ABSTRACT
Objective:To investigate the effects of interleukin-17 on tumor,we transfected interleukin-17 gene into mouse colon cancer cells(C26)and set up an animal model in tumor.Methods:By plasmid vector,IL-17 gene was transfected into C26.Meanwhile, empty plasmid vector(pcDNA3.1)and C26 cells were transfected as control groups.C26/pcDNA3.1-IL-17,C26/pcDNA3.1,and C26 cells were subcutaneously inoculated into mice respectively and the tumor volume and the survival time were observed.Proliferation of splenocyte and NK activity were detected.Detect the characteristic cytokines and transcriptional factors of Th1,Th2,Th17 and Treg cells in splenic lymphocyte.Proliferation of TIL was detected.The characteristic cytokines IL-10 of M1 and the characteristic cytokines IL-12 of M2 in tumor infiltrating macrophages were detected.Results: The growth of tumor in mice inoculated with C26/pcDNA3.1-IL-17 cells was significantly retarded ( P0.05).The proliferation of the splenocytes from C26/pcDNA3.1-IL-17 inoculated mice was higher than those of C26/pcDNA3.1,C26 groups(P0.05),the proliferation of the splenocytes from C26/pcDNA3.1 and C26 inoculated mice was slow than those of normal groups(P0.05 ).The splenocytes from the mice inoculated with C26/pcDNA3.1-IL-17 cells secreted more IFN-γ( the characteristic cytokines of Th1 ) , IL-4 ( the characteristic cytokines of Th2),GATA-3,ROR-γt,IL-10(the characteristic cytokines of Treg)mRNA(P<0.05).The proliferation of TIL from C26/pcDNA3.1-IL-17 inoculated mice was higher than those of C26/pcDNA3.1,C26 groups(P<0.05),the proliferation of TIL from C26/pcDNA3.1-IL-17,C26/pcDNA3.1 and C26 inoculated mice was lower than those of normal groups( P<0.05).And there′s no differences among every groups of the express of cytokines IL-10 and IL-12 mRNA in tumor infiltrating macrophages(P<0.05).Conclusion: The transfection of IL-17 gene inhibited tumor growth in the mice,inoculated with enhancing the immune function.
ABSTRACT
Objective: To investigate the mechanism of vascular endothelial growth factor ( VEGF)165 and hepatocyte growth factor (HGF) improving cardiomyocyte proliferation in experimental porcine after myocardial infarction (MI). Methods: The MI model was established by left anterior descending artery ligation in 15 male pigs and the animals were divided into 3 groups, n=5 in each group. Control group, the pigs received normal saline injection at the infarct and peri-infarct zones. VEGF group, the pigs received (1×1010 ) pfu of viral titers of Ad-VEGF injection. HGF group, the pigs received (1×1010 ) pfu of viral titers of Ad-HGF injection. The myocardial perfusion and cardiac function were examined by SPECT, the protein expressions of VEGF165 and HGF were measured by Western blot analysis, cardiomyocyte proliferation was analyzed by immunolfuorescence and immunoprecipitation method. Results: ① Compared with Control group, the expressions of VEGF165 and HGF were higher at the infarct and peri-infarct zones in both treatment groups; ② Both treatment groups had better cardiac function and myocardial perfusion; ③ Both treatment groups had improved cardiomyocyte proliferation at the infarct and peri-infarct zones.④VEGF165 promoted cardiomyocyte proliferation via p27 pathway;⑤HGF promoted cardiomyocyte proliferation via p21 and p27 pathways. Conclusion: VEGF165 and HGF could improve myocardial perfusion and function in experimental porcine after MI, VEGF165 and HGF promote cardiomyocyte proliferation via different pathways.