1. Academic Validation
  2. Vaccarin hastens wound healing by promoting angiogenesis via activation of MAPK/ERK and PI3K/AKT signaling pathways in vivo

Vaccarin hastens wound healing by promoting angiogenesis via activation of MAPK/ERK and PI3K/AKT signaling pathways in vivo

  • Acta Cir Bras. 2020 Feb 7;34(12):e201901202. doi: 10.1590/s0102-865020190120000002.
Bao Hou 1 Weiwei Cai 2 Ting Chen 3 Zhixuan Zhang 3 Haifeng Gong 3 Wei Yang 3 Liying Qiu 4
Affiliations

Affiliations

  • 1 Assistant Experimentalist, Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, China. Technical procedures, manuscript preparation.
  • 2 Experimentalist, Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, China. Histological examinations, manuscript preparation.
  • 3 Master, Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, China. Acquisition of data, statistics analysis.
  • 4 PhD, Professor, Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, China. Critical revision, final approval.
Abstract

Purpose: To explore the potential role and unclear molecular mechanisms of vaccarin in wound healing.

Methods: Rats' skin excision model to study the effects of vaccarin on wound healing in vivo . Hematoxylin and eosin staining was performed to evaluate Histopathologic characteristics. Immunohistochemistry was employed to assess the effects of vaccarin in accelerating angiogenesis. Western blot was used to evaluate relative protein expressed levels.

Results: Vaccarin could significantly promote wound healing and endothelial cells and fibroblasts proliferation in the wound site. Immunohistochemistry and Western blot studies showed that the nodal proteins and receptor (bFGFR) related to angiogenesis signaling pathway were activated, and the microvascular density in the wound site was markedly higher than that in the control group.

Conclusions: The present study was the first to demonstrate that vaccarin is able to induce angiogenesis and accelerate wound healing in vivo by increasing expressions of p-Akt, p-Erk and p-bFGFR. This process is mediated by MAPK/ERK and PI3K/Akt signaling pathways.

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