摘要
目的探讨p38丝裂原活化蛋白激酶(p38 MAPK)在慢性非细菌性前列腺炎(CNP)大鼠模型中的表达,与细胞因子肿瘤坏死因子-α(TNF-α)、环氧合酶-2(COX-2)、基质金属蛋白酶-9 (MMP-9)的关系及它们在发病机制中可能的作用。方法将成年雄性SD大鼠去势后皮下注射苯甲酸雌二醇连续4周建模,对照组不做任何处理。HE染色,光镜下观察两组前列腺组织的病理学表现,免疫组化检测两组TNF-α、MMP-9、COX-2、磷酸化p38(p-p38)蛋白的表达,逆转录-聚合酶链反应(RT-PCR)检测p38 mRNA的水平变化。结果光镜下对照组前列腺组织无炎症反应,模型组表现为明显的炎症反应。对照组前列腺组织TNF-α、MMP-9、COX-2、p-p38蛋白表达量极少,而模型组明显增加,两组差异有统计学意义(P<0.05)。对照组p38 mRNA的表达为模型组的37.3%。结论在大鼠CNP中p38 MAPK信号转导途径被激活。细胞因子TNF-α、MMP-9、COX-2的表达可能是通过p38 MAPK调节。这为CNP的研究和治疗提供了一条新的途径。
Objective To study the expression of p38 MAPK in rat CNP model and its relationship with TNF-α, MMP-9, COX-2, p-p38 in the development of CNP. Methods The adult male SD rats CNP model was established by four weeks subcutaneously hypodermic injection with benzestrofol after castration, and other SD rats without pretreat were as controls. The pathological changes of prostate tissue in two groupes were analyzed with H.E. staining. The protein expression of TNF-α, MMP-9, COX-2, p-p38 were examined by immunohistochemistry, and the mRNA level of p38 was detected by RT-PCR. Results Obvious inflammatory reaction was found in prostate tissue of rat CNP model whereas no inflammatory reaction in controls. The protein expression of TNF-α, MMP-9, COX-2, p-p38 in control group were lower than that in model group. There was significant differences in factors mentioned above between two groups （P〈0.05）. The p38 mRNA level of control group was only 37.3% of that of model group. Conclusion Signal transduction pathway of p38 MAPK might be activated in CNP and the expression of TNF-α, MMP-9, COX-2 might be regulated by p38 MAPK, which provided a new way for elucidating the mechanism of CNP.
出处
《中国男科学杂志》
CAS
CSCD
2008年第12期10-14,共5页
Chinese Journal of Andrology
