Study on the expression and mechanism of monocyte chemoattractant protein-1 in interstitial cystitis rats / 中华泌尿外科杂志

ABSTRACT

Objective To observe the expression and mechanism of monocyte chemoattractant protein-1 (MCP-1) in interstitial cystitis (IC) rats.Methods Twenty weight of 250-300 g of female SD rats were divided into IC group (n =10) and control group (n =10).IC group were treated by transurethral instillation with 10 mg/ml protamine sulfate (PS) 1 ml reserved for 45 min,and then instillation with 750 ug/ml of lipopolysaccharide (LPS) 1 ml reserved for 30 min.The same operations were repeated after 24 hours,and the rats were killed obtaining the bladder tissue and urine after three days.Control group was given PBS solution perfusion.MCP-1 and histamine (HA) expression levels in the rat bladder tissue and urine were detected by ELISA.The inflammation of bladder tissue was observed and inflammatory score was used by HE staining.MC degranulation count was used by MC special staining.MCP-1 expression and distribution in bladder tissue was observed by immunohistochemical method.The relationship between the MCP-1 and MC was detected by immunofluorescence method.Results By ELISA,the expression levels of MCP-1 and HA in the bladder tissue and urine in IC group were significantly increased compared with control group (P ＜0.01 ).More inflammatory cell infiltration in the bladder mucosa,edema mucosa,congestion and hemorrhage were seen by HE staining.The inflammatory score in IC and control group were (76.5 ±9.8) and (18.5± 9.8)/field (P ＜ 0.01 ).With MC special staining,degranulation MC count in IC and control group were (6.4±3.1 ) and (0.7 ±0.3)/field (P ＜0.01 ),and the degranulation in the bladder tissue of IC group was significantly higher than control group (P ＜ 0.01 ).MCP-1 has a higher expression in the bladder epithelium,and more MCP-1 were found gathering round MC surface by immunofluorescence.Conclusions MCP-1 is highly expressed in IC rats,and could induced activation of MC,which could release HA,aggravating the pathological process of inflammatory and fibrosis in IC.