Antioxidants最新文献

Ascorbic acid (AsA) is an important antioxidant for human health. The concept of "oil-vegetable-duel-purpose" can significantly enhance the economic benefits of the rapeseed industry. Rapeseed, when utilized as a vegetable, serves as a valuable food source of AsA. In this study, we integrated transcriptome and metabolome analyses, along with substrate feeding, to identify the L-galactose pathway as the primary source for AsA production, which is primarily regulated by light. Through seven different photoperiod treatments from 12 h/12 h (light/dark) to 24 h/0 h, we found that AsA content increased with longer photoperiods, as well as chlorophyll, carotenoids, and soluble sugars. However, an excessively long photoperiod led to photooxidative stress, which negatively affected biomass accumulation in rapeseed seedlings and subsequently impacted the total accumulation of AsA. Furthermore, different enzymes respond differently to different photoperiods. Analysis of the correlation between the expression levels of AsA biosynthesis-related genes and AsA content highlighted a dynamic balancing mechanism of AsA metabolism in response to different photoperiods. The study revealed that the 16 h/8 h photoperiod is optimal for long-term AsA accumulation in rapeseed seedlings. However, extending the photoperiod before harvest can enhance AsA content without compromising yield. These findings offer novel insights into an effective strategy for the biofortification of AsA in rapeseed.

Heart failure and cardiovascular disease represent a significant burden on healthcare systems worldwide. Recent evidence associates an increased expression of the dual-specificity tyrosine phosphorylation-regulated kinase 1B (DYRK1B) with an impaired cardiac function in mice. However, there remains a paucity of data on myocardial DYRK1B expression in patients with cardiovascular disease in the context of other comorbidities. In our study, we examined DYRK1B mRNA expression in human right atrial appendage biopsies from 159 patients undergoing elective coronary artery bypass surgery. Each patient was tested for sleep-disordered breathing the night prior to surgery. In this large representative study cohort with cardiovascular high-risk patients, we found that an impaired cardiac function as well as sleep-disordered breathing (SDB), including various oxidative stress parameters, were associated with an increased myocardial DYRK1B expression. A multivariate regression analysis revealed left ventricular ejection fraction and the presence of SDB as significant predictors of the myocardial DYRK1B expression independent of other clinical covariates. Based on these findings, DYRK1B represents a promising molecular target in patients with heart failure and reduced ejection fraction as well in patients with sleep-disordered breathing.

Migraine is one of the most common neurological disorders and the second most disabling human condition. The molecular mechanisms of migraine have been linked to neuropeptide release, endothelial dysfunction, oxidative stress and inflammatory processes. Acid sphingomyelinase (aSMase) is a secreted enzyme that leads to sphingomyelin degradation to produce ceramide. Its activity has been associated with several molecular processes involved in migraine. Therefore, this cross-sectional study aims to study the potential role of aSMase in patients with episodic and chronic migraine. In this cross-sectional pilot study, serum samples from female healthy controls (n = 23), episodic migraine (EM) patients (n = 31), and chronic migraine (CM) patients (n = 28) were studied. The total serum levels of aSMase were determined by ELISA. In addition, the serum levels of sphingomyelin (SM), dihydro-sphingomyelin (dhSM), ceramide (Cer), and dihydro-ceramide (dhCer) were determined by mass spectrometry as biomarkers involved in the main molecular pathways associated with aSMase. aSMase serum levels were found significantly elevated in both EM (3.62 ± 1.25 ng/mL) and CM (3.07 ± 0.95 ng/mL) compared with controls (1.58 ± 0.72 ng/mL) (p < 0.0001). ROC analysis showed an area under the curve (AUC) of 0.94 (95% CI: 0.89-0.99, p < 0.0001) and 0.90 (95% CI: 0.81-0.99, p < 0.0001) for EM and CM compared to controls, respectively. Regarding other biomarkers associated with aSMase's pathways, total SM serum levels were significantly decreased in both EM (173,534 ± 39,096 pmol/mL, p < 0.01) and CM (158,459 ± 40,010 pmol/mL, p < 0.0001) compared to the control subjects (219,721 ± 36,950 pmol/mL). Elevated serum levels of aSMase were found in EM and CM patients compared to the control subjects. The decreased SM levels found in both EM and CM indicate that aSMase activity plays a role in migraine. Therefore, aSMase may constitute a new therapeutic target in migraine that should be further investigated.

Diabetic patients experience hyperglycemia, which can affect multiple organs, including brain function, leading to disabling neurological complications. Hyperglycemia plays a key role in promoting neuroinflammation, the most common complication in diabetic individuals, through the activation of microglia. Attenuating hyperglycemia-related neuroinflammation in microglia may reduce diabetes-associated neurological comorbidities. Natural remedies containing phenolic compounds have shown efficacy in mitigating microglia-mediated neuroinflammation. The aim of this study was to investigate the potential of a Melissa officinalis L. (MO) phytocomplex, obtained from plant cell cultures and enriched in its main polyphenolic constituent, rosmarinic acid (RA), in attenuating hyperglycemia-induced neuroinflammation in microglia. A time-course morphological analysis of BV2 microglial cells exposed to high glucose (HG) levels showed a shift towards a proinflammatory phenotype, peaking after 48 h, which was reversed by pretreatment with MO. Biochemical assays revealed increased expression of the microglial marker CD11b (187%), activation of the NF-κB pathway (179%), expression of iNOS (225%), enhanced phosphorylation of ERK1/2 (180%), and increased expression of the proinflammatory cytokine IL-6 (173%). Pretreatment with MO prevented the aberrant expression of these proinflammatory mediators and restored SIRT1 levels. Exposure of neuronal SH-SY5Y cells to the conditioned medium from HG-exposed microglia significantly reduced cell viability. MO counteracted this effect, exhibiting neuroprotective activity. RA showed efficacy comparable to that of MO. In conclusion, MO and RA attenuated microglia-mediated oxidative imbalance and neuroinflammation under HG exposure by inhibiting the morphological shift toward a proinflammatory phenotype induced by HG and abrogating the subsequent activation of the downstream ERK1/2-NF-κB-iNOS pathway.

Photoreceptor/retinal degeneration is the major cause of blindness. Induced and inherited mouse models of retinal degeneration are valuable tools for investigating disease mechanisms and developing therapeutic interventions. This study investigated the potential of the antioxidant resveratrol to relieve photoreceptor degeneration using mouse models. Clinical studies have shown a potential association between thyroid hormone (TH) signaling and age-related retinal degeneration. Excessive TH signaling induces oxidative stress/damage and photoreceptor death in mice. C57BL/6 (rod-dominant) and Nrl^-/- (cone-dominant) mice at postnatal day 30 (P30) received triiodothyronine (T3) via drinking water (20 µg/mL) with or without concomitant treatment with resveratrol via drinking water (120 µg/mL) for 30 days, followed by evaluation of photoreceptor degeneration, oxidative damage, and retinal stress responses. In experiments using Leber congenital amaurosis model mice, mother Rpe65^-/- and Rpe65^-/-/Nrl^-/- mice received resveratrol via drinking water (120 µg/mL) for 20 days and 10-13 days, respectively, beginning on the day when the pups were at P5, and pups were then evaluated for cone degeneration. Treatment with resveratrol significantly diminished the photoreceptor degeneration induced by T3 and preserved photoreceptors in Rpe65-deficient mice, manifested as preserved retinal morphology/outer nuclear layer thickness, increased cone density, reduced photoreceptor oxidative stress/damage and apoptosis, reduced upregulation of genes involved in cell death/inflammatory responses, and reduced macroglial cell activation. These findings demonstrate the role of oxidative stress in photoreceptor degeneration, associated with TH signaling and Rpe65 deficiency, and support the therapeutic potential of resveratrol/antioxidants in the management of retinal degeneration.

The aim of this study was to investigate the antioxidant capacity of fruit wines and their protective effects against hydrogen peroxide-induced oxidative stress in rat synaptosomes in vitro. The wines were produced from strawberries and drupe fruits (i.e., plum, sweet cherry, peach, and apricot) through microvinification with a pure S. cerevisiae yeast culture. Fruit wines were produced with and without added sugar before the start of fermentation, whereas subvariants with and without pits were only applied to drupe fruit wines. First, synaptosomes were treated with the wines, while oxidative stress was induced with H₂O₂. Subsequently, the activities of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)) and the content of malondialdehyde (MDA), an indicator of membrane injury, were determined. In addition, the Briggs-Rauscher reaction (BR) was used to evaluate the inhibition capacity against free radicals. All investigated fruit wines increased the activity of the studied antioxidant enzymes and decreased MDA content compared to the corresponding controls (synaptosomes treated with H₂O₂). After synaptosomal treatment with plum wine, the highest activities were observed for SOD (5.57 U/mg protein) and GPx (0.015 U/mg protein). Strawberry wine induced the highest CAT activity (0.047 U/mg protein) and showed the best ability to reduce lipid peroxidation, yielding the lowest MDA level (2.68 nmol/mg). Strawberry, plum, and sweet cherry wines were identified as samples with higher antioxidant activity in both principal component analysis (PCA) and hierarchical cluster analysis (HCA). Finally, plum wine exhibited the highest inhibitory activity in the BR reaction (397 s). The results suggest that fruit wines could be considered potential functional food due to their protective effects against oxidative stress.

The petals of flowering plants should retain unique antioxidants that have not been found in the fruits, as the petals need to stay open to attract pollinators against photooxidation and devise a solution to avoid eating attacks. We reported that the yellow petals of freesia cultivars (Freesia x hybrida) accumulated original apocarotenoids, mono- and di-neapolitanosyl crocetin. Here, in the yellow petals, we discovered eight novel flavonoids by their structural determination, including four 3'-caffeoylquercetin 3,7-glycosides, one 3'-caffeoylquercetin 3-glycoside, and three 4'-caffeoylkaempferol 3,7-glycosides. The 3-carbon sugar part was a minor hexose dimer [D-glucosyl-D-glucoside or D-glucosyl-L-rhamnoside] with the β1,2-linkage, while the 7-carbon was usually O-glycosylated with D-glucose, L-rhamnose, or D-glucuronic acid. Such caffeoyl-flavonol glycosides were also present in freesia white petals, regardless of the cultivars and wild species. When dihydroflavonols, the last common precursors between flavonols and anthocyanins, switch to the flavonol route, these caffeoyl-flavonol glycosides are likely to be synthesized via quercetin or kaempferol. All the eight flavonoids exerted in vitro antioxidant activities against both lipid peroxidation and radical generation. Specifically, 3'-caffeoylquercetin 3-sophoroside and its 7-glucuronide showed superior antioxidant activity. Freesia yellow and white flowers have been utilized as edible flowers, indicating the importance of evaluating the human benefits and risks of newly identified flavonoids.

Citrus fruits, mainly grapefruit (Citrus x paradisi L.), are rich in bioactive compounds with potential antioxidant properties. This study investigated the antioxidant effects of naringin (NR) and ethanolic Citrus x paradisi L. peel (E) in reducing aluminum chloride (AlCl₃)-induced oxidative stress in mice. Quantitative analysis using HPLC identified optimal extraction conditions, combination ultrasound and reflux extraction (UH50), resulting in high concentrations of naringin (49.13 mg/g) and naringenin (63.99 µg/g). Mice were treated with NR and E to evaluate their effects on key markers of oxidative stress: reduced glutathione (GSH), malondialdehyde (MDA), and catalase (CAT). The E effectively reduced MDA levels in blood, brain, and liver tissues, with a more substantial effect on controlling lipid peroxidation. In contrast, NR was more effective in restoring GSH levels and CAT activity, suggesting a broader enhancement of antioxidant defense. These findings provide information about specific mechanisms of NR and E and their therapeutic potential in managing oxidative stress and developing products with synergistic efficacy.

High concentrations of non-esterified fatty acids (NEFA) in the blood contribute to various metabolic disorders and are linked to endometritis in dairy cows. Isorhamnetin (ISO), a flavonoid found in many plants, is known for its antioxidant, anti-inflammatory, and anti-obesity properties. This study systematically assessed NEFA-induced damage in bovine endometrial epithelial cells (bEECs) and investigated whether ISO alleviates NEFA-induced cell damage and its underlying molecular mechanisms. Our observations revealed that excessive NEFA inhibited proliferation and induced apoptosis in bEECs, accompanied by an increase in the expression of BAX and cleaved caspase-3. We further observed that NEFA could induce lipid accumulation, reactive oxygen species (ROS) generation, and the release of pro-inflammatory factors IL-1β, IL-6, and TNF-α in bEECs. RNA sequencing and Western blot analysis revealed that NEFA induced damage in bEECs by activating MAPK signaling pathway. Notably, ISO treatment ameliorated these effects induced by NEFA, as evidenced by decreased protein levels of BAX, cleaved caspase-3, and PPAR-γ, along with reductions in triglyceride content, ROS generation, and levels of IL-1β, IL-6, and TNF-α. Mechanistically, our experimental results demonstrated that ISO inhibited NEFA-induced activation of MAPK signaling. Overall, ISO shows promise for therapeutic development to address NEFA-related endometritis in dairy cows.