Abstract
Cystitis cystica et glandularis (CCEG) is a chronic cystitis that causes extreme agony in affected patients. However, there are lack of effective conservative treatments. In this study, it is evident that intravesicular sodium hyaluronate (SH) therapy significantly improved the clinical symptoms of CCEG patients and ameliorated the bladder mucosal inflammation and cell proliferation characteristics of the disease. Immunohistochemical staining showed that the staining intensities of hyaluronidase (HYAL 1/2), CD44, IL-6 and phosphorylated signal transducer and activator of transcription 3 (p-Stat3) in bladder mucosal tissue were significantly increased in CCEG patients compared with control patients and that intravesicular SH treatment suppressed these protein expression. We established a CCEG rat model by treating rats with E. coli intravesicularly, and we found that HYAL 1/2 and CD44 expression levels were significantly increased in the E. coli group compared with the NC group. Activation of the IL-6/JAK2/Stat3 pathway and the expression levels of the downstream pro-apoptotic proteins Mcl-1 and Bcl-xL were also significantly increased in the E. coli group compared with the NC group. The above changes were significantly mitigated by intravesicular SH treatment. Therefore, SH may serve as an effective therapy for CCEG by inhibiting bladder mucosal inflammation and proliferation.
Highlights
Cystitis cystica et glandularis (CCEG) is a chronic reactive inflammatory disorder thought to be attributable to chronic urothelial irritation caused by infections, tumors, calculi or outlet obstructions[1]
The results showed that IL-6, p-JAK2 and p-Stat[3] expression levels were significantly increased in the E. coli group compared with the NC group and significantly decreased in the E. coli + sodium hyaluronate (SH) group compared with the E. coli + NS group (Figs 7 and 8)
We found that HYAL1/2 and CD44 expression levels were significantly increased in the bladder mucosa of rats with CCEG compared with the bladder mucosa of normal control rats
Summary
Cystitis cystica et glandularis (CCEG) is a chronic reactive inflammatory disorder thought to be attributable to chronic urothelial irritation caused by infections, tumors, calculi or outlet obstructions[1]. Given that CCEG is a chronic reactive inflammatory disorder that causes pathologic proliferative changes in the bladder mucosa, we elected to focus on the mechanisms responsible for the inflammation and cell proliferation characteristic of CCEG in this study. The IL-6/JAK2/Stat[3] pathway plays a critical role in inflammation and proliferation Both of inflammation and proliferation occur in the bladder mucosa in CCEG. In this study, we investigated the activity of the IL-6/JAK2/Stat[3] signaling pathway and assessed the expression of the downstream anti-apoptotic biomarkers Mcl-1 and Bcl-xL to elucidate the molecular mechanisms underlying the development of CCEG. In the present study, we evaluated the effects of treatment with SH on CCEG patients and elucidated the mechanisms linking the IL-6/JAK2/Stat[3] pathway to CCEG in a CCEG rat model
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