Neurogenic bladder (NB) is a type of double renal dysfunction caused by nerve lesions. The interstitial cells of Cajal (ICC) damage are involved in bladder dysfunction. The aim of this study is to investigate the effect of stem cell factor (SCF)/c-kit signaling pathway on ICC damage in NB model rats. Maximum cystometric capacity (MCC), bladder leak point pressures (BLPP), and bladder compliance (BC) were measured in sham-operated and NB model rats. Immunofluorescent staining for c-kit was performed to determine ICC count in rat bladder trigone. The morphology and ultrastructure changes of ICCs were observed under an electron microscope. The mRNA levels of c-kit and SCF in bladder tissues were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The protein levels of c-kit, SCF, p-JAK, p-STAT1, and p-STAT3 in bladder tissues were determined by western blot. ICC proliferation was detected by CCK-8 assay. NB resulted in changes in ultrastructure changes of ICCs and a decrease in the number of ICCs and in expression of c-kit, SCF, p-JAK, p-STAT1, and p-STAT3 in NB tissues. Inhibition of SCF/c-kit signaling pathway suppressed ICC proliferation by inhibiting JAK/STAT3 pathway. Moreover, inhibition of SCF/c-kit signaling pathway impaired the SCF-induced attenuation of ICC damage in NB model rats. Collectively, our data indicate that SCF/c-kit signaling pathway participates in ICC damage in NB.

神经源性膀胱（NB）是一种由神经病变引起的双肾功能障碍。Cajal (ICC) 损伤的间质细胞与膀胱功能障碍有关。本研究旨在探讨干细胞因子（SCF）/c-kit信号通路对NB模型大鼠I​​CC损伤的影响。在假手术和 NB 模型大鼠中测量最大膀胱容量 (MCC)、膀胱泄漏点压力 (BLPP) 和膀胱顺应性 (BC)。对 c-kit 进行免疫荧光染色以确定大鼠膀胱三角区的 ICC 计数。在电子显微镜下观察ICCs的形态和超微结构变化。通过逆转录-定量聚合酶链反应 (RT-qPCR) 测定膀胱组织中 c-kit 和 SCF 的 mRNA 水平。c-kit、SCF、p-JAK、p-STAT1、通过蛋白质印迹测定膀胱组织中的p-STAT3和p-STAT3。通过CCK-8测定检测ICC增殖。NB 导致 ICC 超微结构的变化和 ICC 数量的减少以及 NB 组织中 c-kit、SCF、p-JAK、p-STAT1 和 p-STAT3 的表达。SCF/c-kit 信号通路的抑制通过抑制 JAK/STAT3 通路来抑制 ICC 增殖。此外，SCF/c-kit 信号通路的抑制削弱了 SCF 诱导的 NB 模型大鼠 ICC 损伤的衰减。总的来说，我们的数据表明 SCF/c-kit 信号通路参与了 NB 中的 ICC 损伤。和 NB 组织中的 p-STAT3。SCF/c-kit 信号通路的抑制通过抑制 JAK/STAT3 通路来抑制 ICC 增殖。此外，SCF/c-kit 信号通路的抑制削弱了 SCF 诱导的 NB 模型大鼠 ICC 损伤的衰减。总的来说，我们的数据表明 SCF/c-kit 信号通路参与了 NB 中的 ICC 损伤。和 NB 组织中的 p-STAT3。SCF/c-kit 信号通路的抑制通过抑制 JAK/STAT3 通路来抑制 ICC 增殖。此外，SCF/c-kit 信号通路的抑制削弱了 SCF 诱导的 NB 模型大鼠 ICC 损伤的衰减。总的来说，我们的数据表明 SCF/c-kit 信号通路参与了 NB 中的 ICC 损伤。