谷氨酰胺对慢性阻塞性肺疾病患者外周血单个核细胞中P38MAPK及IL-17的影响

    Effect of Glutamine on P38MAPK and IL-17 Expression in PBMC of Patients with Chronic Obstructive Pulmonary Disease

    • 摘要: 目的 通过观察谷氨酰胺(glutamine,Gln)对慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者外周血单个核细胞(peripheral blood mononuclear cell,PBMC)中P38丝裂原活化蛋白激酶(P38 mitogen-activated protein kinases,P38MAPK)活性和白介素17(IL-17)水平的影响,探讨Gln在COPD患者治疗中的抗炎作用。方法 选择32例COPD患者在COPD急性加重期(acute exacerbation of chronic obstructive pulmonary disease,AECOPD)和经治疗后转为稳定期(stable chronic obstructive pulmonary disease,SCOPD)的PBMC各32例为研究对象,各分为Gln组和空白对照组,并选择16例健康体检者的PBMC为健康对照组。采用实时定量荧光PCR(RT-PCR)法检测5组PBMC中P38MAPK、IL-17的基因表达水平。结果 AECOPD空白对照组、SCOPD空白对照组P38MAPK、IL-17的表达水平均高于健康对照组(P<0.01或P<0.05),且AECOPD空白对照组高于SCOPD空白对照组(P<0.05);AECOPD Gln组P38MAPK、IL-17的表达水平高于健康对照组(P<0.05),而SCOPD Gln组P38MAPK、IL-17的表达水平与健康对照组比较差异无统计学意义;AECOPD Gln组、SCOPD Gln组P38MAPK、IL-17的表达水平分别低于其对应的空白对照组(P<0.01或P<0.05)。结论 Gln可抑制COPD患者炎细胞中P38MAPK通路的活化并下调IL-17的表达水平。

       

      Abstract: OBJECTIVE To determine the effects of glutamine on the p38 mitogen-activated protein kinases(P38MAPK) activity and IL-17 expression in peripheral blood mononuclear cells(PBMC) of patients with chronic obstructive pulmonary disease(COPD). METHODS Thirty-two patients with acute exacerbation of COPD(AECOPD) were enrolled. After the treatment, all patients’ conditions were controlled in stable COPD(SCOPD). Venous blood of patients was collected in the acute and stable period, and PBMC were extracted immediately. Then divided into glutamine(Gln) group and blank control group. Sixteen healthy people’s PBMC were used as the normal group. The levels of P38MAPK and IL-17gene expression in PBMCs were detected by real-time PCR. RESULTS The levels of P38MAPK and IL-17 gene expression were higher in AECOPD blank control group and SCOPD blank control group than those in the normal group (P<0.01 and P<0.05, respectively). Moreover, there was a significantly increase both P38MAPK and IL-17 gene expression in AECOPD blank control group compared with SCOPD blank control group (P<0.05); The levels of P38MAPKand IL-17 gene expression were higher in AECOPD Gln group than those in the normal group (P<0.05), while there was no significant difference between SCOPD Gln group and the normal group; The levels of P38MAPK and IL-17 gene expression in AECOPD Gln group and SCOPD Gln group were significantly lower than those in blank control group (P<0.01 and P<0.05, respectively). CONCLUSION Gln plays an anti-inflammatory role on COPD patients by inhibiting P38MAPK Cell signaling pathway and reducing the expression of IL-17.

       

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