ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023
Selective inhibition of PKR by C16 accelerates diabetic wound healing by inhibiting NALP3 expression in mice.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- Huiyang Shengji Unguent Promotes Lymphangiogenesis and Wound Healing in Diabetic Chronic Wounds: Combined Insights from Proteomics and in vivo and in vitro Analyses.Journal of inflammation research · 2025Article
- The Mechanism of Pyroptosis and Its Application Prospect in Diabetic Wound Healing.Journal of inflammation research · 2024Review
- Eukaryotic translation initiation factor 2α kinase 2 in pancreatic cancer: An approach towards managing clinical prognosis and molecular immunological characterization.Oncology letters · 2023Article
- Oxidative stress and programmed cell death in diabetic wounds: A comprehensive review.Science progressReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
OBJECTIVE AND
designTo understand the expression of dsRNA-dependent protein kinase R (PKR) in impaired diabetic wounds, hyperglycemia was induced in C57/BL6 mice with streptozotocin. Murine macrophage cell line, Raw 264.7, stimulated with high glucose and LPS was used to mimic diabetic wound environment in in-vitro. MATERIALS: Macrophages stimulated with HG + LPS, in presence and absence of PKR inhibitor (C16) and wound tissue samples from topically treated mice with C16, were analyzed for the expression of PKR, NALP3, active caspase-1, mature IL-1β and phosphorylation of PKR and eIF2α. Wounds tissues were also analyzed for inflammatory cell infiltration by immunohistochemistry, angiogenesis by CD31 staining, collagen expression by western blotting, expression of CD206+ macrophages by flow cytometry and wound strength by texture analyzer.
resultsPKR and NALP3 were found to be upregulated in macrophages stimulated with HG + LPS as well as in impaired diabetic wounds. PKR inhibition using C16 ameliorated expression of NALP3, caspase-1, IL-1β and phosphorylation of PKR and eIF2α, in macrophages and also in diabetic wounds. Treatment with C16 promoted the wound healing in diabetic mice by increasing collagen synthesis, reducing infiltration of F4/80
conclusionPKR inhibition using C16 accelerates the wound healing process in diabetic mice by decreasing NALP3-mediated IL-1β maturation.
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