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目的:探讨前列腺组织中的肥大细胞在Ⅲ型前列腺炎(CP/CPPS)中的作用。方法:选取雄性SD大鼠45只,分为对照组(0.9%NaCl盆腔区域及双侧肩胛皮下多点注射)、自身免疫性前列腺炎(EAP)模型组(完全弗氏佐剂与前列腺组织混合悬液盆腔区域及双侧肩胛皮下多点注射)、干预组(EAP模型组基础上加入肥大细胞类胰蛋白酶脱落抑制剂色甘酸钠),每组15只。建立EAP模型过程中,用Von-Frey测痛纤维在第5、10、20、30、40天对对照组、EAP组进行骨盆区域痛觉测试。建模成功后,干预组予色甘酸钠连续腹腔内注射10 d,每两天对其及EAP组进行痛觉测试。选取3组大鼠的前列腺,进行HE染色及甲苯胺蓝染色病理学检查;并通过免疫组化和Western印迹法检测肥大细胞类胰蛋白酶的表达。结果:Von-Frey测痛结果显示:EAP模型组大鼠骨盆疼痛表现较对照组明显,干预组大鼠骨盆疼痛表现较EAP组减轻。HE染色提示:EAP组大鼠前列腺间质内淋巴细胞和中性粒细胞浸润,腺体周围充血。对照组未见明显炎症细胞浸润。与EAP组对比,干预组腺体充血及炎症细胞浸润情况较之减轻。甲苯胺蓝染色提示:EAP组大鼠的前列腺组织中,肥大细胞总数及脱颗粒的肥大细胞数目较对照组增加(P<0.01),干预组较EAP组减少(P<0.05)。免疫组化染色提示:EAP组大鼠的前列腺组织中,肥大细胞类胰蛋白酶较对照组表达增加(主要表达于细胞核和细胞质中)(P<0.01),干预组较EAP组减少(P<0.05)。Western印迹提示:EAP组大鼠的前列腺组织中,肥大细胞类胰蛋白酶较对照组表达增加(P<0.01),干预组较EAP组减少(P<0.01)。结论:EAP大鼠前列腺组织中肥大细胞的总数及脱颗粒的肥大细胞数目增加,肥大细胞是导致Ⅲ型前列腺炎骨盆区域疼痛介质之一,可作为干预及治疗Ⅲ型前列腺炎中一个靶向指标。
Objective: To investigate the role of mast cells in prostatic tissue in type Ⅲ prostatitis (CP / CPPS). Methods: Forty-five male Sprague-Dawley rats were divided into control group (0.9% NaCl pelvic region and subcutaneous scapular subcutaneous injection), autoimmune prostatitis (EAP) model group (complete Freund’s adjuvant mixed with prostate tissue Suspension pelvic area and bilateral scapular subcutaneous injection), intervention group (EAP model group based on the addition of mast cell tryptase shedding inhibitor cromolyn), each group of 15. During the establishment of the EAP model, pelvic regional pain tests were performed on the 5th, 10th, 20th, 30th and 40th days in the control and EAP groups with Von-Frey sore fibers. After the modeling was successful, the intervention group was given cromolyn sodium continuously for 10 days, and the pain group and EAP group were pain tested every two days. Prostate of 3 rats were selected for HE staining and toluidine blue staining, and the expression of tryptase in mast cells was detected by immunohistochemistry and Western blot. Results: The results of Von-Frey pain test showed that the pelvic pain in EAP model group was more obvious than that in the control group. The pelvic pain in the intervention group was relieved compared with the EAP group. Hematoxylin-Eosin staining showed that infiltration of lymphocytes and neutrophils in the prostate stroma of rats in the EAP group and hyperemia around the gland. No obvious infiltration of inflammatory cells in the control group. Compared with EAP group, the intervention group, glandular congestion and inflammatory cell infiltration than the reduction. Toluidine blue staining suggested that the number of mast cells and degranulation mast cells in EAP group were significantly increased than those in control group (P <0.01), while those in EAP group were lower than those in EAP group (P <0.05). Immunohistochemical staining showed that the expression of mast cell tryptase in the prostate tissue of EAP group was increased (mainly in the nucleus and cytoplasm) compared with the control group (P <0.01), and decreased in the intervention group compared with the EAP group (P <0.05) ). Western blotting suggested that the expression of mast cell tryptase in EAP group was higher than that in control group (P <0.01), but decreased in EAP group (P <0.01). Conclusion: The number of mast cells and degranulation of mast cells in EAP rat prostate tissue is increased. Mast cell is one of the pain media in the pelvic region of type Ⅲ prostatitis and can be used as a target for intervention and treatment of type Ⅲ prostatitis .