Antioxidants最新文献

To combat influenza A virus (IAV) infection, it is vital to develop effective therapeutic strategies, including immunomodulators. In this study, we examined the antiviral effects of Hovenia dulcis Thunb. honey (HDH) against IAV using RAW 264.7 cells. HDH treatment significantly reduced IAV infection and viral protein expression. Moreover, it enhanced the production of interferon (IFN)-β, activated the innate immune response through the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, and upregulated IFN signaling through signal transducer and activator of transcription (STAT)1/2 phosphorylation and interferon-stimulated gene (ISG) expression. In addition, HDH decreased IAV-induced intracellular and mitochondrial reactive oxygen species (ROS) production by upregulating the expression of antioxidant proteins, such as Sirt3 and SOD2. The results suggest that HDH is a potential therapeutic agent inhibiting viral replication and boosting host antiviral immunity.

Oxidative stress (OS) refers to the production of a substantial amount of reactive oxygen species (ROS), leading to cellular and organ damage. This imbalance between oxidant and antioxidant activity contributes to various diseases, including cancer, cardiovascular disease, diabetes, and neurodegenerative conditions. The body's antioxidant system, mediated by various signaling pathways, includes the AMPK-SIRT1-FOXO pathway. In oxidative stress conditions, AMPK, an energy sensor, activates SIRT1, which in turn stimulates the FOXO transcription factor. This cascade enhances mitochondrial function, reduces mitochondrial damage, and mitigates OS-induced cellular injury. This review provides a comprehensive analysis of the biological roles, regulatory mechanisms, and functions of the AMPK-SIRT1-FOXO pathway in diseases influenced by OS, offering new insights and methods for understanding OS pathogenesis and its therapeutic approaches.

Antioxidants have gained significant importance in modern nutrition [...].

Background: In vitro findings on the biological functions of Lycium barbarum flavonoids (LBFs) as feed additives are limited. This study aimed to explore the effects of different concentrations of LBFs on the growth performance, immune function, intestinal barrier, and antioxidant capacity of meat ducks. A total of 240 one-day-old male meat ducks were randomly allocated to four groups, each receiving a basal diet supplemented with 0 (control), 250, 500, or 1000 mg/kg of LBFs for 42 d. Results: The results showed that dietary supplementation with 500 mg/kg of LBFs resulted in a significant increase in average daily feed intake, body weight, average daily gain, and feed conversion ratio. Dietary supplementation with 500 or 1000 mg/kg of LBFs resulted in significant decreases in serum levels of D-lactic acid and lipopolysaccharide. Dietary supplementation with 500 mg/kg LBFs significantly decreased diamine oxidase activity and enhanced the activities of catalase, total antioxidant capacity, and glutathione peroxidase in the jejunal mucosa, as well as the activity of total superoxide dismutase and the content of glutathione in the ileal mucosa, while significantly lowering the content of malondialdehyde in the ileal mucosa. Dietary supplementation with 500 mg/kg LBFs significantly up-regulated the mRNA expression of genes associated with intestinal barrier function and antioxidant capacity in the jejunal and ileal mucosa, as well as the protein expression of these antioxidant genes, and led to a significant reduction in the mRNA expression of pro-apoptotic and inflammatory-related genes. Conclusions: The addition of LBFs to the diet improved the growth performance, intestinal barrier function, immune response, and antioxidant capacity of the ducks, which may be closely associated with the activation of the Nrf2 signaling pathway and the inhibition of the NF-κB signaling pathway. The optimal dietary inclusion level of LBFs in ducks was 500 mg/kg.

The complement system plays a crucial role in regulating the inflammatory responses in kidney transplantation, potentially contributing to early decline in kidney function. Ischemia-reperfusion injury (IRI) is among the factors affecting graft outcomes and a primary contributor to delayed graft function. Complement activation, particularly the alternative pathway, participates in the pathogenesis of IRI, involving all kidney compartments. In particular, tubular epithelial cells often acquire a dysfunctional phenotype that can exacerbate complement activation and kidney damage. Currently, complement-modulating drugs are under investigation for the treatment of kidney diseases. Many of these drugs have shown potential therapeutic benefits, but no effective clinical treatments for renal IRI have been identified yet. In this review, we will explore drugs that target complement factors, complement receptors, and regulatory proteins, aiming to highlight their potential value in improving the management of renal IRI.

Propolis is a resinous substance produced by bees that has several biomedical properties that could contribute to the repair process of the gastric mucosa, such as antioxidant, anti-inflammatory, healing, and gastroprotective properties. Thus, this study aimed to determine the chemical composition of Mexicali propolis, its antioxidant capacity, and its effect on gastric repair. Three polarity-directed extracts were obtained: the ethanolic extract, the ethyl acetate extract, and the hexane extract. The antioxidant activity, total phenolic content (TPC), and flavone/flavonol content were determined for each extract. The chemical composition was analysed using HPLC-TOF-MS (High-Performance Liquid Chromatography-Time-Of-Flight Mass Spectrometry) and GC-MS (Gas Chromatography-Mass Spectrometry), and a total of 52 compounds were identified. The results revealed that the ethanolic extract had the greatest effect on free radical scavenging and the content of bioactive compounds. On the basis of these results, the effect of the Mexicali ethanolic extract of propolis (MeEEP) on gastric repair was subsequently evaluated. Prior to the evaluation, MeEEP was found to exhibit low oral toxicity, as determined under the Organisation for Economic Co-operation and Development (OECD) 425 guidelines. Gastric injury was induced in male C57BL/6 mice by intragastric administration of indomethacin (10 mg/kg). MeEEP (300 mg/kg) was administered 6 h after the induction of injury using indomethacin and daily thereafter. The mice were sacrificed at 12, 24, and 48 h to assess the effect. As a result, MeEEP enhanced the repair of the gastric lesion by decreasing the percentage of the bleeding area and attenuating the severity of histological damage, as demonstrated by H&E staining. This effect was associated with a reduction in MPO enzyme activity and in the levels of the proinflammatory cytokines TNF-α, IL-1β, and IL-6, maintaining controlled inflammation in gastric tissue. Furthermore, the administration of the extract increased SOD enzymatic activity and GSH levels, reducing the degree of oxidative damage in the gastric tissue, as demonstrated by low MDA levels. Finally, after evaluating the effect on apoptosis via immunohistochemistry, MeEEP was shown to reduce the expression of the proapoptotic marker Bax and increase the expression of the antiapoptotic marker Bcl-2. In conclusion, these findings suggest that MeEEP may enhance gastric repair through a cytoprotective mechanism by controlling inflammation exacerbation, reducing oxidative stress, and regulating apoptosis. These mechanisms are primarily attributed to the presence of pinocembrin, tectochrysin, chrysin, apigenin, naringenin, acacetin, genistein, and kaempferol. It is important to highlight that this study provides a preliminary exploration of the reparative effect of Mexican propolis, describing the potential mechanisms of action of the compounds present in Mexicali propolis.

Whey protein isolate (WPI) has functional properties such as gelation and emulsification. Emulsion gels combine the benefits of both emulsions and hydrogels. In this study, WPI hydrogels and emulsion gels were developed with goji oil (GO) as the oil phase by the inclusion of blueberry extract (BE) in the protein matrix. Heat-denatured WPI (hWPI) particles and emulsions were characterized in terms of size distribution, ζ-potential, interfacial protein, and anthocyanin partition. The inclusion of anthocyanins-rich blueberry extract led to the aggregation of hWPI particles, but it also increased the interfacial protein of 10% goji oil emulsions to 20% and decreased their size distribution to 120 and 325 nm. WPI hydrogels and emulsion gels were analyzed in terms of their water-holding capacity, which decreased from 98% to 82% with the addition of blueberry extract and goji oil. Syneresis, rheological, and morphological characteristics were also analyzed. The gelation time of hWPI particles and emulsions was shortened from 24 h to 12 h when incorporating blueberry extract to form a dense network. The network was the most homogeneous and densest in the presence of 3% blueberry extract and 5% goji oil. The co-inclusion of blueberry extract and goji oil increased the syneresis during the freeze-thaw cycles, with the values rising from 13% to 36% for 5% BE hydrogel and BE-containing emulsion gels after the first cycle. All WPI hydrogels and emulsion gels exhibit predominantly elastic behavior. Moreover, anthocyanin release, antioxidant activity, and the fatty acid composition profile were also analyzed during in vitro digestion. Soluble and free anthocyanins in the digested medium were reduced with the goji oil content but increased with the blueberry extract content. The stability of polyunsaturated fatty acids in the digested medium was improved by the addition of blueberry extract. The antioxidant activity of the digested medium increased with the content of blueberry extract but decreased with the content of goji oil. The ABTS^∙+ scavenging capacities decreased from 63% to 49% by increasing the content of GO from 0% to 10% and they increased from 48% to 57% for 5% BE and 10% GO emulsion gels as the BE content increased from 0% to 5% after 6 h of digestion. The data gathered should provide valuable insights for future efforts to co-encapsulate hydrophilic and hydrophobic agents, thereby enhancing their stability, bioavailability, and functional properties for potential applications in food industries.

Tacrolimus (TAC)-induced chronic nephrotoxicity (TAC nephrotoxicity) is a serious issue for long-term graft survival in kidney transplantation. However, the pathophysiology of TAC nephrotoxicity remains unclear. In this study, we analyzed whole blood samples from mice that developed TAC nephrotoxicity in order to discover its mechanism. Mice were divided into a TAC group and a control group (n = 5 per group). The TAC group received TAC subcutaneously (1 mg/kg/day for 28 days), while the control group received normal saline instead. After the administration period, whole blood was collected and metabolomic analysis was performed, revealing significant changes in 56 metabolites. The major metabolic changes were related to uremic toxins, vascular damage, and NAD⁺. NAD⁺ levels were significantly lower in the TAC group, and ADP-ribose, nicotinamide, and nicotinamide N-oxide, which are degradation products of NAD⁺, were significantly higher, suggesting impairment of the NAD⁺ salvage pathway. NAD⁺ deficiency suggests cellular aging and mitochondrial dysfunction, which may induce vascular damage and chronic kidney disease. Our study demonstrated a correlation between low NAD⁺ levels and the pathophysiology of TAC nephrotoxicity.

Cardiac ischemia-reperfusion injury (IRI) occurs when blood flow is restored to the myocardium after a period of ischemia, leading to oxidative stress and subsequent myocardial cell damage, primarily due to the accumulation of reactive oxygen species (ROS). In our previous research, we identified that miR-25 is significantly overexpressed in pressure overload-induced heart failure, and its inhibition improves cardiac function by restoring the expression of SERCA2a, a key protein involved in calcium regulation. In this study, we aimed to investigate the role of miR-25 in the context of ischemia-reperfusion injury. We found that miR-25 was markedly upregulated under hypoxic conditions in both in vitro and in vivo models. Through in silico analysis, we identified Sestrin3 (SESN3), an antioxidant protein known for its protective effects against oxidative stress, as a novel target of miR-25. Based on these findings, we hypothesized that inhibiting miR-25 would restore Sestrin3 expression, thereby reducing ROS-induced myocardial cell damage and improving cardiac function. To test this hypothesis, we employed two model systems: a hypoxia/reoxygenation (H/R) stress model using H9c2 myoblasts and a surgically induced ischemia-reperfusion injury mouse model. Our results demonstrated that the use of miR-25 inhibitors significantly improved cardiac function and reduced myocardial damage in both models through the restoration of SESN3 expression. In conclusion, our findings suggest that targeting miR-25 may serve as a novel therapeutic modality to alleviate oxidative damage in the heart.

Noise pollution is a known health risk factor and evidence for cardiovascular diseases associated with traffic noise is growing. At least 20% of the European Union's population lives in noise-polluted areas with exposure levels exceeding the recommended limits of the World Health Organization, which is considered unhealthy by the European Environment Agency. This results in the annual loss of 1.6 million healthy life years. Here, we investigated the protective effects of cardiovascular drug interventions against aircraft noise-mediated cardiovascular complications such as elevated oxidative stress or endothelial dysfunction. Using our established mouse exposure model, we applied mean sound pressure levels of 72 dB(A) for 4 d. C57BL/6 mice were treated with the beta-blocker propranolol (15 mg/kg/d s.c. for 5 d) or the alpha-blocker phenoxybenzamine (1.5 mg/kg/d s.c. for 5 d) and noise-exposed for the last 4 d of the drug administration. Short-term noise exposure caused hypertension (measured by tail-cuff blood pressure monitoring) and impaired endothelial function (measured by isometric tension recording in the aorta and video microscopy in cerebral arterioles in response to acetylcholine). Noise also increased markers of oxidative stress and inflammation. Treatment of mice with propranolol and phenoxybenzamine prevented endothelial and microvascular dysfunction, which was supported by a decrease in markers of inflammation and oxidative stress in heart tissue and the brain. Amelioration of noise-induced hypertension (systolic blood pressure) was not observed, whereas pulse pressure was lowered by trend. This study provides a novel perspective mitigating the adverse effects of noise pollution, especially in vulnerable groups with medication, a rationale for further pharmacological human studies.