Approaches of bladder imaging of interstitial cystitis model: Evaluation of effects on inflammation and treatment

在第一项研究中，使用具有GFP阳性骨髓细胞的嵌合体大鼠，骨髓来源干细胞(BMS)没有分化为膀胱炎患者的膀胱组织细胞，尽管许多BMS迁移到膀胱。因此，在膀胱炎模型中，BMS细胞并不直接参与膀胱组织的重组。在第二项研究中，使用荧光素酶分析和流式细胞术检测了NF-KB-TG小鼠中的EGFP，但没有从间质模型中对NF-KB活性的评估中获得足够的数据。需要进一步的研究来建立间质模型中的核因子-KB活性的评估。在第三项研究中，我们利用IL-1B-/-小鼠，研究了IL-1B是否导致部分膀胱出口梗阻(PBOO)后膀胱重塑和下尿路功能障碍。IL-1B具有诱导pBOO患者膀胱重组和恶化尿动力学参数的作用。尤其是通过IL-1B诱导的IGF-1刺激，可导致膀胱肌肉肥大。

In the first study, using chimera rats with GFP-positive bone marrow cells, bone marrow derived stem (BMS) cells did not differentiate into the bladder tissue cells with cystitis, although many BMS migrated to the bladder. Thus, BMS cells were not directly contribute to reorganization of the bladder tissue in cystitis models. In the second study using luciferase assay and flow cytometry for EGFP in NF-KB-Tg mice, enough data were not obtained from evaluation of NF-KB activity in interstitial models. Further studies are necessary to establish evaluation of NF-KB activity in interstitial models. In the third study using IL-1B-/- mice, we investigated whether IL-1Binduced remodeling of the urinary bladder and lower urinary tract dysfunctions after partial bladder outlet obstruction (pBOO). IL-1B has the potential to induce bladder reorganization and deteriorate urodynamic parameters in pBOO. Especially, muscle hypertrophy in the bladder could occur via IGF-1 stimulation induced by IL-1B.