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oai:figshare.com:article/33872254 2026-09-17T05:57:23Z category_19 portal_316 item_type_3 month_year_09_2026

Data Sheet 1_Scutellarein promotes diabetic wound repair and preserves fibroblast calcium-mitochondrial homeostasis.pdf Yizhuo Huang (14027409) Shengzhou Shan (23458469) Mengling Chang (9039553) Yi Liu (36759) Yucheng Yao (3391736) Jun Yang (2084) Fei Liu (21082) Pharmacology calcium signaling diabetic wound fibroblast mitochondrial dysfunction oxidative stress P2RX1 scutellarein Background<p>Diabetic wounds are characterized by delayed repair associated with persistent inflammation, oxidative stress, fibroblast dysfunction, mitochondrial injury, and impaired angiogenesis. 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. 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> 2026-09-17T05:57:23Z Dataset Dataset 10.3389/fphar.2026.1925629.s001 https://figshare.com/articles/dataset/Data_Sheet_1_Scutellarein_promotes_diabetic_wound_repair_and_preserves_fibroblast_calcium-mitochondrial_homeostasis_pdf/33872254 CC BY 4.0