Abstract
Objective To explore the effect of C-phycocyanin (C-PC) on voiding behavior and histological changes in cyclophosphamide- (CYP-) induced cystitis in mice. Methods Sixty female mice were included. The mice in the C-PC group received C-PC (25 mg/kg, twice, i.p.) and then CYP (200 mg/kg, i.p.) two hours later, while the mice in the CYP group only received the equivalent CYP. Saline was injected in the mice in the control group. A voided stain on paper (VSOP) test was conducted to analyze the micturition. The bladders were harvested for histological evaluation and measurements of inflammatory factors. Results C-PC reduced the micturition frequency in the mice with CYP-induced cystitis. The bladder/body weight ratio and edema were remarkably higher in the CYP group compared to the C-PC group. C-PC suppressed the expressions of COX-2, PGE2, and EP4 (prostaglandin E receptor 4) according to the ELISA assay. Immunohistochemical staining also indicated that C-PC reduced the expressions of COX-2 in urothelium and EP4 in smooth muscles. Conclusions C-PC relieved symptoms associated with CYP-induced cystitis in mice by inhibiting bladder inflammation through COX-2 and EP4 expression.
Highlights
Bladder pain syndrome/interstitial cystitis (BPS/IC) is defined by suprapubic chronic pain and/or discomfort associated with bladder storage without well-established pathogenesis such as urinary tract infection or neoplasm
Cyclooxygenase-2(COX-2), which catalyzes the conversion of arachidonic acid to prostaglandins, especially Prostaglandin E2 (PGE2) in the lower urinary tract, was shown to be involved in the pathogenesis of BPS/IC in a murine model [4]
C-PC Relieved the Bladder Inflammation Caused by CYP
Summary
Bladder pain syndrome/interstitial cystitis (BPS/IC) is defined by suprapubic chronic pain and/or discomfort associated with bladder storage without well-established pathogenesis such as urinary tract infection or neoplasm. Prostaglandin E2 (PGE2) is a cytoprotective compound that is upregulated in tumors, bladder overactivity, and urinary tract infection [2]. Cyclooxygenase-2(COX-2), which catalyzes the conversion of arachidonic acid to prostaglandins, especially PGE2 in the lower urinary tract, was shown to be involved in the pathogenesis of BPS/IC in a murine model [4]. Intravesical botulinum toxin A has proven to efficiently suppress bladder hyperactivity by preventing the elevation of PGE2 and COX-2 in cyclophosphamide- (CYP-) induced cystitis in rats [5]. Adverse events, including urine retention and subsequent infections can occur
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