目的 探讨前列闭尔通栓对自身免疫性前列腺炎（EAP）大鼠的影响及作用机制。方法 50只SD大鼠采用前列腺蛋白提纯液联合完全弗氏佐剂制备EAP大鼠模型，另取10只作为对照组，造模成功大鼠随机分为模型组、前列通栓（0.42 g·只^-1）组和前列闭尔通栓低、中、高剂量（0.33、0.66、0.99 g·只^-1）组，直肠给药28 d。压力换能器测定膀胱内压变化速率，显微镜计数测定前列腺液中卵磷脂小体、白细胞数量，ELISA法检测前列腺组织炎症因子，HE染色观察前列腺组织病理变化，Westernblotting检测前列腺组织核因子κB（NF-κB）p65、磷酸化κB抑制因子激酶（p-IKK-α）/IKK-α、肿瘤坏死因子-α（TNF-α）、磷酸化IκB激酶-α（p-IκB-α）/IκB-α、环氧化酶-2（COX-2）蛋白表达；实时荧光定量PCR（qRT-PCR）法检测重组人趋化因子配体5（CXCL5）、白细胞介素-6（IL-6）、TNF-α、COX-2基因表达。结果 与对照组比较，模型组大鼠膀胱内压变化速率显著降低（P<0.01）；白细胞数量显著增加、卵磷脂小体数量显著减少（P<0.01）；前列腺组织TNF-α、IL-8水平显著升高（P<0.01），IL-10水平显著降低（P<0.01）；前列腺组织炎症反应明显，病理评分显著升高（P<0.01）；前列腺组织NF-κB p65、p-IKK-α、p-IκB-α、TNF-α、COX-2蛋白表达显著升高（P<0.05、0.01）；前列腺组织CXCL5、COX-2、TNF-α基因表达升高（P<0.05）。与模型组比较，前列闭尔通栓中剂量组膀胱内压变化速率显著升高（P<0.01）；各剂量组白细胞数量显著减少、卵磷脂小体数量显著增加（P<0.01）；中、高剂量组TNF-α、IL-8水平显著降低（P<0.05、0.01）；各剂量组前列腺组织炎症反应明显减轻，病理评分显著降低（P<0.01）；各剂量组前列腺组织p-IκBα/IκBα、COX-2蛋白表达显著降低（P<0.01）；低剂量组前列腺组织p-IKK-α/IKK-α蛋白表达显著降低（P<0.05）；低、高剂量组前列腺组织NF-κB p65蛋白表达显著降低（P<0.05）；中剂量组前列腺组织TNF-α蛋白表达显著降低（P<0.05） ；各剂量组前列腺组织CXCL5、IL-6、COX-2基因表达显著降低（P<0.05）。结论 前列闭尔通栓可有效改善EAP大鼠前列腺组织病理形态，减轻炎症反应，其作用机制可能与抑制NF-κB信号通路相关蛋白NF-κB p65、p-IKK-α、TNF-α、p-IκB-α表达相关。

Objective To investigate the effect and mechanism of Qianlie-Biertong Suppository (QBS) on autoimmune prostatitis (EAP) rats. Methods Totally 50 SD rats were used to prepare EAP rat model with prostate protein purification solution and complete Freund's adjuvant, and the other 10 rats were used as control group. The 50 EAP rats that were successfully modeled were randomly divided into model group, low, middle and high dose (0.33, 0.66, and 0.99 g·piece^-1) groups of QBS, and Qianlie-tong Suppository (0.42 g·piece^-1) group. After 28 days of rectal administration, rate of changes in bladder internal pressure, the number of lecithin corpuscles and white blood cells were measured, the inflammatory factors of prostate tissue were detected by ELISA, the pathological changes of prostate tissue were observed by HE staining, and the prostate tissue NF-κB p65, p-IKK-α, p-IκB-α, TNF-α, COX-2 protein expression was detected by Western blotting, CXCL5, IL-6, TNF-α, COX-2 gene expression detection by qRT-PCR. Results Compared with control group, rate of changes in bladder internal pressure in the model group decreased (P < 0.01), the number of white blood cells increased and the number of lecithin bodies decreased (P < 0.01), the content of IL-8, TNF-α in prostate tissue increased (P < 0.01), and the content of IL-10 decreased (P < 0.01). The inflammatory reaction of prostate tissue were obvious, and the pathological score of model group compared with control group significantly increased (P < 0.01). The prostate tissue NF-κB p65, p-IKK-α, p-IκB-α, TNF-α, and COX-2 protein expression of model group compared with control group increased significantly (P < 0.05 and 0.01). Prostate tissue CXCL5, TNF-α, and COX-2 gene expression of model group compared with control group increased significantly (P < 0.05). Compared with the model group, rate of changes in bladder internal pressure in the middle dose group of QBS increased significantly (P < 0.01), the number of white blood cells decreased significantly and the number of lecithin corpuscles increased significantly in each dose group of QBS (P < 0.01), the content of IL-8, TNF-α in middle and high dose groups of QBS was decreased significantly (P < 0.05 and 0.01). Compared with the model group, the inflammatory response of prostate tissue in each dose group of QBS was significantly reduced, and the pathological score was significantly reduced (P < 0.01). Compared with the model group, the protein expression p-IκBα/IκBα, COX-2 in each dose group, p-IKK-α/IKK-α in low-dose group, NF-κB p65 in low and high dose group, TNF-α in medium dose group were significantly reduced (P < 0.05). The expression of CXCL5, IL-6, and COX-2 genes in prostate tissue was significantly reduced in each dose group of QBS compared with the model group (P < 0.05). Conclusion QBS can effectively improve the pathological morphology of prostate tissue and reduce inflammatory reaction in EAP rats, and its mechanism may be related to the inhibition of NF-κB signal pathway related protein NF-κB p65, p-IKK-α, TNF-α, p-IκB-α express relevance.

R285.5

西藏自治区科技计划项目（XZ201801-GA-16）