Objective To explore the development of nitrergic neurons in the tongue of human fetus. Methods Using histochemical method of NADPH\|diaphorase, the differentiation, migration and development of the nitrergic neurons in the tongue of human fetus were studied. Results At the fourth month of the gestation, the round cells of epithelial tissue in tongue differentiated into fusiform nitrergic nerve cells, which moved from the epithelial tissue to subepithelial and muscular tissue. The bodies of nitrergic neurons were small, the positive reaction of nitric oxide synthase(NOS) was weak. The development of the process of nitrergic neurons might be divided into two phases:The first phase, the growth and development phase, occured from the fourth to the seventh month, the somatic size enlarged gradually, the numbers increased, the positive reaction of NOS increased gradually and reached its peak at the seventh month. The morphology of neurons was characterized by the development from the fusiform form to the tadpole form and then a diversity of shape. The second phase, the maturation phase, denoted the eighth to tenth month, the bodies of nitrergic neurons were obviously enlarged, the staining intensity of NOS was increased. The nitrergic neurons were scattered in the subepithelial layer and muscular tissue and the typical ganglionic cells were observed. Conclusion Nitrergic neurons of tongue originate from its epithelial tissue at the time of early fetal development. By the differentiation, migration, multiplication, growth and maturation, mature nitrergic neurons are formed. [

OBJECTIVE: To investigate whether kirenol, the major pharmacologically active compound of the Chinese medicinal herb , can protect mice from dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). METHODS: C57BL/6 mice with or without kirenol pretreatment were treated with DSS in drinking water for 7 days to induce UC. The symptoms of UC including weight loss, diarrhea and bloody stool were observed daily and graded using the disease activity index (DAI). Colon injury of the mice was assessed by measuring the length of the colon and HE staining of the colon tissue. The levels of inflammatory cytokines produced by the mesenteric lymph nodes (MLNs) lymphocytes were measured using enzyme-linked immunosorbent assay; the apoptosis of the lymphocytes and CD4 T cells was analyzed using flow cytometry. RESULTS: The mice receiving pretreatment with kirenol showed obviously ameliorated symptoms of UC and milder pathological changes in the colon as compared with the control mice. Kirenol treatment significantly down-regulated the secretion of IFN-γ, IL-17A, IL-6 and TNF-α by the MLNs lymphocytes and increased the apoptosis of lymphocytes, especially CD4 T cells in the DSS-treated mice. CONCLUSIONS Kirenol can protect against T cell-mediated colon injury in DSS-treated mice possibly by suppressing the secretion of inflammatory mediators and inducing apoptosis of the inflammatory lymphocytes.
Animals ; Apoptosis ; Colitis, Ulcerative ; Cytokines ; Dextran Sulfate ; Diterpenes ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes