AIM: Cyclooxygenase-2 (COX-2) has been suggested to be associated with carcinogenesis. We sought to investigate the effect of the selective COX-2 inhibitor, Nimesulide on proliferation and apoptosis of SMMC-7721 human...AIM: Cyclooxygenase-2 (COX-2) has been suggested to be associated with carcinogenesis. We sought to investigate the effect of the selective COX-2 inhibitor, Nimesulide on proliferation and apoptosis of SMMC-7721 human hepatoma cells.METHODS: This study was carried out on the culture of hepatic carcinoma SMMC-7721 cell line. Various concentrations of Nimesulide (0, 200 micromol/L, 300 micromol/L, 400 micromol/L) were added and incubated. Cell proliferation was detected with MTT colorimetric assay, cell apoptosis by electron microscopy, flow cytometry and TUNEL.RESULTS: Nimesulide could significantly inhibit SMMC-7721 cells proliferation dose-dependent and in a dependent manner compared with that of the control group. The duration lowest inhibition rate produced by Nimesulide in SMMC-7721 cells was 19.06%, the highest inhibition rate was 58.49%. After incubation with Nimesulide for 72 h, the most highest apoptosis rate and apoptosis index of SMMC-7721 cells comparing with those of the control were 21.20%+/-1.62% vs 2.24%+/-0.26% and 21.23+/-1.78 vs 2.01+/-0.23 (P【0.05). CONCLUSION:The selective COX-2 inhibitor, Nimesulide can inhibit the proliferation of SMMC-7721 cells and increase apoptosis rate and apoptosis index of SMMC-7721 cells. The apoptosis rate and the apoptosis index are dose-dependent. Under electron microscope SMMC-7721 cells incubated with 300 micromol and 400 micromol Nimesulide show apoptotic characteristics. With the clarification of the mechanism of selective COX-2 inhibitors, These COX-2 selective inhibitors can become the choice of prevention and treatment of cancers.展开更多
In this paper a delayed mathematical model for tumor growth under the action of external inhibitors is studied. The delay represents the time taken for cells to undergo mitosis. External inhibitor means that an inhibi...In this paper a delayed mathematical model for tumor growth under the action of external inhibitors is studied. The delay represents the time taken for cells to undergo mitosis. External inhibitor means that an inhibitor is either developed from the immune system of the body or administered by medical treatment to distinguish with that secreted by tumor itself. Non-negativity of solutions is studied. Local and global stabilities of the stationary solutions are proved for some parameter values. The analysis of the effect of inhibitor＇s parameters on tumor＇s growth is presented. The results show that dynamical behavior of solutions of this model is similar to that of solutions for corresponding nondelayed model for some parameter values.展开更多
Objective： To explore the influence of charred Gossamer urocteae （CGU） on the functions of primary cultured mouse oral fibroblasts and reveal its mechanism in wound healing. Methods： CGU was extracted with differe...Objective： To explore the influence of charred Gossamer urocteae （CGU） on the functions of primary cultured mouse oral fibroblasts and reveal its mechanism in wound healing. Methods： CGU was extracted with different solvents and ethanol extract （EE）, ethyl acetate fraction （EF）, n-butanol fraction （BF） and aqueous fraction （AF） were obtained. The effects of different fractions on the proliferation, matrix metaUoproteinase-2,9 （MMP-2,9） activities, synthesis of collagen and tissue inhibitor of metalloproteinase 1 （TIMP-1） in the mouse oral fibroblasts were determined by MTT, gelatin zymography, chloramine-T method, and enzyme-linked immunosorbent assay （ELISA） respectively. Results： EE, EF and BF at high concentrations could significantly inhibit proliferation of fibroblasts （P〈0.05 or P〈0.01）, and at low concentrations EF and BF could promote proliferation of fibroblasts, and BF and AF could significantly inhibit collagen synthesis （P〈0.05 or P〈0.01）. EE, EF and AF at high concentrations could significantly increase the MMP-9 activity, and BF and AF could significantly inhibit synthesis of TIMP-1. Conclusion： CGU at high concentrations can inhibit the proliferations of fibroblasts and synthesis of collagen, and in healing of wound, CGU at high concentrations possibly has the functions of anti-fibrosis and anti-scar, and the mechanism to promote degradation of collagen is possibly related to the increase in MMP-9 activity and the inhibition of TIMP-1 synthesis.展开更多
文摘AIM: Cyclooxygenase-2 (COX-2) has been suggested to be associated with carcinogenesis. We sought to investigate the effect of the selective COX-2 inhibitor, Nimesulide on proliferation and apoptosis of SMMC-7721 human hepatoma cells.METHODS: This study was carried out on the culture of hepatic carcinoma SMMC-7721 cell line. Various concentrations of Nimesulide (0, 200 micromol/L, 300 micromol/L, 400 micromol/L) were added and incubated. Cell proliferation was detected with MTT colorimetric assay, cell apoptosis by electron microscopy, flow cytometry and TUNEL.RESULTS: Nimesulide could significantly inhibit SMMC-7721 cells proliferation dose-dependent and in a dependent manner compared with that of the control group. The duration lowest inhibition rate produced by Nimesulide in SMMC-7721 cells was 19.06%, the highest inhibition rate was 58.49%. After incubation with Nimesulide for 72 h, the most highest apoptosis rate and apoptosis index of SMMC-7721 cells comparing with those of the control were 21.20%+/-1.62% vs 2.24%+/-0.26% and 21.23+/-1.78 vs 2.01+/-0.23 (P【0.05). CONCLUSION:The selective COX-2 inhibitor, Nimesulide can inhibit the proliferation of SMMC-7721 cells and increase apoptosis rate and apoptosis index of SMMC-7721 cells. The apoptosis rate and the apoptosis index are dose-dependent. Under electron microscope SMMC-7721 cells incubated with 300 micromol and 400 micromol Nimesulide show apoptotic characteristics. With the clarification of the mechanism of selective COX-2 inhibitors, These COX-2 selective inhibitors can become the choice of prevention and treatment of cancers.
文摘In this paper a delayed mathematical model for tumor growth under the action of external inhibitors is studied. The delay represents the time taken for cells to undergo mitosis. External inhibitor means that an inhibitor is either developed from the immune system of the body or administered by medical treatment to distinguish with that secreted by tumor itself. Non-negativity of solutions is studied. Local and global stabilities of the stationary solutions are proved for some parameter values. The analysis of the effect of inhibitor＇s parameters on tumor＇s growth is presented. The results show that dynamical behavior of solutions of this model is similar to that of solutions for corresponding nondelayed model for some parameter values.
文摘Objective： To explore the influence of charred Gossamer urocteae （CGU） on the functions of primary cultured mouse oral fibroblasts and reveal its mechanism in wound healing. Methods： CGU was extracted with different solvents and ethanol extract （EE）, ethyl acetate fraction （EF）, n-butanol fraction （BF） and aqueous fraction （AF） were obtained. The effects of different fractions on the proliferation, matrix metaUoproteinase-2,9 （MMP-2,9） activities, synthesis of collagen and tissue inhibitor of metalloproteinase 1 （TIMP-1） in the mouse oral fibroblasts were determined by MTT, gelatin zymography, chloramine-T method, and enzyme-linked immunosorbent assay （ELISA） respectively. Results： EE, EF and BF at high concentrations could significantly inhibit proliferation of fibroblasts （P〈0.05 or P〈0.01）, and at low concentrations EF and BF could promote proliferation of fibroblasts, and BF and AF could significantly inhibit collagen synthesis （P〈0.05 or P〈0.01）. EE, EF and AF at high concentrations could significantly increase the MMP-9 activity, and BF and AF could significantly inhibit synthesis of TIMP-1. Conclusion： CGU at high concentrations can inhibit the proliferations of fibroblasts and synthesis of collagen, and in healing of wound, CGU at high concentrations possibly has the functions of anti-fibrosis and anti-scar, and the mechanism to promote degradation of collagen is possibly related to the increase in MMP-9 activity and the inhibition of TIMP-1 synthesis.
