The therapeutic effect of human umbilical cord mesenchymal stem cells (hUCMSCs) combined with intestinal probiotics on the wound healing of diabetic mice and its potential mechanism were explored. A diabetic wound mouse model was established, and 25 male C57BL/6J mice were randomly divided into five groups: blank control group, model group, hUCMSCs treatment group, probiotics treatment group, and hUCMSCs combined with probiotics treatment group. The wound healing conditions were photographed and recorded on days 0, 3, 6, 9, and 12 after modeling, and the differences in wound healing rates among the groups were analyzed. HE and Masson staining were used to observe the histopathological changes and collagen deposition. CD31 immunofluorescence was used to detect angiogenesis. Collagen I immunohistochemistry was used to evaluate the formation of type I collagen. ELISA was used to detect the expression levels of anti-inflammatory factors (Arg1) and pro-inflammatory factors (IL-6, IL-1β, TNF-α) in wounded skin tissue and serum. The results showed that on day 12 after modeling, compared with the other groups, the combined treatment group had the most significant wound contraction and the fastest healing rate. HE and Masson staining showed that the combined treatment group had the fastest epithelialization and the most collagen deposition. Immunofluorescence and immunohistochemistry showed that the combined treatment group had the highest expression levels of CD31 and Collagen I. ELISA results indicated that the combined treatment group had higher expression levels of Arg1 in wound skin tissue and serum than the other groups, while the expression levels of IL-6, IL-1β, and TNF-α were significantly lower. These results suggest that the combined treatment of hUCMSCs and intestinal probiotics can accelerate wound healing in diabetic mice through mechanisms such as promoting angiogenesis, enhancing collagen deposition, and regulating the inflammatory microenvironment. The therapeutic effect was significantly better than that of single treatment, providing a new potential strategy for the clinical treatment of diabetic foot.

Objective To investigate the mechanism of protective effects of 17-β estradiol on the experimental model of spinal cord injury (SCI) rats.Methods First,the primary astrocytes were cultured and identified.When the third generation astrocytes were cultured,they were induced by H202 whose concentrations were established by the method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT).The cells were randomly divided into five groups:control group; the group of treatment with 400 μmol/L H2O2 for 24 hours; the group of treatment with 20 nmol/L estrogen for 2 hours prior to exposure to 400 μmol/L H2O2 for 24 hours; the group of treatment with 20 nmol/L estrogen for 26 hours and the group of treatment with dimethyl sulfoxide for 26 hours.The proteins which were extracted from these cells after treatments with H2O2 for 24 hours were detected by Western blotting.Results The absorbances of the astrocytes of treatments with H2O2 were reduced( q' =-11.45,P =0.001 ).But exposure to estrogen prior to exposure to H2O2 provided partial restoration of the absorbances (q' =7.025,P =0.0025 ).The absorbances of the astrocytes among different groups showed significant differences( F =69.69,P =0.0025 ).The results suggested that estrogen might increase the cell viability in astrocytes.Compared with the group of treatment cells with H2O2,treatment cells with 17-β estradiol prior to H2O2 exposure down-regulated the expressions of both phosphatase and tensin homologue deleted on chromosome 10 ( PTEN ) ( F =290.003,P =0.001 ) and caspase-3 ( F =46.158,P =0.023 ).And,17-β estradiol treatment of cells increased the levels of p-Akt ( F =49.173,P =0.033 ) and Bcl-2 ( F =115.916,P =0.001 ) when compared with the group of treatment astrocytes with H2O2.Conclusion These findings suggest that the attenuation of PTEN expression mediated by estrogen is associated with an increase in phosphorylation/activation of the Akt and the Bel-2 expressions.These results suggest that the protective effects of 17-β estradiol on the experimental model of SCI rats may depend on the estrogen protection to the astrocytes which may be mediated by decreasing the PTEN expression.