Objective To explore the influence of chronic neuropathic pain on cellular immune function of mice models.Methods The mice models were established by ligating tibeal nerve and common peroneal nerve on one side,and the influence of chronic neuropathic pain on cellular immune function and tumor necrosis factor-?(TNF-?) and interleukin-6(IL-6) was observed with lymphocyte cell increase experiment(MTT method) and enzyme linked immunosorbent assay(ELISA).Results The increased reactivity of T lymphocyte of the model group was significantly higher than that of the sham group and the control group.At the same time,content of TNF-? and IL-6 in blood of the model group also increased.Conclusion Cellular immune function of mice is increased in the state of chronic neuropathic pain.

OBJECTIVETo isolate the side population (SP) and non-side population (NSP) cells from A431 cells and compare their difference in tumorigenicity in mice and the expression profiles of epithelial-mesenchymal transition (EMT) markers.

METHODSA431 cells stained with Hoechst 33342 were sorted with flow cytometry. The isolated SP cells and NSP cells were inoculated into NOD/SCID mice and the tumorigenicity of the cells was observed. EMT markers E-cadherin, β-catenin, vimentin, AXL, and Erbb3 in the tumor tissues were detected by immunohisto-staining.

RESULTSThe tumors generated by SP cells were larger than those by NSP cells in NOD/SCID mice. Compared with the tumors generated by NSP cells, the cells in the periphery of tumors generated by SP cells showed up-regulated expressions of AXL, vimentin and β-catenin and down-regulated ERBB3 and E-cadherin.

CONCLUSIONThe SP cells in A431 cells have a strong tumorigenicity and show more EMT phenotypes in tissues.

Animals ; Biomarkers, Tumor ; metabolism ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition ; Humans ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplastic Stem Cells ; metabolism ; Side-Population Cells ; metabolism ; Skin Neoplasms ; metabolism ; pathology