摘要
AIM: To investigate the feasibility and effectiveness of c-myc shRNA in inhibiting the hyperplastic behavior and lithogenic potentiality of chronic proliferative cholangitis (CPC), in order to prevent stone recurrence and biliary restenosis.METHODS: An animal model of CPC was established by giving intralumenally 0.5 mL of c-myc shRNA. Then, the effects of c-myc shRNA on hyperplastic behavior and lithogenic potentiality of CPC were evaluated by histological observation, immunohistochemistry, real-time PCR and Western blotting for c-myc, proliferating cell nuclear antigen (PCNA), procollagen TM mucin5AC, enzymatic histochemistry for β-glucuronidase, and biochemistry for hydroxyproline in the diseased bile duct.RESULTS: Treatment with c-myc shRNA efficiently suppressed the hyperplasia of biliary epithelium, submucosal gland, and collagen fiber by inhibiting mRNA and protein expression of c-myc. More importantly, it decreased the lithogenic potentiality of CPC by inhibiting the expression of mucin 5AC and the secretion of endogenous β-glucuronidase. Further investigation indicated that c-myc shRNA-3 had a better inhibitory effect on CPC.CONCLUSION: Treatment with c-myc shRNA-3 can control CPC and reduce the lithogenic potentiality of CPC.
AIM： To investigate the feasibility and effectiveness of c-myc shRNA in inhibiting the hyperplastic behavior and lithogenic potentiality of chronic proliferative cholangitis （CPC）, in order to prevent stone recurrence and biliary restenosis. METHODS： An animal model of CPC was established by giving intralumenally 0.5 mL of c-myc shRNA. Then, the effects of c-myc shRNA on hyperplastic behavior and lithogenic potentiality of CPC were evaluated by histological observation, immunohistochemistry, real- time PCR and Western blotting for c-myc, proliferating cell nuclear antigen （PCNA）, procollagen m, mucin 5AC, enzymatic histochemistry for 13-glucuronidase, and biochemistry for hydroxyproline in the diseased bile duct. RESULTS： Treatment with c-myc shRNA efficiently suppressed the hyperplasia of biliary epithelium, submucosal gland, and collagen fiber by inhibiting mRNA and protein expression of c-myc. More importantly, it decreased the lithogenic potentiality of CPC by inhibiting the expression of mucin 5AC and the secretion of endogenous 13-glucuronidase. Further investigation indicated that c-myc shRNA-3 had a better inhibitory effect on CPC. CONCLUSION： Treatment with c-myc shRNA-3 can control CPC and reduce the lithogenic potentiality of CPC.
