前列腺Ⅰ号方通过调控p38MAPK信号通路抑制Ⅲ型前列腺炎模型大鼠炎症反应

Observation of prostateⅠprescription inhibiting inflammatory response in rat model of typeⅢprostatitis by regulating p38MAPK signaling pathway

目的本研究旨在探究前列腺Ⅰ号方对Ⅲ型前列腺炎模型大鼠炎症反应及p38MAPK信号通路的影响。方法Ⅲ型前列腺炎模型大鼠随机分为4组,每组10只,分别是模型组和高、中、低剂量给药组,10只健康正常大鼠作为正常对照组。高、中、低给药组分别给予前列腺Ⅰ号方40g/kg、20g/kg、10g/kg灌胃;正常对照组和模型组给予等量的生理盐水,每天灌胃给药1次,连续给药10周。苏木精-伊红(HE)染色观察大鼠前列腺组织病理变化;ELISA法检测大鼠血清炎症因子白细胞介素(IL)-8、肿瘤坏死因子(TNF)-α及内皮中性粒细胞激活肽(ENA)-78水平;Western blot法检测大鼠前列腺组织p38MAPK信号通路蛋白表达水平。结果与正常对照组相比,模型组大鼠前列腺指数、血清炎症因子IL-8、TNF-α及ENA-78水平和前列腺组织基质金属蛋白酶(MMP)-9、总p38MAPK及p-p38MAPK蛋白表达水平明显升高,差异具有统计学意义(P<0.05);与模型组相比,各给药组大鼠的前列腺指数、血清炎症因子IL-8、TNF-α及ENA-78水平和前列腺组织MMP-9、总p38MAPK及p-p38MAPK蛋白表达水平均有不同程度降低,高剂量给药组与模型组相比,差异具有统计学意义(P<0.05)。结论前列腺Ⅰ号方对Ⅲ型前列腺炎模型大鼠的炎症反应具有明显的改善作用,其作用机制可能与抑制p38MAPK信号通路的表达有关。

Objective To investigate the effects of prostate I prescription on the inflammatory response and p38 MAPK signaling pathway in type III prostatitis rats.Methods 40 typeⅢprostatitis rats were randomly divided into 4 groups,including model group,high,medium and low dose groups,10 rats in each group.And 10 healthy normal rats were selected as normal control group.The high,medium and low dose groups were intragastrically administered with 40 g/kg,20 g/kg,and 10 g/kg of prostateⅠprescription,once a day for 10 weeks.The normal control group and the model group were intragastrically administered with an equal dose of normal saline,once a day for 10 weeks.Hematoxylin-eosin(HE)staining was used to observe the pathological changes of prostate tissue in rats.The levels of serum inflammatory factors,including IL-8,TNF-αand ENA-78 were detected by ELISA.The protein expression of MMP-9,p38 MAPK and p-p38 MAPK in rat prostate tissue was detected by Western blot.Results Compared with the control group,the prostate index,the levels of serum inflammatory factors,including IL-8,TNF-αand ENA-78 in the model group and the protein expression levels of MMP-9,p38 MAPK and p-p38 MAPK in prostate tissues were significantly increased,with statistically significant differences(P<0.05).Compared with the model group,the prostate index,serum IL-8,TNF-αand ENA-78 levels and the protein expression of MMP-9,total p38 MAPK and p-p38 MAPK in prostate tissue in each group were reduced to different extents,and the difference between the high dose group and the model group was statistically significant(P<0.05).Conclusions ProstateⅠprescription has remarkable effects on improving the inflammatory response of typeⅢprostatitis rats,which may be related to the inhibition of p38 MAPK signaling pathway.