ABSTRACT
UNLABELLED: OBJECTITVE: To investigate the effect of human umbilici mesenchymal cells (HUMSCs) implantation on the brain derived neurotrophic factor (BDNF) expression in diabetic foot rats. METHODS: SD rats were divided into three groups (n = 12): normal group, diadetic foot model group and HUMSC treatment group. Diabetic foot model in rats was established, then prepared HUMSC were implanted on the diabetic foot ulcers in rats, and control ones were administrated with saline only. The area of ulceration, sensory function, BDNF expression and its localization were determined by using morphology, physiological function measurement, RT-PCR and immunohistochemistry assay. RESULT: Siglificantly decreased area of ulceration in diabetic foot rats of HUMSC implantation group was observed. This was simultaneously companied with the sensory function improvement (P < 0.05). RT-PCR showed that BDNF mRNA expression was significantly up regulated (P < 0.05). BDNF immunstaining was located in epithelia tissue and the protein level of BDNF was markedly increased (P < 0.05). CONCLUSION: HUMSC implantation maybe an effective strategy on the treatment of ulceration in diabetic foot rats, and the possible mechanism may involve in BDNF expression.
Subject(s)
Brain-Derived Neurotrophic Factor/metabolism , Diabetic Foot/therapy , Mesenchymal Stem Cell Transplantation/methods , Umbilical Cord/cytology , Animals , Brain-Derived Neurotrophic Factor/genetics , Diabetes Mellitus, Experimental/complications , Diabetic Foot/metabolism , Humans , Male , Rats , Rats, Sprague-Dawley , Wound Healing/physiologyABSTRACT
It has been known that parasites developed sophisticated strategies to escape from the host immune assault. More recently, one strategy to induce immune evasion involved CD4(+)CD25(+) regulatory T cells (Tregs). Mice were infected with Schistosoma japonicum cercariae and then injected intraperitoneally with anti-CD25 monoclonal antibody (anti-CD25 mAb). The results showed that the percentages of CD4(+)CD25(+) Tregs in mice were expanded by S. japonicum infection, and it could be partially blocked by anti-CD25 mAb. Worm burden in anti-CD25 mAb group (23.17 ± 6.94) was significantly lower than that in infected group (30.17 ± 5.85). The level of interferon gamma was increased with anti-CD25 mAb administration; meanwhile, lower concentration of interleukin 10 was observed in the same group. These results suggest that CD4(+)CD25(+) Tregs contribute to the escape of S. japonicum from the host immune responses, while anti-CD25 mAb can partially block CD4(+)CD25(+) Tregs and enhance the protective immunity to the parasite by Th1-type immune response.
