京尼平苷对慢性前列腺炎大鼠前列腺组织中细胞因子的影响

【目的】探讨京尼平苷对慢性前列腺炎（chronic prostatitis，CP）模型大鼠治疗作用机制。【方法】采用前列腺内注射消痔灵方法复制慢性前列腺炎模型，随机分为模型组、阳性药组（前列康片组，2g／kg）及京尼平苷高、中、低剂量组（20、10、5mg／kg）。28d后处死大鼠，取前列腺组织，观察前列腺病理改变，并对前列腺组织内炎细胞、成纤维细胞、腺体数量和腺腔面积等形态学变化情况进行分析。同时ELISA法检测前列腺组织匀浆中白介素-1β（IL-1β）、白介素-6（IL-6）、肿瘤坏死因子（TNF-α）和白介素-10（IL-10）的含量。【结果】京尼平苷高剂量组、前列康片组与模型组比较，前列腺间质中炎细胞数、成纤维细胞数均显著降低，腺体数量与腺腔面积明显升高（P〈0.05或P〈0.01）；CP大鼠前列腺中IL-1β、IL-6、TNF-α明显降低，IL-10含量显著上升（P〈0.01或P〈0.05）。【结论】京尼平苷对大鼠慢性前列腺炎的治疗作用与其降低前列腺内炎性细胞因子（IL-1β、IL-6、TNF-α）、提高抑炎细胞因子（IL-10）水平、减轻炎细胞浸润、抑制纤维组织增生有关。

Effect of Geniposide on the cytokine of prostatic tissue in chronic prostatitic rats

Objective] To observe the mechanism of Geniposide in treating experimental chronic prostatis （CP） rats.Methods] The animal model of CP was made by injecting Xiaozhiling （Chinese medicine） into the rat＇s prostate gland. Rats in experiment group were randomly devided into model group, Qianliekang tablets group （2 g/kg） and Geniposide （high, middle, low） dose groups （20, 10, 5 mg/kg）. After 28 days the rats were killed and prostatic tissue was taken and histopathological changes were observed. Quantitation of inflammatory cell, fibroblasts, glandular organ, calculation of glandular cavity area, and their changes of morphology were analyzed. The contents of interleukin-1β（IL-1β）, interleukin-6（IL-6）, tumor necrosis factor-α （TNF-α） and interleukin-10（IL-10） were detected in prostatic homogenate by enzyme linked immunosorbent assay （ELISA）. Results] Compared with model group, the number inflammatory cells and fibroblasts in Qianliekang tablets group, high dose Geniposide group were decreased, and the quantity of glandular organ and area of glandular cavity in these groups were increased （P 〈 0.05 or P 〈 0.01）. Compared with model group, the content of IL-1β, IL-6 and TNF-α in Qianliekang tablets group, high dose Geniposide group obviously were decreased （P 〈 0.05 or P 〈 0.01）, while the content of IL-10 in these groups were remarkably increased （P 〈 0.05 or P 〈 0.01）. Conclusions] The principal mechanism of Geniposide in treating chronic prostatitis is related to both the decrease of proinflammatory cytokines levels （IL-1β, IL-6 and TNF-α）, and the increase of the antiinflammatory cytokine levels （IL-10）, and thus leucocytes infiltration is reduced, the hyperplasia of fibrous tissue is restrained.