Therapeutic Potential of Luteolin on Impaired Wound Healing in Streptozotocin-Induced Rats

doi:doi.org/10.3390/biomedicines9070761

中山醫學大學機構典藏 CSMUIR > 健康管理學院 > 營養學系暨碩士班 > 期刊論文 > Item 310902500/22415

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/22415

Title:	Therapeutic Potential of Luteolin on Impaired Wound Healing in Streptozotocin-Induced Rats
Authors:	Chen, Li-You;Cheng, Hsin-Lin;Kuan, Yu-Hsiang;Tang-Jun Liang;Chao, Yun-Yi;Lin, Hsing-Chun
Keywords:	luteolin;diabetes;wound healing;anti-oxidation;anti-inflammation
Date:	2021-06-30
Issue Date:	2022-06-13T02:32:12Z (UTC)
Publisher:	MDPI
Abstract:	Long-term hyperglycemia may lead to diabetic microvascular and macrovascular complications that can affect the peripheral vascular system, particularly in wound healing capacity. Impaired angiogenesis and delayed wound healing are significant clinically. Luteolin (3′, 4′, 5, 7-tetrahydroxyflavone) is a naturally occurring flavonoid that is ubiquitously found in plants. Recent evidence has shown that luteolin is an anti-inflammatory and anti-oxidative agent. However, the effect of systemic luteolin administration on diabetic wound restoration remains unclear. Herein, we explored the effectiveness of luteolin for improving delayed and impaired healing of skin wound and further clarified the underlying mechanisms. The results indicated that luteolin significantly attenuates blood glucose concentration, improves impaired healing and accelerates re-epithelization of skin wound in streptozotocin (STZ)-induced diabetic rats. Histopathological staining and immunoblotting revealed an inhibitory effect of luteolin on inflammatory cell and cytokine production. We also observed remarkable decreases in protein expressions of inflammatory factors including matrix metalloproteinase (MMP)-9, tumor necrosis factor (TNF)-α, interleukin (IL-6), and IL1-β and downregulation of nuclear factor (NF)-κB, as well as increases in anti-oxidative enzymes such as superoxide dismutase 1 (SOD1) and glutathione peroxidase (GSH-Px) induced by nuclear factor erythroid 2-related factor (Nrf)-2 following luteolin supplementation. Furthermore, luteolin decreased the expression of vascular endothelial growth factor (VEGF) and increased the expression of ubiquitin carboxy-terminal hydrolase (UCH)-L1, as evidenced by angiogenesis and neuronal regeneration in completely healed wound. In conclusion, systemic administration of luteolin promotes wound restoration by ameliorating inflammation and oxidative stress through the inactivation of NF-κB and upregulation of Nrf2 in STZ-induced diabetic rats.
URI:	https://ir.csmu.edu.tw:8080/handle/310902500/22415
Relation:	Biomedicines, 9(7), 761
Appears in Collections:	[營養學系暨碩士班] 期刊論文

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