CAJ | 학술논문

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 ERK1／2、p －ERK1／2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。
목적：탐토대서방광출구경조중ERK화p－ERK적변화，이급단삼동ⅡA대ERK통로활화적영향。방법 SD대서수궤분위Sham、PBOO、STS삼조，매조8지。 Sham조위가수술조，PBOO조건립대서방광출구부분경조모형조，STS위PBOO모형조＋단삼동ⅡA광산납치료，우4주말，취방광조직검측。채용HE염색관찰방광벽형태적변화，Masson염색관찰방광벽섬유적변화，통과면역조화검측 ERK1／2、p －ERK1／2단백적표체。결과 HE염색시방광출구경조후방광벽증후，핍뇨기증생。 Masson염색시효원섬유표체면적，PBOO조여Sham조상비，명현증다（ P ＜0．05），STS 조여 PBOO 상비，명현강저（ P ＜0．05）。ERK단백면역조화시Sham、PBOO、STS삼조평균IOD치차이무통계학의의（ P ＞0．05）。 p－ERK단백면역조화평균IOD치，PBOO조고우Sham조（ P ＜0．05），STS조교PBOO조강저（ P ＜0．05）。결론 MAPK통로중적ERK도경적활화가능여방광출구부분경조인기적방광벽효원섬유증생유관，이단삼동ⅡA광산납가능통과억제해통로적활화，발휘항섬유화적작용。
Objectives To investigate the expression of ERK or p-ERK in the rat bladder outlet obstruc-tion, and the impact of tanshinone ⅡA on the activated ERK pathway.Methods 24 SD rats were randomly di-vided into three groups equally:Sham group, PBOO group, and tanshinoneⅡA group.The bladder tissues were har-vested 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 PBOO model group, but obviously lower in tanshinone ⅡA 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 ⅡA play a role in anti-fibrosis by inhibiting the pathway .