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ObjectiveTo investigate the effect of recombinant interleukin-2 (rIL-2) combined with allicin in the treatment of pancreatic cancer and related mechanisms. MethodsA nude mouse xenograft model was established. A total of 60 nude mice were randomized into control group, rIL-2 treatment group, allicin treatment group, and combined treatment group. At 4 weeks after treatment, peripheral blood was collected, tumor volume, tumor weight, and survival time were recorded, and survival rates were calculated. Flow cytometry was used to analyze the apoptosis of tumor cells and measure the percentages of CD4+ T, CD8+ T, and natural killer (NK) cells, ELISA was used to measure the level of interferonγ (IFNγ), and Western blot was used to measure the expression of Bcl-2 protein in tumor tissue. An analysis of variance was used for comparison of continuous data between groups, and SNK-q test was used for further comparison between any two groups. ResultsAt 4 weeks after treatment, the rIL-2 treatment group, allicin treatment group, and combined treatment group showed significant reductions in tumor volume compared with the control group (all P＜0.05), and the combined treatment group showed the greatest reduction (P＜0.01). The combined treatment group had a tumor inhibition rate of 90.5% and a prolonged survival time (60% of the mice survived at 55 days). Compared with the control group, the combined treatment group showed significant increases in the apoptosis rate of tumor cells (233%±4.3% vs 90%±3.7%, P＜0.05) and the expression of pro-apoptotic protein Bcl-2. The treatment groups showed significant increases in the percentages of CD4+ T, CD8+ T, and NK cells compared with the control group (F=23.74, 26.38, and 1972, all P＜0.001). Compared with the other three groups, the combined treatment group showed a significant increase in the IFNγ level (F=9.84, P=0.026). ConclusionCombined treatment with allicin and rIL-2 can enhance the innate immunity and adaptive immunity and thus improve the survival of pancreatic cancer.
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Objective To investigate the correlation between the ratio change of circulating myeloid-derived suppressor cells (MDSCs) and cellular immune function in healthy volunteers,chronic gastritis patients,gastric intraepithelial neoplasia patients and gastric cancer patients.Methods From February 2011 to July 2011,129 peripheral blood samples were collected,including 32 healthy volunteers,48 chronic gastritis patients,27 gastric intraepithelial neoplasia patients and 22 gastric cancer patients.The percentages of peripheral blood MDSC,T lymphocyte subsets and regulatory T cells (Treg) were determined by flow cytometry.The data were analyzed by one way analysis of variance,pearson and spearman correlation.Results The percentages of circulating MDSC,CD8+ T lymphocyte and Treg were highest in gastric cancer patients (9.63％±3.24％,10.03％ ± 1.26％,69.45％±3.42％) and lowest in healthy volunteers (0.92％±0.33％,4.12％ ±0.99％,32.35％ ±4.83％).Those of gastric intraepithelial neoplasia patients (5.13％ ± 1.30％,7.54％ ± 0.79％,53.26％±4.30％) were lower than gastric cancer patients but higher than chronic gastritis patients (2.76％ ±0.64％,6.28％ ±0.61％,42.37％ ±4.02％).The differences among each groups were statistically significant (F=24.85,20.88,37.84,all P＜0.05).However,the percentage of circulating CD4+T lymphocyte was highest in healthy volunteers (65.10％±4.10％),55.15％ ± 4.00％ in chronic gastritis group,42.23％ ± 3.91％ in gastric intraepithelial neoplasia group,and lowest in gastric cancer group (26.84％ ± 3.69％).The differences among each groups were statistically significant (F=46.80,P＜0.05).A significant correlation between circulating MDSC and TNM stages of gastric cancer was also observed (r=0.856,P＜0.01).The percentage of circulating MDSC was positively correlated with Treg percentage (r =0.862,P ＜ 0.01),and negatively correlated with CD4+/CD8+ ratio (r=-0.768,P＜0.01).Conclusion The increase of MDSC percentage in peripheral blood is correlated with human cellular immune function,which might play an important role in the tumor immune evasion during the development of gastric cancer.