Study On The Effect Of Compound Rhizome Nucleating Agent On IFN-??IL-17 And The Expression Of CTSD?C-myc In S180 Tumor Bearing Mice

Objective:To investigate compound rhizome nucleating agent effecti on S180 mice serum IFN-y?IL-17?CTSD?c-myc protein expression levels.This paper analysed more systematic that compound rhizome nucleating agent improve the inhibiton on the on tumor immune system,and impact on tumor invasion and metastasis,and further in-depth study compound rhizome nucleating agent antitumor mechanism.Methods:In vivo method,50 inbred ICR mice,half male and female,are divided into five groups,the normal group,model group,Chinese herb medicine group,CTX group and combination group.Except the normal group,S180 mice as research models,drug treatment after 10 days,peel the thymus,spleen,weighing,calculating each group of mice organ index;separating mice serum,ELISA(Enzyme-Linked Immunosorbent assay)is taking to measure the content of IFN-?,IL-17 levels in serum cytokines;detecting telomerase concentration in serum in mice,the tumor tissue as sample,using immunohistochemical techniques,determination Compound root mixture effect on mice tumor tissue CTSD?c-myc protein expression.Results:?Compound rhizome nucleating agent can enhance tumor-induced thymus index decreased,thus decreasing the combined treatment group spleen index;?Compound rhizome nucleating agent can increase IFN-y levels in the serum of tumor-bearing mice,lower levels of IL-17,and it had a significant statistical significance compared with model group(P<0.01);?Compound rhizome nucleating agent compared with the model group,CTSD?c-myc protein expression was significant(P<0.01),can be reduced CTSD?c-myc protein expression.Conclusion:Compound rhizome nucleating agent can reduce the IL-17 levels by increasing IFN-y in S180 mice,adjust immunosuppressed status of tumor-bearing mice,play a role in anti-tumor;and reduce CTSD?c-myc protein expression,provide a theoretical basis for compound rhizome nucleating agent anti-tumor invasion and metastasis mechanism.