丹参酮ⅡA磺酸钠对PB00大鼠膀胱ERK信号通路的影响

Expression of tanshinone 11A on ERK signaling pathway in PBO0 rats

目的探讨大鼠膀胱出口梗阻中ERK和P—ERK的变化，以及丹参酮ⅡA对ERK通路活化的影响。方法sD大鼠随机分为Sham、PBOO、STS三组，每组8只。Sham组为假手术组，PBOO组建立大鼠膀胱出口部分梗阻模型组，STS为PBOO模型组＋丹参酮ⅡA磺酸钠治疗，于4周末，取膀胱组织检测。采用HE染色观察膀胱壁形态的变化，Masson染色观察膀胱壁纤维的变化，通过免疫组化检测ERKl／2、P—ERKl／2蛋白的表达。结果HE染色示膀胱出口梗阻后膀胱壁增厚，逼尿肌增生。Masson染色示胶原纤维表达面积，PBOO组与Sham组相比，明显增多（P〈0．05），STS组与PBOO相比，明显降低（P〈0．05）。ERK蛋白免疫组化示Sham、PBOO、STS三组平均IOD值差异无统计学意义（P〉0．05）。P—ERK蛋白免疫组化平均IOD值，PBOO组高于Sham组（P〈0．05），STS组较PBOO组降低（P〈0．05）。结论MAPK通路中的ERK途径的活化可能与膀胱出口部分梗阻引起的膀胱壁胶原纤维增生有关，而丹参酮ⅡA磺酸钠可能通过抑制该通路的活化，发挥抗纤维化的作用。

Objectives To investigate the expression of ERK or p - ERK in the rat bladder outlet obstruction, and the impact of tanshinone Ⅱ A on the activated ERK pathway. Methods 24 SD rats were randomly divided into three groups equally ： Sham group, PBOO group, and tanshinone Ⅱ A group. The bladder tissues were harvested after four weeks. The morphology of bladder tissues was observed by H＆E staining. The expression of collagen fibrils was determined by Masson trichrome staining. The expression of ERK1/2 or p - ERK1/2 protein was detected by immunohistochemistry. Results The expression of bladder collagen fibrils was significantly lower in STS group than in the PBOO model group（ P 〈 0.05 ）. The expression of ERK had no statistic significance among three groups （ P 〉 0.05 ）. The levels of p - ERK protein was significantly higher in PBOOmodel group, but obviously lower in tanshinone Ⅱ A therapy groups （ P 〉 0.05 ）. Conclusions The activation of MAPK/ERK pathway in PBOO model may be in relation to the higher expression of bladder collagen fibrilse, and therefore, tanshinone Ⅱ A play a role in anti - fibrosis by inhibiting the pathway.