| Summary: | 碩士 === 國立嘉義大學 === 微生物免疫與生物藥學系研究所 === 104 === Long-term ketamine abuse has been shown to affect the lower urinary tract and result in interstitial cystitis-like syndrome. However, the causative mechanism of ketamine-induced dysfunction is still not clear. This present study was to investigate the physiological, histological and molecular changes on ketamine-induced cystitis (KIC) in a mouse model. Both male and female BALB/c mice were separately distributed into the control (normal saline) and ketamine groups which received ketamine (100 mg/kg/day) daily by intraperitoneal injection for a total period of 20 weeks. In each group, the urine was analyzed by GC-MS to measure the concentration of ketamine and its metabolites. Urinary frequency and urine volume were examined to investigate the urinary voiding functions. Mice bladders were excised for cDNA microarray and histological stains. The ketamine and metabolites were detected only in ketamine-treated mice urine. The voiding interval was decreased at the male mice group after 20-week ketamine administration. Moreover, the result of cDNA array analysis revealed a number of gene expressions involved in chronic wound healing response and collagen accumulation, which were closely related to fibrosis progression in the connective tissue. In HE stain of bladder tissue, the ketamine-injected mice showed prominently denser blood vessel distribution in the submucosal layer. However, the results of Masson's trichrome and Periodic acid-Schiff (PAS) stain showed no significant difference on protein expression of collagens as well as mucosubstances, suggesting the pathology may still stay in the initial stage. Taken together, based on the evidence in our experiment, we may build up a mechanism that delineates fibrosis formation of urinary bladder induced by the pathogenesis of ketamine abuse.
|
|---|
