Transmitters derived from vesical urothelium ? in association with the pathogenesis ofInterstitial Cystitis

本研究旨在阐明间质性膀胱炎（IC）的发病机制，IC是一种病因不明的膀胱慢性炎症性疾病。为了实现这一目的，我们将重点放在人类IC患者尿中表达或分泌的递质上。同时，我们也用免疫组织化学方法评估了膀胱组织学，不幸的是，到目前为止，尿标记物和IC症状之间还没有显著的相关性。免疫组化结果显示，IC型溃疡中表达CD 11b和VEGF-A的免疫细胞明显增多。此外，在干燥综合征的IC膀胱组织中，CD 4和CD 8阳性免疫细胞均明显出现，表明每种类型IC的发病机制不同。在动物模型实验中，我们尝试制作氯胺酮诱导的大鼠膀胱炎模型，但目前尚未发现IC症状的产生。我们还用丙烯醛制作了大鼠IC模型，并对膀胱组织中TRPM 8的表达进行了评估。结果表明，IC大鼠排尿频率和排尿量呈动态变化，TRPM 8表达无明显变化，其发病机制和病理生理机制尚不明确，有待进一步研究。

This study was conducted to elucidate the pathogenesis of interstitial cystitis (IC), chronic inflammatory disease of the urinary bladder with unidentified cause. To achieve this purpose, we’ve focused on the transmitters expressed on urothelium or secreted into urine of human IC patients. Also, we’ve assessed bladder histology immuno-histochemically.Unfortunately, no significant correlation between urine markers and IC symptoms has been identified so far. However, histochemistry analysis indicated that immune cells expressing CD11b and VEGF-A significantly increased in ulcer type IC. In addition, in bladder tissue of IC with Sjogren’s syndrome showed significant appearance of both CD4 and CD8 positive immune cells, all of which indicating different pathogenesis in each type of IC.In animal model experiments, we tried to produce ketamine induced cystitis rat model, however, at the moment, IC symptoms of findings were not produced. Also we’ve produced rat IC model using acrolein,he bladder tissue of which was assessed for TRPM8 expression. The rats showed dynamic change in urinary frequency and voided volume, but no significant change in TRPM8 expression was observed.The pathogenesis and pathophysiology of IC are still undefined and need further investigations.