Table · dataset · 2026
Data Sheet 1_Scutellarein promotes diabetic wound repair and preserves fibroblast calcium-mitochondrial homeostasis.pdf
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Background<p>Diabetic wounds are characterized by delayed repair associated with persistent inflammation, oxidative stress, fibroblast dysfunction, mitochondrial injury, and impaired angiogenesis.
Description
Scutellarein (SCU), a structurally defined plant-derived flavonoid metabolite, has documented antioxidant and anti-inflammatory activities; however, its role and the mechanistically relevant pathways engaged in diabetic wound repair, particularly those involving calcium-mitochondrial homeostasis and purinergic signaling, remain incompletely defined.</p>Methods<p>We administered local SCU in a streptozotocin-induced diabetic mouse cutaneous wound model and, in H2O2-injured L929 fibroblasts, assessed scratch closure, survival, redox balance, mitochondrial morphology and function, and calcium overload.
We then used RNA sequencing (RNA-seq) and adenosine triphosphate (ATP) challenge/reversal experiments to examine purinergic calcium signaling. These analyses identified P2rx1—the gene encoding P2RX1 (P2X purinoceptor 1), an ATP-gated cation channel that mediates rapid calcium entry—as a candidate purinergic signal rather than a validated target.</p>Results<p>SCU accelerated wound closure and increased re-epithelialization, Masson-positive collagen deposition, proliferative α-SMA-positive wound cells, and angiogenic indices in diabetic wounds.
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In injured fibroblasts, SCU increased scratch closure, reduced cell death and reactive oxygen species (ROS) accumulation, restored the superoxide dismutase (SOD)/malondialdehyde (MDA) balance, preserved mitochondrial morphology and membrane potential, and increased cellular ATP content. RNA-seq showed P2rx1 downregulation after SCU treatment and enrichment of calcium transport, mitochondrial, inflammatory, and wound-healing pathways.
ATP addition attenuated the SCU-associated reductions in calcium overload, mitochondrial depolarization, and inflammatory gene expression, consistent with a contribution from broad purinergic calcium signaling.</p>Conclusion<p>In experimental models, SCU promoted diabetic wound repair and protected fibroblasts from oxidative injury. The data support preservation of calcium-mitochondrial homeostasis as a mechanistically relevant axis, and broad purinergic signaling, possibly involving P2RX1, may contribute to these effects; direct receptor-perturbation studies are warranted.</p>
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- DOI doi.org/10.3389/fphar.2026.1925629.s001 ↗
DOI / persistent id · from figshare com
Catalogue records · 1
- OAI-PMH record api.figshare.com/v2/oai?verb=GetRecord&metadataPrefix=oai_dc&identifier=oai%3Af… ↗
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Topics
- From keywords
- Astronomy & Astrophysics · Chemistry · Computer Science & AI · Earth & Environmental Science · Economics & Finance · Engineering · Humanities · Life Sciences · Medicine & Health · Ocean & Atmospheric Science · Social Science
- Inferred from text
- RNA sequencing 75% · Sequencing 75%
Provenance · 1 source records, 18 field assertions
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