【摘要】 目的研究JAK2信号通路在前列腺基质细胞中的作用及激酶抑制剂WP1066对其表达的影响。方法采用Western blot检测单纯良性前列腺增生(BPH)者(n=4)和合并重度组织炎症BPH患者(n=4)前列腺组织中的JAK2和STAT3的磷酸化程度来验证其所介导的信号通路的活化情况,并检测其抑制剂WP1066在前列腺基质细胞上抑制JAK2和STAT3由白介素-6(IL-6)带来的活化作用。结果在BPH合并重度组织炎症的前列腺组织中,JAK2的磷酸化水平(pJAK2)升高,使用WP1066处理细胞并不会降低JAK2或STAT3的表达。但在抑制剂WP1066所处理的细胞上,无论是JAK2还是STAT3都无法检测到磷酸化,表明JAK2-STAT3的信号通路被抑制。使用IL-6可增加pJAK2和pSTAT3的表达,此结果可被WP1066阻断。结论 JAK/STAT信号通路在BPH合并重度组织学炎症前列腺组织中呈现活化状态,激酶抑制剂WP1066可抑制STAT3的活化。更多还原

【Abstract】 Objective To study the role of JAK2 signaling pathway in prostate stromal cells and the effect of inhibitor WP1066 on its expression.Methods The phosphorylation of JAK2 and STAT3 in prostate tissues of patients with benign prostatic hyperplasia(BHP)(n=4)and severe histological prostatitis(HP)plus BPH(n=4)was tested by using Western blot to verify the activation of their mediated signaling pathway.Kinase inhibitor WP1066 was added to prostate stromal cells to detect inhibition of the JAK2 and STAT3 activation launched by IL-6.Results JAK2 phosphorylation level(pJAK2)was significantly increased in the patients with severe HP plus BPH,and the expression of JAK2 or STAT3 was not decreased in WP1066 treatment cells.However,neither phosphorylation in JAK2 nor STAT3 was able to be detected in the cells treated with WP1066 or WP1066+IL-6,indicating that the signaling pathway of JAK2-STAT3 was inhibited.Conclusion JAK/STAT signaling pathway is activated in patients with severe HP plus BPH,but could be inhibited by WP1066.更多还原