IL-17和CCL2与大鼠自身免疫性前列腺炎盆腔疼痛关系的研究

发布时间：2018-05-04 15:50

本文选题：前列腺炎 + IL-17　；参考：《昆明医科大学》2017年硕士论文

【摘要】：[目的]探讨细胞因子IL-17和趋化因子CCL2在实验性自身免疫性前列腺炎大鼠模型中表达及其病理作用。[方法]将2个月龄的SD大鼠44只随机分为正常对照组(Control组,n=10)、模型组(EAP组,n=10);剩余24只建模制成EAP大鼠后随机分为他克莫司组(Tacrolimus组,n=8)、塞来昔布组(Celecoxib组,n=8)和盐水对照组(NS组,n=8)。分别将EAP组和Control组进行Von Frey filament行为测试;将Tacrolimus组、Celecoxib组和NS组于干预治疗后进行痛觉测试。取各组SD大鼠前列腺组织进行HE染色和免疫组化、RT-PCR检测、Western blots测定观察IL-17和CCL2的表达。[结果](1)痛觉反应测试中:EAP组异常痛觉诱发明显多于Control组;Celecoxib组异常下降频率较快,而Tacrolimus组则是缓慢下降,NS组则仅为小幅下降(P0.05)。(2)HE染色:EAP组大鼠前列腺呈不规则改变,腺体间质内淋巴细胞和中性粒细胞浸润,腺体周围充血;Control组大鼠前列腺未见明显炎症细胞浸润及充血。免疫组化提示:IL-17和CCL2在EAP组中呈阳性表达。(3)RT-PCR结果、Western blots方法检测发现,与Control组相比,建模后50d,EAP大鼠前列腺IL-17和CCL2的表达明显上调(P0.05)。Celecoxib组、Tacrolimus组在干预后30 d,与NS组相比,大鼠前列腺的IL-17和CCL2表达均明显下调(P0.05)。[结论]IL-17和CCL2在实验性自身免疫性前列腺炎发病中有重要作用,并且可能对盆腔疼痛有介导作用;他克莫司和塞来昔布减少EAP大鼠模型前列腺组织中的炎症细胞且减轻骨盆疼痛,其作用机制可能与抑制IL-17和CCL2的产生有关。
[Abstract]:[objective] to investigate the expression of cytokine IL-17 and chemokine CCL2 in experimental autoimmune prostatitis in rats. [methods] Forty-four SD rats aged 2 months were randomly divided into control group (n = 10) and model group (n = 10), and the remaining 24 rats were randomly divided into two groups: tacrolimus group (Tacrolimus group), celecoxib group (n = 8) and saline control group (NS group, n = 8). The behavior of Von Frey filament was tested in EAP group and Control group, and pain was tested in Tacrolimus group and NS group after intervention. The prostatic tissues of SD rats in each group were stained with HE and detected by RT-PCR. The expression of IL-17 and CCL2 were detected by Western blots. [results] in the pain response test, abnormal nociceptive response was induced more frequently in the Control group than in the Celecoxib group, while in the Tacrolimus group, the abnormal decrease rate was only slightly decreased P0.05N. T2HE staining showed irregular changes in the prostate gland of the rats in the Tacrolimus group. Interstitial lymphocytes and neutrophils were infiltrated in glandular mesenchymal cells, but no inflammatory cell infiltration and congestion were found in the prostate of rats in the control group. Immunohistochemistry showed that the positive expression of CCL2 and IL-17 in EAP group was detected by RT-PCR. Western blots method showed that the expression of IL-17 and CCL2 in the prostate of 50 days after modeling was significantly up-regulated in the control group compared with that in the NS group, compared with the NS group, and the expression of IL-17 and CCL2 in the prostate of 50 d after modeling was significantly up-regulated in the control group, compared with that in the NS group, and the expression of IL-17 and CCL2 in the prostatic gland of the control group was significantly higher than that in the control group (P < 0.05). The expression of IL-17 and CCL2 in rat prostate was significantly down-regulated (P 0.05). [conclusion] IL-17 and CCL2 may play an important role in the pathogenesis of experimental autoimmune prostatitis and may mediate pelvic pain. Tacrolimus and celecoxib reduce inflammatory cells in prostate tissue and relieve pelvic pain in EAP rats. The mechanism of tacrolimus and celecoxib may be related to the inhibition of IL-17 and CCL2 production.
【学位授予单位】：昆明医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R697.33

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