Background The possible role of substance P （SP） during wound healing has been the primary research focus in recent years,but its effect on the healing process after bile duct injury is little understood.This study ...Background The possible role of substance P （SP） during wound healing has been the primary research focus in recent years,but its effect on the healing process after bile duct injury is little understood.This study aimed to investigate the effects of SP on growth of fibroblast-like cells derived from rabbit bile duct.Methods Fibroblast-like cells derived from rabbit bile duct were identified and divided randomly into control and experimental groups.SP-treated cells at different concentrations of 10^-9-10^-5 mol/L and control group were incubated,respectively,for 48 hours.After incubating,the effects of SP on cell proliferation were assessed by cell counts and MTT test.Apoptosis rate （AR） of cells was measured by flow cytometry.Results Cultured rabbit bile duct cells were fibroblast-like in morphology,and these cells were stained positively for vimentin and negatively for desmin.After SP was added to nonconfluent cells for 48 hours,cell numbers were significantly increased in experimental groups than in controls （P 〈0.05）.The maximum stimulation of cell proliferation was achieved at SP of 10^-5 mol/L.Bile duct fibroblast-like cells in the SP group showed a higher proliferating activity and lower AR than those in the control group or in the SP ＋ Spantide group （P 〈0.05）.Spantide partly inhibited the effects of SP on fibroblastlike cells.Examination under transmission electron microscopy revealed rough endoplasmic reticulum and prominent Golgi complexes after SP treatment.Conclusions SP has a growth regulatory property on cultivated bile duct fibroblast-like cells in vitro,suggesting that SP may involve in wound healing after bile duct injury by promoting wound fibroblast proliferation and inhibiting apoptosis and participate in pathological scar formation.展开更多
基金This research was supported by a grant from the National High Technology Research and Development Program of China （the 863 Program, No. 2007AA04Z313） and China Postdoctoral Science Foundation （No. 201003781）.Acknowledgments： The authors thank the staff of the Laboratory Animal Center, Peking University Third Hospital, China, for their competent technical assistance and for the use of animal laboratory facilities.
文摘Background The possible role of substance P （SP） during wound healing has been the primary research focus in recent years,but its effect on the healing process after bile duct injury is little understood.This study aimed to investigate the effects of SP on growth of fibroblast-like cells derived from rabbit bile duct.Methods Fibroblast-like cells derived from rabbit bile duct were identified and divided randomly into control and experimental groups.SP-treated cells at different concentrations of 10^-9-10^-5 mol/L and control group were incubated,respectively,for 48 hours.After incubating,the effects of SP on cell proliferation were assessed by cell counts and MTT test.Apoptosis rate （AR） of cells was measured by flow cytometry.Results Cultured rabbit bile duct cells were fibroblast-like in morphology,and these cells were stained positively for vimentin and negatively for desmin.After SP was added to nonconfluent cells for 48 hours,cell numbers were significantly increased in experimental groups than in controls （P 〈0.05）.The maximum stimulation of cell proliferation was achieved at SP of 10^-5 mol/L.Bile duct fibroblast-like cells in the SP group showed a higher proliferating activity and lower AR than those in the control group or in the SP ＋ Spantide group （P 〈0.05）.Spantide partly inhibited the effects of SP on fibroblastlike cells.Examination under transmission electron microscopy revealed rough endoplasmic reticulum and prominent Golgi complexes after SP treatment.Conclusions SP has a growth regulatory property on cultivated bile duct fibroblast-like cells in vitro,suggesting that SP may involve in wound healing after bile duct injury by promoting wound fibroblast proliferation and inhibiting apoptosis and participate in pathological scar formation.
