前列清浊汤对慢性非细菌性前列腺炎大鼠模型血清TNF-α、IFN-γ的影响

Effects of Qianlie Qingzhuo decoction on serum TNF-α and IFN-γ levels in rat model of chronic nonbacterial prostatitis

目的:探讨前列清浊汤治疗慢性非细菌性前列腺炎的作用机制。方法:将60只健康Wistar大鼠随机分为正常组,模型组,前列康组和前列清浊汤高、中、低剂量组(以下简称高、中、低剂量组),每组10只。对除正常组外的其余组大鼠采用大鼠前列腺蛋白提纯液结合福氏完全佐剂法建立慢性非细菌性前列腺炎模型。造模成功后,各组予相应药物或等量生理盐水灌胃处理,每天1次,连续给药30d。于末次给药24h后处死各组大鼠,光镜下观察前列腺组织病理学变化,用ELISA法测定其前列腺组织中TNF-α、IFN-γ水平,并比较结果。结果:模型组大鼠TNF-α、IFN-γ水平明显高于正常组(P<0.01);高剂量组与前列康组TNF-α水平及高、中剂量组与前列康组IFN-γ水平均低于模型组(P<0.05)。结论:前列清浊汤治疗慢性非细菌性前列腺炎的作用机制可能与其调节TNF-α和IFN-γ的水平有关。

Objective：To investigate the action mechanism of Qianlie Qingzhuo decoction in the treatment of chronic nonbacterial prostatitis. Methods ： Sixty healthy Wistar rats were randomly and equally divided into normal group, model group, Qianliekang group, and high - ,middle - ,and low - dose Qianlie Qingzhuo decoction groups. All rats except those in the normal group were treated with puri- fied prostate protein and complete Freund＇s adjuvant to establish a chronic nonbacterial prostatitis model. Then, all groups received re- spective drugs or an equal volume of normal saline by gavage once daily for 30 d. All rats were sacrificed at 24 h after the final adminis- tration. The pathological changes in prostate tissue were observed under a light microscope ; the levels of tumor necrosis factor - alpha （TNF -α ）and interferon -gamma（ IFN -y）in prostate tissue were measured by enzyme -linked immunosorbent assay. The two groups were compared in terms of the results. Results ： The model group had significantly higher TNF - α and IFN - ylevels than the normal group （P 〈 0. 01 ）. Compared with the model group, the high -dose Qianlie Qingzhuo decoction group and Qianliekang group had signifi- cantly lower TNF-α levels（P 〈0. 05 ） ,and the high - and middle -dose Qianlie Qingzhuo decoction groups and Qianliekang group had significantly lower IFN-y levels（ P 〈 0. 05 ）. Conclusion：The action mechanism of Qianlie Qingzhuo decoction in the treatment of chronic nonbacterial prostatitis may involve its regulation of TNF - α and IFN - y levels.