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.

Polyphenols have been widely recognized for their potential anti-obesity effects. This study aimed to evaluate the impact of a polyphenol compound-epigallocatechin-3-gallate, quercetin, and rutin (EQR) on obesity-related parameters and gut microbiota composition. After four weeks of high-fat diet (HFD) induction, the obese Wistar male rats received EQR treatment for an additional four weeks. EQR supplementation significantly reduced body weight gain, feed efficiency, adipose tissue accumulation, and liver lipid content in obese rats. Additionally, it enhanced fecal short-chain fatty acid (SCFA) levels and modulated gut microbiota composition. Specifically, EQR treatment significantly induced Fusobacteria, Fusobacteriaceae, Christensenellaceae, Christensenellaceae R-7 group, Lachnoclostridium, Enterorhabdus, and Parvibacter levels and reduced Deferribacteres and Mucispirillum levels. Gene expression analysis in liver, white adipose tissue (WAT), and brown adipose tissue (BAT) revealed that EQR upregulated the expression of liver PPAR-α, WAT SIRT-1, and BAT PGC-1α, while downregulating liver PPAR-γ, liver FATP-1, and WAT FAS, indicating its role in promoting fatty acid oxidation and thermogenesis, as well as suppressing lipid synthesis and transport. In conclusion, EQR demonstrated significant anti-obesity effects by modulating gut microbiota and lipid metabolism, suggesting its potential as a functional ingredient for obesity management.

Background/Objectives: Obesity represents a critical risk factor for various chronic illnesses and metabolic dysfunctions, underscoring the urgency of identifying safe, food-based interventions to curb fat over-accumulation. Mesona procumbens Hemsl. (Hsian-tsao) is a traditional Chinese herb known for its antioxidant and health-promoting properties; however, it remains unclear how its phenolic acid profiles contribute to anti-obesity activity. This research explored the anti-adipogenic potential of various Hsian-tsao ethanol extracts, focusing on how their phenolic profiles influence lipid suppression in 3T3-L1 adipocytes. Methods: Ethanol extracts prepared using different ethanol concentrations were analyzed for total polyphenol content, antioxidant capacity, and phenolic acid profiles. Adipocytes were exposed to 0, 100, and 250 μg/mL of Hsian-tsao ethanol extract for 48 h duration to monitor changes in cell count and intracellular triglyceride levels. Results: Among all fractions, the 40% ethanol extract (40EEHT) possessed the most robust antioxidant capacity and highest polyphenol content, specifically showing enriched levels of caffeic acid, p-coumaric acid, and total phenolic acids. Notably, while 40EEHT influenced cell density at certain concentrations, it significantly and specifically reduced intracellular triglyceride content, indicating a potent inhibitory effect on lipid storage independent of changes in cell number. Comparative analysis using phenolic acid standards revealed that caffeic acid exerted the strongest inhibitory effect on lipid accumulation, suggesting that it is a key contributor to the anti-adipogenic activity of 40EEHT. Conclusions: Collectively, these findings demonstrate that phenolic acid profiles, particularly caffeic acid enrichment, critically contribute to the potential anti-adipogenic effects of specific ethanol extracts of M. procumbens. Therefore, Hsian-tsao ethanol extracts represent a promising natural source for the development of functional ingredients targeting obesity and related metabolic disorders.

Objective: Chronic sleep deprivation (CSD) is a major public health issue that causes metabolic dysfunction by disrupting redox homeostasis and triggering hepatic inflammation. Given the strong anti-oxidative and anti-inflammatory properties of alpha lipoic acid (ALA), this study aims to determine whether exogenous ALA supplementation would provide hepatoprotection and therefore, maintain the metabolic activity following CSD. Methods: Adult male Wistar rats were randomly assigned to three groups ( n = 6/group). The first two groups underwent three cycles of 5-day total sleep deprivation followed by 2-day rest, receiving daily 2 mL olive oil (CSD group) or ALA (100 mg/kg in 2 mL olive oil) (CSD + ALA group), respectively. The third group received no treatment serving as yoked control (CSC group). Spectrometric, biochemical, immunoblot, and immunohistochemical analyses were performed to assess the hepatic redox-active Fe ²⁺ intensity, metabolic function, anti-oxidative enzyme expression, and the pro-inflammatory cytokine levels. Results: ALA significantly improves metabolic function as effectively attenuates serum concentrations of AST, ALT, and ALP, and stabilize hepatic Fe ²⁺ intensity. ALA also remarkably decreases the protein level of inflammatory factors including NF-κB, TNF-α, IL-6, IL-1β, and cyclooxygenase-2 (COX2), as well as increases the expression of Nrf2-induced antioxidative enzymes such as SOD1 and glutathione peroxidase (GPx). Moreover, ALA further suppresses apoptosis and ferroptosis by modulating related markers including BAX, Bcl-2, GPx4, and FACL4 activities. Conclusion: These findings clearly demonstrate that ALA confers manifold hepatoprotective effects against CSD-induced dysfunction by significantly restoring redox balance, decreasing hepatic inflammation, suppressing apoptotic and ferroptotic signaling, thereby successfully preserving metabolic activity.