目的 探討前列閉爾通栓對自身免疫性前列腺炎（EAP）大鼠的影響及作用機制。方法 50只SD大鼠采用前列腺蛋白提純液聯(lián)合完全弗氏佐劑制備EAP大鼠模型，另取10只作為對照組，造模成功大鼠隨機分為模型組、前列通栓（0.42 g·只^-1）組和前列閉爾通栓低、中、高劑量（0.33、0.66、0.99 g·只^-1）組，直腸給藥28 d。壓力換能器測定膀胱內(nèi)壓變化速率，顯微鏡計數(shù)測定前列腺液中卵磷脂小體、白細胞數(shù)量，ELISA法檢測前列腺組織炎癥因子，HE染色觀察前列腺組織病理變化，Westernblotting檢測前列腺組織核因子κB（NF-κB）p65、磷酸化κB抑制因子激酶（p-IKK-α）/IKK-α、腫瘤壞死因子-α（TNF-α）、磷酸化IκB激酶-α（p-IκB-α）/IκB-α、環(huán)氧化酶-2（COX-2）蛋白表達；實時熒光定量PCR（qRT-PCR）法檢測重組人趨化因子配體5（CXCL5）、白細胞介素-6（IL-6）、TNF-α、COX-2基因表達。結(jié)果 與對照組比較，模型組大鼠膀胱內(nèi)壓變化速率顯著降低（P<0.01）；白細胞數(shù)量顯著增加、卵磷脂小體數(shù)量顯著減少（P<0.01）；前列腺組織TNF-α、IL-8水平顯著升高（P<0.01），IL-10水平顯著降低（P<0.01）；前列腺組織炎癥反應(yīng)明顯，病理評分顯著升高（P<0.01）；前列腺組織NF-κB p65、p-IKK-α、p-IκB-α、TNF-α、COX-2蛋白表達顯著升高（P<0.05、0.01）；前列腺組織CXCL5、COX-2、TNF-α基因表達升高（P<0.05）。與模型組比較，前列閉爾通栓中劑量組膀胱內(nèi)壓變化速率顯著升高（P<0.01）；各劑量組白細胞數(shù)量顯著減少、卵磷脂小體數(shù)量顯著增加（P<0.01）；中、高劑量組TNF-α、IL-8水平顯著降低（P<0.05、0.01）；各劑量組前列腺組織炎癥反應(yīng)明顯減輕，病理評分顯著降低（P<0.01）；各劑量組前列腺組織p-IκBα/IκBα、COX-2蛋白表達顯著降低（P<0.01）；低劑量組前列腺組織p-IKK-α/IKK-α蛋白表達顯著降低（P<0.05）；低、高劑量組前列腺組織NF-κB p65蛋白表達顯著降低（P<0.05）；中劑量組前列腺組織TNF-α蛋白表達顯著降低（P<0.05） ；各劑量組前列腺組織CXCL5、IL-6、COX-2基因表達顯著降低（P<0.05）。結(jié)論 前列閉爾通栓可有效改善EAP大鼠前列腺組織病理形態(tài)，減輕炎癥反應(yīng)，其作用機制可能與抑制NF-κB信號通路相關(guān)蛋白NF-κB p65、p-IKK-α、TNF-α、p-IκB-α表達相關(guān)。

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

西藏自治區(qū)科技計劃項目（XZ201801-GA-16）