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Abstract Chronic type 2 diabetes mellitus (T2DM) and its associated diseases are major concern among human population and also responsible for significant mortality rate. Hence, the present study aims to evaluate and correlate the invertase inhibition, antioxidant activity and control against DFU causing bacterial pathogens by Pandanus odoratissimus flowers. Two dimensional preparative thin layer chromatography (2D PTLC) was adopted to purify the phenolic acid component and LC-MS2 was done to predict the phenolic acid structures. Standard spectrophotometry methods were adopted to investigate the in vitro invertase inhibitory and antioxidant (CUPRAC and ABTS) activities. Agar well diffusion and broth dilution assays were used to record the antibacterial property against DFU causing pathogens isolated from clinical samples. Statistical analyses were used to validate the experiments. A new and novel diferuloyl glycerate related phenolic acid (m/z 442) purified from PTLC eluate has recorded satisfactory cupric ion reducing power (ED50= 441.4±2.5 µg), moderate ABTS radical scavenging activity (IC50= 450.3±10 µg; 32.5±1.5%), and a near moderate, in vitro, invertase mixed type inhibition (24.5±4.5%; Ki: 400 µg). Similarly, bacterial growth inhibitory kinetics has showed a significant inhibition against E. coli and S. aureus.

Background: Oxidative stress, a condition characterized by excessive production of reactive oxygen species (ROS), can cause significant damage to cellular macromolecules, leading to neurodegeneration. This underscores the need for effective antioxidant therapies that can mitigate oxidative stress and its associated neurodegenerative effects. KC14 peptide derived from liver-expressed antimicrobial peptide-2 A (LEAP 2 A) from Cyprinus carpio L. has been identified as a potential therapeutic agent. This study focuses on the antioxidant and neuroprotective properties of the KC14 peptide is to evaluate its effectiveness against oxidative stress and neurodegeneration., Methods: The antioxidant capabilities of KC14 were initially assessed through in silico docking studies, which predicted its potential to interact with oxidative stress-related targets. Subsequently, the peptide was tested at concentrations ranging from 5 to 45 µM in both in vitro and in vivo experiments. In vivo studies involved treating H 2 O 2 -induced zebrafish larvae with KC14 peptide to analyze its effects on oxidative stress and neuroprotection., Results: KC14 peptide showed a protective effect against the developmental malformations caused by H 2 O 2 stress, restored antioxidant enzyme activity, reduced neuronal damage, and lowered lipid peroxidation and nitric oxide levels in H 2 O 2 -induced larvae. It enhanced acetylcholinesterase activity and significantly reduced intracellular ROS levels (p < 0.05) dose-dependently. Gene expression studies showed up-regulation of antioxidant genes with KC14 treatment under H 2 O 2 stress., Conclusions: This study highlights the potent antioxidant activity of KC14 and its ability to confer neuroprotection against oxidative stress can provide a novel therapeutic agent for combating neurodegenerative diseases induced by oxidative stress., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Endothelial dysfunction is a predictor for cardiovascular disease. Preclinical data suggest longstanding cardiovascular and cerebrovascular dysfunction occurs in offspring with perinatal electronic cigarette (Ecig) exposure. Furthermore, direct use of Ecigs increases reactive oxygen species and impairs cerebrovascular function, but the combined effect of direct use in offspring with a history of perinatal exposure (i.e. double-hit condition) is not known. We tested the hypothesis that offspring with double-hit Ecig exposure will lead to greater cerebrovascular and neurocognitive dysfunction compared with in utero exposure only. Male and female offspring were obtained from time-mated Sprague Dawley female rats exposed to air ( n = 5 dams) or Ecig exposed ( n = 5 dams) and studied at either 3 or 6 mo after birth. Ecig exposure for double-hit offspring began at 1-mo before the timepoints and lasted 4 wk (5 days/wk with 90-min exposure/day). We found double-hit offspring (Ecig:Ecig = exposure dam:offspring) sustained further blunted middle cerebral artery (MCA) reactivity, increased severity of neuronal damage, and increased interactions of astrocytes and endothelial cells compared with offspring with maternal (Ecig:Air) or direct (Air:Ecig) exposure only. Circulating extracellular vesicles (EVs) were increased, whereas sirtuin 1 (SIRT1) was decreased, in all Ecig-exposed groups compared with controls (Air:Air), with Ecig:Ecig group showing the greatest respective change for each. Electron paramagnetic resonance (EPR) spectroscopy revealed oxidative stress was the highest in the plasma of Ecig:Ecig group ( P < 0.05) than the other groups. These data show that a double-hit exposure in adolescent or adult offspring results in a greater decline in cerebrovascular function, biomarkers of neuronal dysfunction, and increased circulation of EVs compared with a single-hit exposure. NEW & NOTEWORTHY These data add to the growing body of literature demonstrating that electronic cigarette (Ecig) use during pregnancy (even without nicotine) is not safe, and primes offspring to have worse cardiovascular health outcomes in early and adult life. A key finding from this work is that a second insult from direct vaping in offspring with prior in utero exposure induces greater vascular dysfunction, increased oxidative stress, and shows evidence of neuronal dysfunction compared with either direct- or maternal-only exposure.

The long-term consequences of electronic cigarette (Ecig) use in humans are not yet known, but it is known that Ecig aerosols contain many toxic compounds of concern. We have recently shown that Ecig exposure impairs middle cerebral artery (MCA) endothelial function and that it takes 3 days for MCA reactivity to return to normal. However, the sources contributing to impairment of the endothelium were not investigated. We hypothesized that the increased levels of oxidative stress markers in the blood are correlated with impaired MCA reactivity. We used electron paramagnetic resonance (EPR) spectroscopy to examine plasma from 4-month-old male Sprague-Dawley rats that were exposed to either air (n = 5) or 1 h Ecig exposure, after which blood samples were collected at varying times after exposure (i.e., 1-4, 24, 48 and 72 h postexposure, n = 4 or 5 in each time group). The EPR analyses were performed using the redox-sensitive hydroxylamine spin probe 1-hydroxy-3-carboxymethyl-2,2,5,5-tetramethyl-pyrrolidine (CMH) to measure the level of reactive oxidant species in the plasma samples. We found that EPR signal intensity from the CM • radical was significantly increased in plasma at 1-4, 24 and 48 h (P < 0.05, respectively) and returned to control (air) levels by 72 h. When evaluating the EPR results with MCA reactivity, we found a significant negative correlation (Pearson's P = 0.0027). These data indicate that impaired cerebrovascular reactivity resulting from vaping is associated with the oxidative stress level (measured by EPR from plasma) and indicate that a single 1 h vaping session can negatively influence vascular health for up to 3 days after vaping. HIGHLIGHTS: What is the central question of this study? Does the time course of oxidative stress triggered by electronic cigarette exposure follow the cerebral vascular dysfunction? What is the main finding and its importance? Electron paramagnetic resonance analysis shows that the oxidative stress induced after a single 1 h exposure to electronic cigarette aerosol takes ≤72 h to return to normal, which mirrors the time course for vascular dysfunction in the middle cerebral artery that we have reported previously., (© 2024 The Author(s). Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

The ability of air pollution to induce acute exacerbation of asthma is well documented. However, the ability of ozone (O 3 ), the most reactive gaseous component of air pollution, to function as a modulator during sensitization is not well established. C57BL/6 J male mice were intranasally sensitized to house dust mite (HDM) (40 μg/kg) for 3 weeks on alternate days in parallel with once-a-week O 3 exposure (1 ppm). Mice were euthanized 24 h following the last HDM challenge. Lung lavage, histology, lung function (both forced oscillation and forced expiration-based), immune cell profiling, inflammation (pulmonary and systemic), and immunoglobulin production were assessed. Compared to HDM alone, HDM + O 3 leads to a significant increase in peribronchial inflammation (p < 0.01), perivascular inflammation (p < 0.001) and methacholine-provoked large airway hyperreactivity (p < 0.05). Serum total IgG and IgE and HDM-specific IgG1 were 3-5 times greater in HDM + O 3 co-exposure compared to PBS and O 3 -exposed groups. An increase in activated/mature lung total and monocyte-derived dendritic cells (p < 0.05) as well as T-activated, and T memory lymphocyte subset numbers (p < 0.05) were noted in the HDM + O 3 group compared to HDM alone group. Concurrent O 3 inhalation and HDM sensitization also caused significantly greater (p < 0.05) lung tissue interleukin-17 pathway gene expression and mediator levels in the serum. Redox imbalance was manifested by impaired lung antioxidant defense and increased oxidants. O 3 inhalation during allergic sensitization coalesces in generating a significantly worse T H 17 asthmatic phenotype., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Oxidative stress disorders and diseases caused by drug-resistant bacteria have emerged as significant public health concerns. Plant-based medications like protease inhibitors are growing despite adverse effects therapies. Consecutively, in this study, trypsin inhibitors from Dioscorea bulbifera L. (DbGTi trypsin inhibitor) ground tubers were isolated, purified, characterized, and evaluated for their potential cytotoxicity, antibacterial, and antioxidant activities. DbGTi protein was purified by Q-Sepharose matrix, followed by trypsin inhibitory activity. The molecular weight of the DbGTi protein was found to be approximately 31 kDa by SDS-PAGE electrophoresis. The secondary structure analysis by circular dichroism (CD) spectroscopy revealed that the DbGTi protein predominantly comprises β sheets followed by α helix. DbGTi protein showed competitive type of inhibition with V max  = 2.1372 × 10 -1  μM/min, K m  = 1.1805 × 10 2 μM, & K i  = 8.4 × 10 -9 M and was stable up to 70 °C. DbGTi protein exhibited 58 % similarity with Dioscorin protein isolated from Dioscorea alata L. as revealed by LC-MS/MS analysis. DbGTi protein showed a non-toxic effect, analyzed by MTT, Haemolytic assay and in vivo studies on zebrafish model. DbGTi protein significantly inhibited K. pneumoniae and has excellent antioxidant properties, confirmed by various antioxidant assays. The results of anti-microbial, cytotoxicity and antioxidant assays demonstrate its bioactive potential and non-toxic nature., Competing Interests: Declaration of competing interest There is no evidence that the authors have conflicting financial or social relationships, which may appear to bias the discoveries of this study., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Prosthetic joint infections (PJI) are associated with orthopaedic morbidity and mortality. Mitochondria, the "cell's powerhouses," are thought to play crucial roles in infection response and in increased risk of sepsis mortality. No current research discusses PJI's effect on mitochondrial function and a lack of understanding of immune-infection interactions potentially hinders patient care. The purpose of this pilot study was to evaluate the impact of simulated PJI on local tissue mitochondrial function. Using an established prosthetic implant-associated in vivo model, tissues were harvested from the surgical limb of a methicillin-sensitive Staphylococcus aureus implant-associated infection group (n = 6) and compared to a noninfected group (n = 6) at postoperative day (POD) 21. Using mitochondrial coupling assays, oxygen consumption rate and extracellular acidification rate were assessed in each group. Electron flow through mitochondrial complexes reflected group activity. Electron Paramagnetic Resonance (EPR) spectrometry measured the oxidizing potential of serum samples from infected versus noninfected groups. On POD21, colony-forming units per gram of tissue showed 5 × 10 9 in the infected group and 10 1 in the noninfected group (p < 0.0001). Maximal respiration and oxygen consumption due to adenosine triphosphate synthesis were significantly lower in isolated mitochondria from infected limbs (p = 0.04). Both groups had similar complex I, III, IV, and V activity (p > 0.1). Infected group EPR signal intensity reflecting reactive oxygen species levels was 1.31 ± 0.30 compared to 1.16 ± 0.28 (p = 0.73) in the noninfected group. This study highlights PJI's role in mammalian cell mitochondrial dysfunction and oxidative tissue damage, which can help develop interventions to combat PJI., (© 2023 The Authors. Journal of Orthopaedic Research ® published by Wiley Periodicals LLC on behalf of Orthopaedic Research Society.)

Recently, aqueous zinc-ion batteries (ZIBs) have become increasingly attractive as grid-scale energy storage solutions due to their safety, low cost, and environmental friendliness. However, severe dendrite growth, self-corrosion, hydrogen evolution, and irreversible side reactions occurring at Zn anodes often cause poor cyclability of ZIBs. This work develops a synergistic strategy to stabilize the Zn anode by introducing a molybdenum dioxide coating layer on Zn (MoO 2 @Zn) and Tween 80 as an electrolyte additive. Due to the redox capability and high electrical conductivity of MoO 2 , the coating layer can not only homogenize the surface electric field but also accommodate the Zn 2+ concentration field in the vicinity of the Zn anode, thereby regulating Zn 2+ ion distribution and inhibiting side reactions. MoO 2 coating can also significantly enhance surface hydrophilicity to improve the wetting of electrolyte on the Zn electrode. Meanwhile, Tween 80, a surfactant additive, acts as a corrosion inhibitor, preventing Zn corrosion and regulating Zn 2+ ion migration. Their combination can synergistically work to reduce the desolvation energy of hydrated Zn ions and stabilize the Zn anodes. Therefore, the symmetric cells of MoO 2 @Zn∥MoO 2 @Zn with optimal 1 mM Tween 80 additive in 1 M ZnSO 4 achieve exceptional cyclability over 6000 h at 1 mA cm -2 and stability (>700 h) even at a high current density (5 mA cm -2 ). When coupling with the VO 2 cathode, the full cell of MoO 2 @Zn∥VO 2 shows a higher capacity retention (82.4%) compared to Zn∥VO 2 (57.3%) after 1000 cycles at 5 A g -1 . This study suggests a synergistic strategy of combining surface modification and electrolyte engineering to design high-performance ZIBs.