AIM: To observe the anti-cancer effect of iNOS selective inhibitor (aminoguanidine, AG) and investigate the relationship between iNOS inhibitor and angiogenesis, infiltration or metastasis in MFC gastric cancer xenogr...AIM: To observe the anti-cancer effect of iNOS selective inhibitor (aminoguanidine, AG) and investigate the relationship between iNOS inhibitor and angiogenesis, infiltration or metastasis in MFC gastric cancer xenografts.METHODS: Fifty athymic mice xenograft models were established by inoculating gastric cancer cell MFC subcutaneously. Twenty-four hours later, 0.9% sodium chloride solution, mitomycin, low dosage AG, high dosage AG, mitomycin and AG were administered by intraperitoneal injection respectively. Thus these mice were divided into five groups of 10 each randomly: control group, MMC group,AGL group, AGH group, MMC+AGH group. Two weeks later the mice were killed, and the tumor weight, inhibitory rate were evaluated. Greiss assay was used to detect the nitric oxide levels in plasma. HE and immunohistochemistry staining were used to examine microvessel density (MVD)and the expression of iNOS, VEGF, and PCNA. Apoptosis was detected by using TUNEL assay.RESULTS: The inhibitory rates in MMC+AGH group and AGH group were 52.9% and 47.1% respectively, which is significant statistically compared with that of control group (0). In treatment groups, the cell proliferation index (PI)was lower and apoptosis index was higher than those of control group. Microvessel density, iNOS, and VEGF in MMC+ AGH group were 8.8±2.6, 2.4±1.1, and 2.1±1.4respectively, which is significant statistically compared with those of control group (68.3±10.6, 11.3±1.3, and 10.3±1.6). The NO level in plasma of MMC+ AGH and AGH group were 12.7±2.1 and 12.9±2.0 μmol/L. Compared with that of control group (46.6±2.3 μmol/L), the difference is statistically significant.CONCLUSION: AG has anticancer effect on gastric cancer,and it has positive synergistic effect with chemotherapeutic drugs. It may play important inhibitory roles in angiogenesis of gastric cancer. The anticancer effect of iNOS inhibitors may include inducing cell apoptosis, suppressing cell proliferation and reducing angiogenesis.展开更多
Objective:The aim of this study was to investigate the inhibition effect of natural killer T(NKT) cells on transplantation hepatocellular carcinoma in mice.Methods:α-galactosylceramide(α-GalCer)-pulsed DC and Hep S ...Objective:The aim of this study was to investigate the inhibition effect of natural killer T(NKT) cells on transplantation hepatocellular carcinoma in mice.Methods:α-galactosylceramide(α-GalCer)-pulsed DC and Hep S were prepared as stimulus.Hepatoma xenograft model was established and mice were randomly divided into 4 groups(n=13 each group):(1) control group,intravenous injection of the same volume of saline.(2) mature DC group,intravenous injection of mature DC cells(4×106 cells).(3) α-GalCer-pulsed HepS group,intravenous injection of α-GalCer-pulsed HepS(4×106 cells).(4) α-GalCer-pulsed mature DC group,intravenous injection of α-GalCer-pulsed DC(4×106 cells).The changes of tumor volume in mice and survival period were measured every 2 days.Percentage of NKT cells in spleens and cytotoxicity of spleen cells were detected by flow cytometry.Tumor tissues were analyzed by histopathological examination.Results:In α-GalCer-pulsed Heps and DC groups,the average survival period was prolonged and tumor volume was markedly decreased,spleen cells and NKT cells were significantly increased,and tumor necrosis was evident,compared to the control group.Conclusion:α-GalCer-pulsed DC and HepS could activate NKT cells in vivo,also increase NKT cells cytotoxicity,inhibit the growth of hepatomas and prolong survival period.展开更多
Objective： This work aimed to study the inhibitory effect and the related mechanism of metformin （MET） on the proliferation of human hepatoma HepG2 cells. Methods： Human hepatoma HepG2 cells were treated with MET ...Objective： This work aimed to study the inhibitory effect and the related mechanism of metformin （MET） on the proliferation of human hepatoma HepG2 cells. Methods： Human hepatoma HepG2 cells were treated with MET （0, 2, 10, and 50 mM）. The inhibitory effect of MET on the proliferation of HepG2 cells was determined by MTT method. The apoptosis of HepG2 cells was detected by flow cytornetry. The expression of cyclin D1 in HepG2 cells was examined by Western blot. ROS-DHE fluorescence probe was used to stain the reactive oxygen species （ROS） generated by HepG2 cells after treat- ment. Results： MET could inhibit the proliferation of HepG2 cells in a dose and time dependent manner. MET promoted the apoptosis of HepG2 cells. In addition, MET suppressed the expression of cell cycle protein cyclin D1 and induced the produc- tion of ROS in HepG2 cells. Conclusion： MET can inhibit the proliferation of human hepatoma HepG2 cells and induce cell apoptosis. Meanwhile, MET has the ability to decrease the expression of cyclin D1 and induce ROS generation, which may be involved in the mechanism of inhibiting hepatoma cells proliferation.展开更多
基金Supported by the Natural Science Foundation of Jilin Province, No. 20010536
文摘AIM: To observe the anti-cancer effect of iNOS selective inhibitor (aminoguanidine, AG) and investigate the relationship between iNOS inhibitor and angiogenesis, infiltration or metastasis in MFC gastric cancer xenografts.METHODS: Fifty athymic mice xenograft models were established by inoculating gastric cancer cell MFC subcutaneously. Twenty-four hours later, 0.9% sodium chloride solution, mitomycin, low dosage AG, high dosage AG, mitomycin and AG were administered by intraperitoneal injection respectively. Thus these mice were divided into five groups of 10 each randomly: control group, MMC group,AGL group, AGH group, MMC+AGH group. Two weeks later the mice were killed, and the tumor weight, inhibitory rate were evaluated. Greiss assay was used to detect the nitric oxide levels in plasma. HE and immunohistochemistry staining were used to examine microvessel density (MVD)and the expression of iNOS, VEGF, and PCNA. Apoptosis was detected by using TUNEL assay.RESULTS: The inhibitory rates in MMC+AGH group and AGH group were 52.9% and 47.1% respectively, which is significant statistically compared with that of control group (0). In treatment groups, the cell proliferation index (PI)was lower and apoptosis index was higher than those of control group. Microvessel density, iNOS, and VEGF in MMC+ AGH group were 8.8±2.6, 2.4±1.1, and 2.1±1.4respectively, which is significant statistically compared with those of control group (68.3±10.6, 11.3±1.3, and 10.3±1.6). The NO level in plasma of MMC+ AGH and AGH group were 12.7±2.1 and 12.9±2.0 μmol/L. Compared with that of control group (46.6±2.3 μmol/L), the difference is statistically significant.CONCLUSION: AG has anticancer effect on gastric cancer,and it has positive synergistic effect with chemotherapeutic drugs. It may play important inhibitory roles in angiogenesis of gastric cancer. The anticancer effect of iNOS inhibitors may include inducing cell apoptosis, suppressing cell proliferation and reducing angiogenesis.
基金Supported by a grant of Eleventh Five Year Plan project of Nanjing Military Region (No. 06MA45)
文摘Objective:The aim of this study was to investigate the inhibition effect of natural killer T(NKT) cells on transplantation hepatocellular carcinoma in mice.Methods:α-galactosylceramide(α-GalCer)-pulsed DC and Hep S were prepared as stimulus.Hepatoma xenograft model was established and mice were randomly divided into 4 groups(n=13 each group):(1) control group,intravenous injection of the same volume of saline.(2) mature DC group,intravenous injection of mature DC cells(4×106 cells).(3) α-GalCer-pulsed HepS group,intravenous injection of α-GalCer-pulsed HepS(4×106 cells).(4) α-GalCer-pulsed mature DC group,intravenous injection of α-GalCer-pulsed DC(4×106 cells).The changes of tumor volume in mice and survival period were measured every 2 days.Percentage of NKT cells in spleens and cytotoxicity of spleen cells were detected by flow cytometry.Tumor tissues were analyzed by histopathological examination.Results:In α-GalCer-pulsed Heps and DC groups,the average survival period was prolonged and tumor volume was markedly decreased,spleen cells and NKT cells were significantly increased,and tumor necrosis was evident,compared to the control group.Conclusion:α-GalCer-pulsed DC and HepS could activate NKT cells in vivo,also increase NKT cells cytotoxicity,inhibit the growth of hepatomas and prolong survival period.
文摘Objective： This work aimed to study the inhibitory effect and the related mechanism of metformin （MET） on the proliferation of human hepatoma HepG2 cells. Methods： Human hepatoma HepG2 cells were treated with MET （0, 2, 10, and 50 mM）. The inhibitory effect of MET on the proliferation of HepG2 cells was determined by MTT method. The apoptosis of HepG2 cells was detected by flow cytornetry. The expression of cyclin D1 in HepG2 cells was examined by Western blot. ROS-DHE fluorescence probe was used to stain the reactive oxygen species （ROS） generated by HepG2 cells after treat- ment. Results： MET could inhibit the proliferation of HepG2 cells in a dose and time dependent manner. MET promoted the apoptosis of HepG2 cells. In addition, MET suppressed the expression of cell cycle protein cyclin D1 and induced the produc- tion of ROS in HepG2 cells. Conclusion： MET can inhibit the proliferation of human hepatoma HepG2 cells and induce cell apoptosis. Meanwhile, MET has the ability to decrease the expression of cyclin D1 and induce ROS generation, which may be involved in the mechanism of inhibiting hepatoma cells proliferation.
