Intracellular Antioxidant Enzymes Research Articles

Peroxiredoxin 3 deficiency exacerbates DSS-induced acute colitis via exosomal miR-1260b-mediated barrier disruption and pro-inflammatory signaling.

Peroxiredoxin3 (Prdx3) is an intracellular antioxidant enzyme that is specifically localized in mitochondria and protects against oxidative stress by removing mitochondrial reactive oxygen species (ROS). The intestinal epithelium provides a physical and biochemical barrier that segregates host tissues from commensal bacteria to maintain intestinal homeostasis. An imbalance between the cellular antioxidant defense system and oxidative stress has been implicated in the pathogenesis of inflammatory bowel disease (IBD). However, the role of Prdx3 in the intestinal epithelium under intestinal inflammation has not been elucidated. To investigate the potential role of Prdx3 in intestinal inflammation, we used intestinal epithelial cell (IEC)-specific Prdx3-knockout mice. IEC-specific Prdx3-deficient mice showed more severe colitis phenotypes with greater degrees of body weight loss, colon shortening, barrier disruption, mitochondrial damage, and ROS generation in IECs. Furthermore, exosomal miR-1260b was dramatically increased in Prdx3-knockdown colonic epithelial cells. Mechanistically, Prdx3 deficiency promoted intestinal barrier disruption and inflammation via P38-MAPK/NFκB signaling. this is the first study to report the protective role of Prdx3 in acute colitis using IEC-specific conditional knockout mice. our study sheds light on the role of exosome-loaded miRNAs, particularly miR-1260b, in IBD. targeting miR-1260b or modulating exosome-mediated intercellular communication may hold promise as potential therapeutic strategies for managing IBD and restoring intestinal barrier integrity.

The Effects and Safety of Silymarin on β-thalassemia in Children and Adolescents: A Systematic Review based on Clinical Trial Studies.

β-thalassemia imposes significant complications on affected patients. Silymarin, a natural flavonoid complex, has potential therapeutic properties. This systematic review aims to comprehensively evaluate the literature on the mechanistic effects of Silymarin on β-thalassemia outcomes in children and adolescents. A systematic search of electronic databases, including MEDLINE/PubMed, Embase, Scopus, Cochrane Library, and Web of Science (WOS), was done to identify relevant clinical trials before January 2024. Various data were extracted, including study characteristics, outcomes measured (hematological parameters, oxidative stress markers, iron metabolism, and other outcomes), proposed mechanisms, and safety. By iron chelation effects, Silymarin can reduce reactive oxygen species (ROS) production, increase intracellular antioxidant enzyme glutathione (GSH), and insert antioxidant effects. It also attenuated inflammation through reduced tumor necrosis factor-alpha (TNF-α), transforming growth factor-β1 (TGF-β1), interferon-gamma (IFNγ), C-reactive protein (CRP), interleukin 6 (IL-6), IL-17, and IL-23 levels and increase in IL-4 and IL-10 levels. By reducing iron overload conditions, Silymarin indicates modulatory effects on immune abnormalities, inhibits red blood cell (RBC) hemolysis, increases RBC count, and minimizes the need for a transfusion. Moreover, it reduces myocardial and hepatic siderosis, improves liver function tests, and modifies abnormal enzymes, particularly for aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), total bilirubin, and total protein levels. Silymarin also reduces iron overload, increases antioxidant and anti-inflammatory capacity in cardiomyocytes, and reveals antioxidant effects. Silymarin indicates promising effects on various aspects of children and adolescents with β-thalassemia and has no serious side effects on the investigated dosage.

Walnut protein isolate-epigallocatechin gallate nanoparticles: A functional carrier enhanced stability and antioxidant activity of lycopene

Walnut isolate protein (WPI)-epigallocatechin gallate (EGCG) conjugates can be employed to creat food-grade delivery systems for preserving bioactive compounds. In this study, WPI-EGCG nanoparticles (WENPs) were developed for encapsulating lycopene (LYC) using the ultrasound-assisted method. The results indicated successful loading of LYC into these WENPs, forming the WENPs/LYC (cylinder with 200–300 nm in length and 14.81–30.05 nm in diameter). Encapsulating LYC in WENPs led to a notable decrease in release rate and improved stability in terms of thermal, ultraviolet (UV), and storage conditions compared to free LYC. Simultaneously, WENPs/LYC exhibited a synergistic and significantly higher antioxidant activity with an EC50 value of 23.98 μg/mL in HepG2 cells compared to free LYC’s 31.54 μg/mL. Treatment with WENPs/LYC led to a dose-dependent restoration of intracellular antioxidant enzyme activities (SOD, CAT, and GSH-Px) and inhibition of intracellular malondialdehyde (MDA) formation. Furthermore, transcriptome analysis indicated that enrichment in glutathione metabolism and peroxisome processes following WENPs/LYC addition. Quantitative real-time reverse transcription PCR (qRT-PCR) verified the expression levels of related genes involved in the antioxidant resistance pathway of WENPs/LYC on AAPH-induced oxidative stress. This study offers novel perspectives into the antioxidant resistance pathway of WENPs/LYC, holding significant potential in food industry.

Metabolic effects of phospholipids extracted from capelin (Mallotus villosus) roe on HepG2 cells

This study aimed to evaluate the effects of capelin roe phospholipid (CPL) on lipid accumulation, fatty acid profile, oxidative stress, and changes in target macromolecular structure in HepG2 cells using multidimensional hyperspectral technique. The results showed that CPL significantly inhibited oleic acid-induced accumulation of intracellular lipids and increased the activity of intracellular antioxidant enzymes (CAT, GSH-Px, SOD). The control and CPL-treated groups promoted accumulation of unsaturated fatty acids and reduced deposition of saturated fatty acids. The therapeutic effects of CPL positively correlated with its concentration. Fourier transform infrared spectroscopy and two-dimensional correlation infrared analysis indicated that CPL decreased the relative contents of intracellular carbohydrate, nucleic acid, –CH2-, and ν(C=O)/νas (CH2+CH3), and maintained the order of intracellular protein structure. Fourier transform infrared spectroscopy could be used for label-free cell sorting. This work provided a direction for the subsequent development of functional lipids in aquaculture.

Kaempferia galanga (L.): An Updated Overview of In Vitro and In Vivo Antioxidant Properties

Kaempferia galanga L. (K. galanga) locally called aromatic ginger or “kencur" in Bahasa is traditionally for the treatment of various diseases related to antioxidants such as anti-inflammatory, anti-cancer, and immunomodulator. This paper aims to provide a critical review of the current antioxidant activity of K. galanga using in vitro and in vivo assays. The information and data of K. galanga were collected from various resources such as Scopus, PubMed, Science Direct, and Google Scholar. The results showed that K. galanga plays a role in defense systems against oxidative stress. Several in vitro assays have been used to measure the antioxidant activity of K. galanga, namely,1-diphenyl-2-picrylhydrazyl (DPPH), ferric reduction of antioxidant power (FRAP), 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid (ABTS). Whereas, the parameter in vivo antioxidant assay of K galanga including lifespan, survival life, intracellular reactive oxygen species (ROS) level, malondialdehyde (MDA) level, and antioxidant enzyme activities: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Based on the findings, it can be indicated that K. galanga has powerful antioxidant activities and, therefore could have the potential as a natural antioxidant.

Anticandidal Activity of a Siderophore from Marine Endophyte Pseudomonas aeruginosa Mgrv7.

An endophytic symbiont P. aeruginosa-producing anticandidal siderophore was recovered from mangrove leaves for the first time. Production was optimal in a succinate medium supplemented with 0.4% citric acid and 15 µM iron at pH 7 and 35 °C after 60 h of fermentation. UV spectra of the acidic preparation after purification with Amberlite XAD-4 resin gave a peak at 400 nm, while the neutralized form gave a peak at 360 nm. A prominent peak with RP-HPLC was obtained at RT 18.95 min, confirming its homogeneity. It was pH stable at 5.0-9.5 and thermally stable at elevated temperatures, which encourages the possibility of its application in extreme environments. The minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) against Candida spp. Were in the range of 128 µg/mL and lower. It enhanced the intracellular iron accumulation with 3.2-4.2-fold (as judged by atomic absorption spectrometry) with a subsequent increase in the intracellular antioxidative enzymes SOD and CAT. Furthermore, the malondialdehyde (MDA) concentration due to cellular lipid peroxidation increased to 3.8-fold and 7.3-fold in C. albicans and C. tropicalis, respectively. The scanning electron microscope (SEM) confirmed cellular damage in the form of roughness, malformation, and production of defensive exopolysaccharides and/or proteins after exposure to siderophore. In conclusion, this anticandidal siderophore may be a promising biocontrol, nonpolluting agent against waterborne pathogens and pathogens of the skin. It indirectly kills Candida spp. by ferroptosis and mediation of hyperaccumulation of iron rather than directly attacking the cell targets, which triggers the activation of antioxidative enzymes.

Protective Mechanism of Rosa roxburghii Tratt Fermentation Broth against Ultraviolet-A-Induced Photoaging of Human Embryonic Skin Fibroblasts.

This study takes the fruit of Rosa roxburghii Tratt (RRT) as a fermentation substrate and carries out a quantitative visual analysis of the domestic and foreign literature on screenings of five different lactic acid bacteria to obtain a fermentation broth. Systemic anti-photoaging effects are analyzed at the biochemical, cellular, and molecular biological levels. DPPH and ABTS free radical scavenging activities are used to verify the antioxidant capacity of the RRT fruit fermentation broth in vitro. Human embryonic skin fibroblasts (HESs) are used to establish a UVA damage model, and the antioxidant capacity of the RRT fruit fermentation broth is verified in terms of intracellular reactive oxygen species (ROS) and antioxidant enzyme activity. RT-qPCR and ELISA are used to detect the expression of TGF-β/Smad, MMPs, and the MAPK/AP-1 and Nrf2/Keap-1 signaling pathways in order to explore the anti-oxidation and anti-photoaging effects of the RRT fruit fermentation broth by regulating different signaling pathways. The results show that an RRT fruit fermentation broth can effectively protect cells from oxidative stress caused by UVA and has significant anti-photoaging effects, with the co-cultured Lactobacillus Yogurt Starter LYS-20297 having the highest overall effect.

Aging effects of titanium dioxide on Cu toxicity to Daphnia magna: Exploring molecular docking and significance of surface properties

Cosmetics and personal care products containing titanium dioxide nanoparticles (TiO2 NPs) may enter aquatic environments, where the surface coatings of TiO2 NPs may change with aging due to environmental factors such as light, and potentially affect their bioaccumulation and toxicity. This study examined how aging impacted the physicochemical properties of three commercially available TiO2 NPs and subsequent influence on the bioaccumulation and toxicity of copper (Cu) in Daphnia magna (D. magna). We demonstrated that aging significantly affected the hydrophobicity of TiO2 NPs, which affected their binding to water molecules and adsorption of Cu. Changes of bioaccumulation of TiO2 NPs and Cu in D. magna ultimately affected the activities of intracellular antioxidant enzymes such as SOD, CAT, GSH-Px, and the transmembrane protein Na+/K+–ATPase. Molecular docking calculations demonstrated that changes of activities of these biological enzymes were due to the interaction between TiO2 NPs, Cu, and amino acid residues near the sites with the lowest binding energy and active center of the enzyme. Such effect was closely related to the hydrophobicity of TiO2 NPs. Our study demonstrated the close relationship between surface properties of TiO2 NPs and their biological effects, providing important evidence for understanding the behavior of nanomaterials in aquatic environments.

Nb2CTx MXene coating with inhibition of oxidative stress prepared by Marangoni effect for hemodialysis therapy

Oxidative stress is an important risk factor for end-stage renal disease (ESRD), that can further aggravate the disease during dialysis of patients and eventually lead to various complications. Here, Nb2CTx MXene was deposited using the Marangoni force to tightly stack them on the polyvinylidene fluoride (PVDF) substrate membrane, conferring the alleviation of oxidative stress. Owing to the excellent antioxidant activity of Nb2CTx MXenes, PVDF/Nb2CTx membranes can scavenge a wide range of reactive oxygen species (ROS) to inhibit advanced glycation end-products (AGEs). Additionally, the functionalized membranes modulated the intracellular antioxidant enzyme activity and maintained an intracellular oxidative-antioxidant system balance. In the simulated dialysis experiment, the optimised hemodialysis membrane (MMX-0.2 membrane) exhibited the high clearance of middle and small uraemic toxins (72.6% of lysozyme and 90.0% of urea) owing to the unique lamellar structure of Nb2CTx. Protein adhesion experiments showed that Nb2CTx MXenes improved membrane hydrophilicity and hindered protein adsorption. The functionalized membranes exhibited excellent hemocompatibility and cytocompatibility, meeting the biocompatibility requirements for hemodialysis membranes. In this work constructed PVDF/Nb2CTx functionalized membranes with excellent oxidative stress inhibition and high dialysis performance are proposed as a novel hemodialysis membrane preparation method to improve patient prognosis.

Feasibility and mechanism of removing Microcystis aeruginosa and degrading microcystin-LR by dielectric barrier discharge plasma

Harmful cyanobacterial bloom is one of the serious environmental problems worldwide. Microcystis aeruginosa is a representative harmful alga in cyanobacteria bloom. It is of great significance to develop new technologies for the removal of Microcystis aeruginosa and microcystins. The feasibility and mechanism of removing microcystis aeruginosa and degrading microcystins by dielectric barrier discharge (DBD) plasma were studied. The suitable DBD parameters obtained in this study are DBD (41.5 W, 40 min) and DBD (41.5 W, 50 min), resulting in algae removal efficiency of 77.4% and 80.4%, respectively; scanning electron microscope and LIVE-DEATH analysis demonstrate that DBD treatment can disrupt cell structure and lead to cell death; analysis of elemental composition and chemical state indicated that there are traces of oxidation of organic nitrogen and organic carbon in microcystis aeruginosa; further intracellular ROS concentration and antioxidant enzyme activity analysis confirm that DBD damage microcystis aeruginosa through oxidation. Meanwhile, DBD can effectively degrade the microcystin-LR released after cell lysis, the extracellular microcystin-LR concentration in the DBD (41.5 W) group decreased by 88.7% at 60 min compared to the highest concentration at 20 min; further toxicity analysis of degradation intermediates indicated that DBD can reduce the toxicity of microcystin-LR. The contribution of active substances to the inactivation of microcystis aeruginosa is eaq− >•OH > H2O2 > O3 > 1O2 >•O2− >ONOO−, while on the degradation of microcystin-LR is eaq− >•OH > H2O2 > O3 >•O2− >1O2 > ONOO−. The application of DBD plasma technology in microcystis aeruginosa algae removal and detoxification has certain prospects for promotion and application.

Programmed microalgae-gel promotes chronic wound healing in diabetes

Chronic diabetic wounds are at lifelong risk of developing diabetic foot ulcers owing to severe hypoxia, excessive reactive oxygen species (ROS), a complex inflammatory microenvironment, and the potential for bacterial infection. Here we develop a programmed treatment strategy employing live Haematococcus (HEA). By modulating light intensity, HEA can be programmed to perform a variety of functions, such as antibacterial activity, oxygen supply, ROS scavenging, and immune regulation, suggesting its potential for use in programmed therapy. Under high light intensity (658 nm, 0.5 W/cm2), green HEA (GHEA) with efficient photothermal conversion mediate wound surface disinfection. By decreasing the light intensity (658 nm, 0.1 W/cm2), the photosynthetic system of GHEA can continuously produce oxygen, effectively resolving the problems of hypoxia and promoting vascular regeneration. Continuous light irradiation induces astaxanthin (AST) accumulation in HEA cells, resulting in a gradual transformation from a green to red hue (RHEA). RHEA effectively scavenges excess ROS, enhances the expression of intracellular antioxidant enzymes, and directs polarization to M2 macrophages by secreting AST vesicles via exosomes. The living HEA hydrogel can sterilize and enhance cell proliferation and migration and promote neoangiogenesis, which could improve infected diabetic wound healing in female mice.

In vitro evaluation of antioxidant potential of polysaccharides and oligosaccharides extracted from three different seaweeds.

Bioactive polysaccharides and oligosaccharides were successfully extracted from three distinct seaweeds: Sargassum sp., Graciallaria sp., and Ulva sp. utilizing various extraction techniques. The obtained polysaccharides and oligosaccharides were subjected to comprehensive characterization, and their potential antioxidant properties were assessed using a Hep G2 cell model. Analysis via FTIR spectroscopy unveiled the presence of sulfate groups in the polysaccharides and oligosaccharides derived from Sargassum sp. The antioxidant capabilities were assessed through various assays (DPPH, ABTS, Fe-ion chelation, and reducing power), revealing that SAR-OSC exhibited superior antioxidant activity than others. This was attributed to its higher phenolic content (24.6μg/mg), FRAP value (36μM Vitamin C/g of extract), and relatively low molecular weight (5.17kDa). The study also investigated the protective effects of these polysaccharides and oligosaccharides against oxidative stress-induced damage in Hep G2 cells by measuring ROS production and intracellular antioxidant enzyme expressions (SOD, GPx, and CAT). Remarkably, SAR-OSC demonstrated the highest efficacy in protecting Hep G2 cells reducing ROS production and downregulating SOD, GPx, and CAT expressions. Current findings have confirmed that the oligosaccharides extracted by the chemical method show higher antioxidant activity, particularly SAR-OSC, and robust protective abilities in the Hep G2 cells.

Oxyphenbutazone ameliorates carfilzomib induced cardiotoxicity in rats via inhibition of oxidative free radical burst and NF-κB/IκB-α pathway

Carfilzomib (CFZ), a chemotherapeutic agent used for multiple myeloma treatments reported to cause high incidence of cardiac events either new onset and/or exacerbate formerly diagnosed heart failure with ventricular and myocardial dysfunction.Purpose: Current research designed to explore and examine the preventive effect of oxyphenbutazone in the CFZ -instigated cardiotoxicity. Methodology: Female Wistar Rats weighing 200–250 g selected randomly and grouped as follows: Group 1 designated as the Normal control and receive normal saline only. Group 2 served toxic control and exposed to CFZ (4 mg/kg, intraperitoneally [i.p.]). Group 3 & 4 served as treatment groups and administered with CFZ concomitantly orally fed with oxyphenbutazone at doses of 35 and 70 mg/kg/three times a week, respectively. The total duration of experimental protocol was of 21 days. After completion of the experiments animals subjected to blood collection using light ether anesthesia and serum was separated for biochemical analysis further. The serum levels of Mg+2, Ca+2 and cardiac enzymes (aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase-MB (CK-MB) levels were estimated. Later animals sacrificed and heart tissue isolated for further examinations. Intracellular proteins NFkB and IkBα were estimated by western blot. Results: The serum analysis revealed that CFZ administration significantly elevated the levels of LDH, CK and CKMB in CFZ exposed animals when compared to normal animals while administration of oxyphenbutazone significantly reduced these biochemical changes, Intracellular antioxidant enzymes and NF-kB in treatment groups as compared to disease control animals. Conclusion: Findings of the research protocol suggests significant injuries to cardiac tissues when animals exposed to CFZ and Oxyphenbutazone protected the cardiac tissues.

Niacin treatment prevents bone loss in iron overload osteoporotic rats via activation of SIRT1 signaling pathway

Recently, more and more studies have revealed that iron overload can lead to osteoporosis by inducing oxidative stress. Niacin (NAN), also known as nicotinate or vitamin B3, has been confirmed to possess potent antioxidative effects. In addition, very little is currently known about the protective effects of NAN on iron overload in osteoporotic bone tissue. Therefore, we aimed to evaluate the protective effect of niacin on iron overload-induced bone injury and to investigate the effect and underlying mechanisms of the niacin and iron overload on intracellular antioxidant properties. When MC3T3-E1 and RAW264.7 cells were cultured in the presence of ammonium ferric citrate(FAC), NAN therapy could increase the matrix mineralization and promote expression of osteogenic markers in MC3T3-E1, inhibit osteoclastic differentiation of RAW264.7 cells, while increasing intracellular reactive oxygen species (ROS) levels and strengthening mitochondrial membrane potential (MMP). In the ovariectomized (OVX) rat model, NAN had an obvious protective effect against iron-overloaded injury. Meanwhile, superoxide dismutase 2 (SOD2), intracellular antioxidant enzymes and silent information regulator type 1 (SIRT1), were up-regulated in response to NAN exposures in MC3T3-E1. Furthermore, SIRT1 inhibitor EX527 attenuated the protective effects of NAN. Results revealed that NAN could stimulate osteogenic differentiation, inhibit osteoclastic differentiation and markedly increased antioxidant properties in cells through the induction of SIRT1. Studies suggest that niacin is a promising agent for preventing bone loss in iron overload conditions.

Effects of Two Different Self-Paced Training Modalities on the Aerobic Fitness Levels, Psychophysiological Responses, and Antioxidant Status in Physically Active Young Adults

This study aims to investigate the effects of self-paced high-intensity interval training (Sp-HIIT) vs. self-paced moderate-intensity continuous training (Sp-MICT) on aerobic fitness levels, psychophysiological responses, and antioxidant status to assess the relationship between aerobic fitness levels and antioxidant markers. Physically active young adults were randomised into Sp-HIIT and Sp-MICT groups. The intervention consisted of three weekly sessions during an eight-week period. Sp-HIIT consisted of performing two sets of 12–24 × 30 s high-intensity runs ≥ 85% HRmax followed by 30 s rest periods, while Sp-MICT consisted of performing 24–48 min of continuous running at 60–75% HRmax. Pre- and post-intervention testing included a maximal oxygen uptake (VO2max) assessment during a 30-15 intermittent fitness test (30-15 IFT), as well as resting blood samples, which were analysed for oxidative stress markers (malondialdehyde (MDA)) and activity of intracellular antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD) and reduced (GSH) and oxidized glutathione (GSSG)). The Sp-HIIT group showed a greater improvement in velocity of 30-15 IFT, VO2max, and MDA responses. Furthermore, the Sp-HIIT group demonstrated higher psychophysiological responses than the Sp-MICT group, except for anger responses. In conclusion, these results suggest that Sp-HIIT has a higher level of beneficial exercise-induced effects in physiological responses with greater perceived exertion in physically active young adults.

Inhibition of FSP1 impairs early embryo developmental competence in pigs

Ferroptosis suppressor protein 1 (FSP1) is a glutathione-independent ferroptosis inhibitory factor. FSP1 has been found to play a crucial role in the regulation of mitochondrial function and ferroptosis. However, its function in porcine early embryonic development remains unknown. In the present research, we found that FSP1 was expressed at different stages during porcine early embryo development. Compared with the control condition, inhibition of FSP1 reduced the cleavage rate at 24 h and 48 h and the blastocyst rate at 144 h. In addition, inhibiting FSP1 reduced the blastocyst diameter, total cell number, and proliferation capacity. Further analysis showed that inhibition of FSP1 significantly increased the levels of ferrous ions (Fe2+) and MDA but not GPX4. We also found that inhibition of FSP1 significantly decreased mitochondrial membrane potential and ATP levels, which in turn caused excessive accumulation of ROS and decreased the levels of GSH and the activity of the intracellular antioxidant enzymes SOD and CAT in embryos. In conclusion, FSP1, an important regulator, participates in regulating the development and quality of porcine early embryos. Inhibition of FSP1 impairs blastocyst formation, induces glutathione-independent ferroptosis, and further leads to oxidative stress due to mitochondrial dysfunction, ultimately affecting the developmental competence and impairing the quality of porcine early embryos.

Identification of novel antioxidant collagen peptides for preventing and treating H2 O2 -induced oxidative stress in HepG2 cells through in vitro and in silico approaches.

Nowadays, the prevalence of oxidative stress-related chronic diseases is increasing. The identification of novel antioxidant collagen peptides to counteract oxidative stress for individuals' health has gained significant attention. In this study, collagen peptides with antioxidant activities were separated and identified by ion chromatography, reversed-phase high-performance liquid chromatography and liquid chromatography-tandem mass spectrometry. The identified antioxidant collagen peptides were further screened by molecular docking for Keap1-targeted peptide inhibitors and their theoretical interaction mechanisms were investigated. Four novel antioxidant collagen peptides, GPAGPIGPVG, GPAGPpGPIG, ISGPpGPpGPA and IDGRPGPIGPA, with high binding affinity to Keap1 were selected. Molecular docking results demonstrated that the putative antioxidant mechanism of the four antioxidant collagen peptides contributed to their blockage of Keap1-Nrf2 interactions. The results of antioxidant activity of the four antioxidant collagen peptides proved that IDGRPGPIGPA exerted a high scavenging capacity for DPPH and ABTS free radicals, while GPAGPpGPIG improved the resistance of cells to hydrogen peroxide-induced oxidative damage by promoting the activation of intracellular antioxidant enzymes and the production of reduced glutathione in human hepatoma (HepG2) cells. The antioxidant collagen peptides (GPAGPIGPVG, GPAGPpGPIG, ISGPpGPpGPA and IDGRPGPIGPA) will be developed as novel functional food for human health in the near future. © 2023 Society of Chemical Industry.

Investigative on the molecular mechanism of novel antioxidation peptides by 3D-QSAR, in vitro assay and MD simulations

Three novel antioxidant peptides MHW, YHW and FHW were designed by the analysis of 3D-QSAR. Two accurate CoMFA (Q2 = 0.886 and R2 = 0.988) and CoMSIA (Q2 = 0.737 and R2 = 0.955) models were established. The FTC assay showed that activities of the new peptides on lipid peroxidation is significantly better than that of the template molecule LHW. The results of erythrocyte hemolysis assay demonstrated that MHW, YHW and FHW significantly inhibited AAPH-induced erythrocyte hemolysis by scavenging free radicals at the cellular level. It caused the restoration of intracellular antioxidant enzyme (GSH, CAT and SOD) activities at an acceptable pace and the silencing of intracellular MDA formation. Furthermore, MTT toxicity assay showed that the novel antioxidant peptides had good biocompatibility and no cytotoxicity. Molecular docking and molecular dynamics simulations were used to investigate the molecular mechanism. The results showed that Ser363, Arg380, Asn414 and Arg415 residues played key roles in the antioxidant activity of MHW, YHW and FHW. And they mainly binded to the important residues of Keap1 protein stably by electrostatic force, van der Waals force, H-bonds and hydrophobic interactions, which can better fit the Kelch pocket structural domain of Keap1. Therefore, MHW, YHW and FHW had strong potential to interfere with Keap1-Nrf2 interaction and promoted the enzymatic expression of Nrf2-ARE downstream target pathway.

Quercetin attenuates avermectin-induced cardiac injury in carp through inflammation, oxidative stress, apoptosis and autophagy

As an important antibiotic, avermectin (AVM) has been widely used in China, but its unreasonable application has caused serious harm to the water environment. In view of the various pharmacological effects of quercetin (QUE), such as anti-inflammatory and antioxidant, the scientific hypothesis that “QUE may cause carp poisoning by inhibiting AVM” was proposed in this study. However, its protective effect in AVM -induced heart damage has not been reported. QUE reduced the symptoms of AVM toxicity and decreased the levels of creatine kinase, lactate dehydrogenase, and creatine kinase in the serum of carp. By histological observation, QUE was found to significantly reduce cardiac fiber swelling in carp. A DHE fluorescence probe study showed that QUE was able to inhibit AVM -induced accumulation of reactive oxygen species (ROS) in carp myocardium. We found that QUE significantly increased the intracellular antioxidant enzymes CAT, T-AOC and GSH enzyme activity and reduced intracellular MDA content. In addition, QUE significantly increased il-10 and tgf-β1 expression, and significantly down-regulated tnf-α, il-6, il-1β and inos expression. Tunel assay showed that QUE attenuated AVM -induced apoptosis, significantly decreased the transcript levels of pro-apoptosis-related genes, and increased the expression of anti-apoptosis-related genes. We also detected the protein expression of LC3 in the AVM group and QUE + AVM group, and found that the expression of LC3 was significantly increased in both groups compared with the Control group, but after adding QUE, the expression of LC3 was significantly decreased compared with the AVM group. In addition, the transcript levels of p62 and atg5 were also detected by qPCR. QUE significantly increased the expression of p62 and decreased the expression of atg5, suggesting that QUE could attenuate AVM -induced cardiac autophagy in carp. This study will provide preliminary evidence of the principle of QUE attenuating AVM -induced myocardial injury in carp from four aspects, including oxidative stress, inflammatory response, apoptosis and autophagy, and provide a theoretical basis for its prevention and treatment.

Study on the antioxidant activity of peptides from soybean meal by fermentation based on the chemical method and AAPH-induced oxidative stress.

Preparation and antioxidant activities of soybean peptides using solid fermentation to decrease the content of trypsin inhibitor (TI) and antigen protein were investigated in this study. The results showed the optimal fermentation conditions were as follows: fermentation time 48 h, the ratio of material to solvent 1:2, inoculum size 12%, and the ratio of Lactic acid bacteria and Aspergillus oryzae 2:1. The hydrolysate was were divided into four components of <1, 1-3, 3-5, and >5 kDa by ultrafiltration based on molecular weight, and the <1 kDa peptides expressed the highest antioxidant activities. Meanwhile, the cell antioxidant activity of the <1 kDa soybean peptides was investigated using AAPH-induced erythrocyte hemolysis, which effectively inhibited erythrocyte hemolysis with the inhibit rate of 85.8% through inhibition of the ROS intracellular generation. In addition, soybean peptides could significantly restore the intracellular antioxidant enzymes (SOD, GSH-Px, and CAT) activities, as well as inhibited intracellular MDA generation and depletion of GSH. The intracellular antioxidant detoxifying mechanism of soybean peptides was associated with both non-enzymatic and enzymatic defense systems. According to this study, fermentation could effectively improve the antioxidant activities of soybean peptides.