title: Bone marrow mesenchymal stem cells accelerate the hyperglycemic refractory wound healing by inhibiting an excessive inflammatory response.
abstract: The aim of the present study was to evaluate the healing effect of bone marrow-derived mesenchymal stem cells administered to hyperglycemia model mice with skin wounds, and to explore the underlying mechanism contributing to their effects in promoting refractory wound healing. A full‑thickness skin wound mouse model was established, and refers to a wound of the skin and subcutaneous tissue. The mice were randomly divided into three groups: Blank control group, hyperglycemic group and a hyperglycemic group treated with stem cells. Wound healing was monitored and the wound‑healing rate was determined at 3, 6, 9, and 12 days following trauma. The structure of the organization of new skin tissue was observed by hematoxylin and eosin staining, and expression levels of the inflammatory cytokines interleukin (IL)‑6 and tumor necrosis factor (TNF)‑α were determined from 1 to 6 days following trauma. The wound healing of the hyperglycemic group was slower than that of the blank group, and the hyperglycemic mice treated with stem cells presented faster healing than the hyperglycemia group. The horny layer and granular layer of the skin were thinner and incomplete in the new skin tissue of the hyperglycemic group, whereas the new skin wound tissue basal layer was flat and demonstrated better fusion with the wound edge in the other two groups. The expression of inflammatory cytokines (IL‑6 and TNF‑α) was significantly increased in all three groups, with continuously higher expression in the hyperglycemic group and decreased expression in the other two groups over time. Hyperglycemia refractory wounds are likely related to the excessive expression of inflammatory cytokines surrounding the wound area. Stem cells may be able to alleviate the excessive inflammatory reaction in the wound tissue of hyperglycemic mice, so as to promote wound healing.
authors.affiliation: Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Wenbin
authors.initials: W
authors.lastname: Nan
authors.affiliation: Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Zhihao
authors.initials: Z
authors.lastname: Xu
authors.affiliation: Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Zhibin
authors.initials: Z
authors.lastname: Chen
authors.affiliation: Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Xin
authors.initials: X
authors.lastname: Yuan
authors.affiliation: Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Juntang
authors.initials: J
authors.lastname: Lin
authors.affiliation: Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Huigen
authors.initials: H
authors.lastname: Feng
authors.affiliation: Research Center of Stem Cell and Biotherapy Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Jie
authors.initials: J
authors.lastname: Lian
authors.affiliation: Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
authors.forename: Hongli
authors.initials: H
authors.lastname: Chen
mesh_terms: D000818:Animals; D000067696:Ataxin-1 / Q000378:metabolism; D001854:Bone Marrow Cells / Q000166:cytology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005260:Female; D018960:Hyaluronan Receptors / Q000378:metabolism; D006943:Hyperglycemia / Q000150:complications* / Q000473:pathology; D019012:Integrin beta1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D012867:Skin / Q000378:metabolism / Q000473:pathology; D012871:Skin Diseases / Q000150:complications / Q000473:pathology / Q000628:therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014945:Wound Healing
chemical_list: D000067696:Ataxin-1; C000593750:Atxn1 protein, mouse; D018960:Hyaluronan Receptors; D019012:Integrin beta1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha