with a complex and multifactorial etiology.Declined gallbladder motility reportedly contributes to CG pathogenesis.Furthermore,interstitial Cajal-like cells(ICLCs)are reportedly present in human and guinea pig gallbla...with a complex and multifactorial etiology.Declined gallbladder motility reportedly contributes to CG pathogenesis.Furthermore,interstitial Cajal-like cells(ICLCs)are reportedly present in human and guinea pig gallbladder tissue.ICLCs potentially contribute to the regulation of gallbladder motility,and aberrant conditions involving the loss of ICLCs and/or a reduction in its pacing potential and reactivity to cholecystokinin may promote CG pathogenesis.This review discusses the association between ICLCs and CG pathogenesis and provides a basis for further studies on the functions of ICLCs and the etiologies of CG.展开更多
BACKGROUND Loss and/or dysfunction of interstitial Cajal-like cells(ICLCs)in the gallbladder may promote cholesterol gallstone formation by decreasing gallbladder motility.AIM To study the effect of cholesterol on the...BACKGROUND Loss and/or dysfunction of interstitial Cajal-like cells(ICLCs)in the gallbladder may promote cholesterol gallstone formation by decreasing gallbladder motility.AIM To study the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders.METHODS Guinea pig gallbladder ICLCs were isolated and cultured in vitro.The cells were exposed to cholesterol solutions at different concentrations(0,25,50,and 100 mg/L)for 24 h.Then,cell proliferation was detected by the CCK-8 method and the apoptosis rate was detected by flow cytometry.Further,the expression of the c-Kit protein was detected by Western blot and the expression level of c-Kit m RNA in the cells was detected by real-time quantitative PCR.RESULTS After ICLCs were cultured with cholesterol at concentrations of 25,50,and 100 mg/L,the proliferation rates decreased significantly(P<0.05),whereas the apoptosis rates increased significantly(P<0.05).Moreover,the expression of cKit protein and m RNA decreased significantly(P<0.05).CONCLUSION High cholesterol concentrations can inhibit the proliferation of ICLCs and promote apoptosis.This decrease in the ICLC proliferation rate might be caused by the inhibition of the stem cell factor/c-Kit signaling pathway.展开更多
Objective：To observe the reversion of multi-drug resistance by proteasome inhibitor bortezomib in K562/DNR cell line and to analyze the possible mechanism of reversion of multidrug-resistance.Methods：MTT method was ...Objective：To observe the reversion of multi-drug resistance by proteasome inhibitor bortezomib in K562/DNR cell line and to analyze the possible mechanism of reversion of multidrug-resistance.Methods：MTT method was used to determine the drug resistance of K562/DNR cells and the cellular toxicity of bortezomib.K562/DNR cells were cultured for 12 hours,24 hours and 36 hours with 100 μg/ml DNR only or plus 4 μg/L bortezomib.The expressions of NF-κB,IκB and P-gp of K562/DNR were detected with Western blot method,the activity of NF-κB was tested by ELISA method and the apoptosis rate was observed in each group respectively.Results：The IC50 of DNR on cells of K562/S and K562/DNR groups were 1.16 μg/ml and 50.43 μg/mL,respectively.The drug-resistant fold was 43.47.The IC10 of PS-341 on Cell strain K562/DNR was 4 μg/L.Therefore,4 μg/L was selected as the concentration for PS-341 to reverse drug-resistance in this study.DNR induced down-regulation of IκB expression,up-regulation of NF-κB and P-gp expression.After treatment with PS-341,a proteasome inhibitor,the IκB degradation was inhibited,IκB expression increased,NF-κB and P-gp expression decreased in a time dependent manner.Compared to DNR group,the NF-κB p65 activity of DNR＋PS-341 group was decreased.Compared to corresponding DNR group,DNR induced apoptosis rate increases after addition of PS-341 in a time dependent manner.Conclusion：Proteasome inhibitor bortezomib can convert the leukemia cell drug resistance.The mechanism may be that bortezomib decreases the degradation of IκB and the expression of NF-κB and P-gp,therefore induces the apoptosis of multi-drug resistant cells.展开更多
基金National Natural Science Foundation of China,No.81000183and Natural Science Foundation of Liaoning Province,No.20180550125.
文摘with a complex and multifactorial etiology.Declined gallbladder motility reportedly contributes to CG pathogenesis.Furthermore,interstitial Cajal-like cells(ICLCs)are reportedly present in human and guinea pig gallbladder tissue.ICLCs potentially contribute to the regulation of gallbladder motility,and aberrant conditions involving the loss of ICLCs and/or a reduction in its pacing potential and reactivity to cholecystokinin may promote CG pathogenesis.This review discusses the association between ICLCs and CG pathogenesis and provides a basis for further studies on the functions of ICLCs and the etiologies of CG.
基金Supported by the National Natural Science Foundation of China,No.81000183the Natural Science Foundation of Liaoning Province,No.20180550125。
文摘BACKGROUND Loss and/or dysfunction of interstitial Cajal-like cells(ICLCs)in the gallbladder may promote cholesterol gallstone formation by decreasing gallbladder motility.AIM To study the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders.METHODS Guinea pig gallbladder ICLCs were isolated and cultured in vitro.The cells were exposed to cholesterol solutions at different concentrations(0,25,50,and 100 mg/L)for 24 h.Then,cell proliferation was detected by the CCK-8 method and the apoptosis rate was detected by flow cytometry.Further,the expression of the c-Kit protein was detected by Western blot and the expression level of c-Kit m RNA in the cells was detected by real-time quantitative PCR.RESULTS After ICLCs were cultured with cholesterol at concentrations of 25,50,and 100 mg/L,the proliferation rates decreased significantly(P<0.05),whereas the apoptosis rates increased significantly(P<0.05).Moreover,the expression of cKit protein and m RNA decreased significantly(P<0.05).CONCLUSION High cholesterol concentrations can inhibit the proliferation of ICLCs and promote apoptosis.This decrease in the ICLC proliferation rate might be caused by the inhibition of the stem cell factor/c-Kit signaling pathway.
基金supported by Educational Commission of Liaoning Province, China (No. 20060985)
文摘Objective：To observe the reversion of multi-drug resistance by proteasome inhibitor bortezomib in K562/DNR cell line and to analyze the possible mechanism of reversion of multidrug-resistance.Methods：MTT method was used to determine the drug resistance of K562/DNR cells and the cellular toxicity of bortezomib.K562/DNR cells were cultured for 12 hours,24 hours and 36 hours with 100 μg/ml DNR only or plus 4 μg/L bortezomib.The expressions of NF-κB,IκB and P-gp of K562/DNR were detected with Western blot method,the activity of NF-κB was tested by ELISA method and the apoptosis rate was observed in each group respectively.Results：The IC50 of DNR on cells of K562/S and K562/DNR groups were 1.16 μg/ml and 50.43 μg/mL,respectively.The drug-resistant fold was 43.47.The IC10 of PS-341 on Cell strain K562/DNR was 4 μg/L.Therefore,4 μg/L was selected as the concentration for PS-341 to reverse drug-resistance in this study.DNR induced down-regulation of IκB expression,up-regulation of NF-κB and P-gp expression.After treatment with PS-341,a proteasome inhibitor,the IκB degradation was inhibited,IκB expression increased,NF-κB and P-gp expression decreased in a time dependent manner.Compared to DNR group,the NF-κB p65 activity of DNR＋PS-341 group was decreased.Compared to corresponding DNR group,DNR induced apoptosis rate increases after addition of PS-341 in a time dependent manner.Conclusion：Proteasome inhibitor bortezomib can convert the leukemia cell drug resistance.The mechanism may be that bortezomib decreases the degradation of IκB and the expression of NF-κB and P-gp,therefore induces the apoptosis of multi-drug resistant cells.
