Department of Urology, Faculty of Medicine Universitas Padjadjaran, Hasan Sadikin General Hospital Bandung, Jln. Pasteur No. 38, Bandung, Indonesia.
BMC Urol. 2022 Apr 24;22(1):69. doi: 10.1186/s12894-022-01019-2.
Bladder outlet obstruction (BOO) was caused by a series of histological and biochemical changes in the bladder wall, through the inflammation process in the bladder wall, hypertrophy and fibrosis. ADSC has an important role in bladder regeneration.
This study was an experimental randomized study using male Wistar rats which were monitored at 2 and 4 weeks to determine the effect of ADSC therapy on TGF-β1 type I collagen, and degree of fibrosis.
Rats were divided into 5 groups. In the week 2 BOO group, 1 sample included in the category of moderate fibrosis, 1 sample that was given ADSC with mild fibrosis category, 3 samples included in severe fibrosis category, 3 samples that were given ADSC included in the category of moderate fibrosis. The concentration of TGF-β1 in the hADSC therapy group was significantly lower than the control group at the 2nd and 4th week of monitoring (p2 = 0.048, p4 = 0.048), and also with more type I collagen on 2nd and the 4th week (p2 = 0.048, p4 = 0.048).
ADSC therapy can reduce the concentration of TGF-β1, type I collagen, and degree of fibrosis in the male Wistar BOO model.
膀胱出口梗阻(BOO)是由一系列膀胱壁的组织学和生化变化引起的,通过膀胱壁的炎症过程,发生肥大和纤维化。ADSC 在膀胱再生中具有重要作用。
本研究为使用雄性 Wistar 大鼠进行的实验性随机研究,在 2 周和 4 周时进行监测,以确定 ADSC 治疗对 TGF-β1 型胶原蛋白和纤维化程度的影响。
大鼠分为 5 组。在 BOO 组第 2 周,1 个样本归入中度纤维化范畴,1 个样本给予 ADSC,纤维化程度为轻度,3 个样本归入重度纤维化,3 个样本给予 ADSC,纤维化程度为中度。在第 2 和第 4 周监测时,hADSC 治疗组 TGF-β1 的浓度明显低于对照组(p2=0.048,p4=0.048),第 2 周和第 4 周的 I 型胶原蛋白也更多(p2=0.048,p4=0.048)。
ADSC 治疗可降低雄性 Wistar BOO 模型中 TGF-β1、I 型胶原蛋白和纤维化程度的浓度。