Scientific reports · 2017
Intravesicular administration of sodium hyaluronate ameliorates the inflammation and cell proliferation of cystitis cystica et glandularis involving interleukin-6/JAK2/Stat3 signaling pathway.
Клиническое исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Ni Yongliang, Zhao Shaohua, Yin Xiaoxuan, Wang Haixin, Guang Qianqian, Hu Guangxia, Yang Yi, Jiao Shoubin, Shi Benkang
Аннотация
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.
Предметные рубрики MeSH
Administration, IntravesicalAdultAnimalsCell ProliferationCystitisCystoscopyEscherichia coliHumansHyaluronan ReceptorsHyaluronic AcidHyaluronoglucosaminidaseInflammationInterleukin-6Janus Kinase 2Middle AgedPhosphorylationRNA, MessengerRatsSTAT3 Transcription FactorSignal TransductionUrinary Bladder