胞因子IFN-γ、IL-17A、IL-21、IL-22,以及促炎症因子IL-6,抑炎症因子IL-10 mRNA的表达变化。流式CBA法检测模型小鼠血浆TNF-α含量。结果,采用烟碱喂饲关节炎模型小鼠能够有效减缓关节炎病症进展,减轻模型小鼠关节炎症状。病理切片显示对照组小鼠患处充血、水肿及中等量炎症细胞浸润;而相应烟碱实验组小鼠病理症状较轻。相比对照组,烟碱实验组Th17细胞比例明显降低(7.63%vs 12.53%);且烟碱实验组IL-17A、IFN-γmRNA比值低于对照组,具有显著性差异,P<0.05。烟碱干预能有效降低实验小鼠IL-6、IL-21 mRNA含量,P<0.05。另外,烟碱实验组小鼠血浆TNF-α含量明显低于对照组(10.82±2.22)pg/ml和(30.14±4.12)pg/ml,两者具有显著性差异,P<0.01。提示,烟碱干预能够有效减缓关节炎小鼠病症进展,减轻小鼠关节炎症状;这一效应是通过降低Th17细胞比例、降低炎症因子IL-17A/IFN-γ比例,减少IL-6、IL-21、TNF-α等多因素共同参与的过程。
To observe the effect of nicotine on collagen-induced arthritis model mice, and to explore its immunological and molecular mechanisms, to establish a model of collagen-induced arthritis, with PBS solution-fed mice as control, semi-quantitative scoring system and pathology Slides were used to evaluate the progression of arthritis model mice and nicotine experimental group. The spleen CD4 + cell phenotype of control group and nicotine experimental group were determined by flow cytometry. Th1 / Th17 cytokines IFN-γ and IL-17A of splenocytes in control group and nicotine group were detected by RT-PCR , IL-21, IL-22, as well as the expression of proinflammatory cytokines IL-6 and IL-10. Flow cytometry was used to detect plasma TNF-α in model mice. As a result, nicotine-fed arthritis model mice effectively slowed the progression of arthritic conditions and alleviated the arthritic symptoms in model mice. The pathological sections showed congestion, edema and moderate infiltration of inflammatory cells in mice in the control group, while the mice in the corresponding nicotine group had lighter pathological symptoms. Compared with the control group, the proportion of Th17 cells in the nicotine group was significantly decreased (7.63% vs 12.53%). The ratio of IL-17A and IFN-γmRNA in the nicotine group was significantly lower than that in the control group (P <0.05). Nicotine intervention can effectively reduce the experimental mice IL-6, IL-21 mRNA content, P <0.05. In addition, the plasma TNF-αlevels in the nicotine experimental group were significantly lower than those in the control group (10.82 ± 2.22 pg / ml and (30.14 ± 4.12) pg / ml, respectively), with significant difference between the two groups (P <0.01). These results suggest that nicotine intervention can effectively reduce the progression of arthritis in mice and alleviate the arthritis symptoms in mice. This effect can be achieved by reducing the proportion of Th17 cells, decreasing the proportion of inflammatory cytokines IL-17A / IFN-γ, decreasing IL-6, IL -21, TNF-α and other factors involved in the process.