Stromal vascular fraction gel promoted wound healing and peripheral nerve repair in diabetic rats via TLRs/MyD88/NF-κB signaling pathway

Author:

Xing Nan1,Yang Jincun1,Wang Haitao1ORCID,Peng Lei2,Liu Xiaowen1,Chen Jiong3,Liu Yan4

Affiliation:

1. Burn plastic surgery, Weihai Municipal Hospital, Shandong University, Weihai, Shandong, China

2. Trauma center, Weihai Municipal Hospital, Shandong University, Weihai, Shandong, China

3. Burn plastic and skin repair surgery, Third Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

4. Department of Ophthalmology and stomatology, Weihai Municipal Hospital, Shandong University, Weihai, Shandong, China

Abstract

Diabetes mellitus (DM) contributes to impaired wound healing. This study was aimed to evaluate the effect of stromal vascular fraction (SVF) gel extracted from rats on diabetic ulcers wound healing and peripheral nerve repair. 60 Sprague Dawley (SD) rats were divided into 6 groups, including control, model, SVF-gel low dose (SVF-gel-L), SVF-gel high dose (SVF-gel-H), ST2825, and SVF-gel-H + CL075 groups. Wound closure rate was recorded. The histopathological changes and deposition change of collagen fibre were identified. The content of TNF-α, IL-1β, VEGF, and bFGF were detected. Immunohistochemical, immunofluorescence and western blot were employed to determine the protein expression. We identified SVF-gel could promoted wound healing, restored normal cutaneous structures of the wound, promoted collagen deposition, while diminished fibrosis and inflammation. In addition, SVF-gel promoted angiogenesis and peripheral nerve recovery, diminished the expression of TLRs/MyD88/NF-κB signaling pathway. However, the protective effect of SVF-gel could be revised by CL075 co-treatment. Furthermore, ST2825 also promoted wound healing, but its effect was lower than that with SVF-gel-H treatment. SVF gel promotes the healing of diabetic skin ulcer tissue and regeneration of damaged peripheral nerve, diminished inflammatory factor infiltration. The mechanism maybe related to suppress the activation of TLRs/MyD88/NF-κB signaling pathway.

Publisher

SAGE Publications

Subject

Biomedical Engineering,Biomaterials

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