Increased Glutathione Peroxidase Research Articles

Berberine alleviates ovarian tissue damage in mice with hepatolenticular degeneration by suppressing ferroptosis and endoplasmic reticulum stress

ObjectiveHepatolenticular degeneration (HLD) is an autosomal recessive disorder that manifests as multiorgan damage due to impaired copper (Cu) metabolism. Female patients with HLD often experience reproductive impairments. This study investigated the protective effect of berberine against ovarian damage in toxic-milk (TX) mice, a murine model for HLD. MethodsMice were categorized into control group, HLD TX group (HLD group), penicillamine (Cu chelator)-treated TX group and berberine-treated TX group. Body weight, ovary weight and the number of ovulated eggs were recorded. Follicular morphology and cellular ultrastructure were examined. Total iron, ferrous iron (Fe2+) and trivalent iron (Fe3+) levels, as well as malondialdehyde (MDA), glutathione (GSH) and oxidized glutathione (GSSG), were measured in the ovaries. Western blot analysis was used to analyze the expression of proteins related to ferroptosis and endoplasmic reticulum (ER) stress. ResultsOvarian tissue damage was evident in the HLD group, with a significant increase in ferroptosis and ER stress compared to the control group. This damage was inhibited by treatment with penicillamine, a Cu chelator. Compared with the HLD group, berberine increased the number of ovulations, and improved ovarian morphology and ultrastructure. Further, we found that berberine reduced total iron, Fe2+, MDA and GSSG levels, elevated GSH levels, decreased the expression of the ferroptosis marker protein prostaglandin-endoperoxide synthase 2 (PTGS2), and increased glutathione peroxidase 4 (GPX4) expression. Furthermore, berberine inhibited the expression of ER stress-associated proteins mediated by the protein kinase RNA-like ER kinase (PERK) pathway. ConclusionFerroptosis and ER stress are involved in Cu-induced ovarian damage in TX mice. Berberine ameliorates ovarian damage in HLD TX mice by inhibiting ferroptosis and ER stress.Please cite this article as: Liu QZ, Han H, Fang XR, Wang LY, Zhao D, Yin MZ, Zhang N, Jiang PY, Ji ZH, Wu LM. Berberine alleviates ovarian tissue damage in mice with hepatolenticular degeneration by suppressing ferroptosis and endoplasmic reticulum stress. J Integr Med. 2024; 22(4): 494–503.

Anti-Vasculogenic, Antioxidant, and Anti-Inflammatory Activities of Sulfated Polysaccharide Derived from Codium tomentosum: Pharmacokinetic Assay.

The purpose of this paper was to investigate the anti-inflammatory and anti-angiogenic activities of sulfated polysaccharide from C. tomentosum (PCT) using carrageenan (CARR)-induced paw edema in a rat model and anti-vasculogenic activity on a chorioallantoic membrane assay (CAM) model. Based on in vitro tests of anti-radical, total antioxidant, and reducing power activities, PCT presents a real interest via its antioxidant activity and ability to scavenge radical species. The in vivo pharmacological tests suggest that PCT possesses anti-inflammatory action by reducing paw edema and leukocyte migration, maintaining the redox equilibrium, and stabilizing the cellular level of several pro-/antioxidant system markers. It could significantly decrease the malondialdehyde levels and increase superoxide dismutase, glutathione peroxidase, and glutathione activities in local paw edema and erythrocytes during the acute inflammatory reaction of CARR. PCT pretreatment was effective against DNA alterations in the blood lymphocytes of inflamed rats and reduced the hematological alteration by restoring blood parameters to normal levels. The anti-angiogenic activity results revealed that CAM neovascularization, defined as the formation of new vessel numbers and branching patterns, was decreased by PCT in a dose-dependent manner, which supported the in silico bioavailability and pharmacokinetic findings. These results indicated the therapeutic effects of polysaccharides from C. tomentosum and their possible use as anti-proliferative molecules based on their antioxidant, anti-inflammatory, and anti-angiogenic activities.

Peroxynitrite-Triggered Carbon Monoxide Donor Improves Ischemic Stroke Outcome by Inhibiting Neuronal Apoptosis and Ferroptosis.

Cerebral ischemia-reperfusion injury produces excessive reactive oxygen and nitrogen species, including superoxide, nitric oxide, and peroxynitrite (ONOO-). We recently developed a new ONOO--triggered metal-free carbon monoxide donor (PCOD585), exhibiting a notable neuroprotective outcome on the rat middle cerebral artery occlusion model and rendering an exciting intervention opportunity toward ischemia-induced brain injuries. However, its therapeutic mechanism still needs to be addressed. In the pharmacological study, we found PCOD585 inhibited neuronal Bcl2/Bax/caspase-3 apoptosis pathway in the peri-infarcted area of stroke by scavenging ONOO-. ONOO- scavenging further led to decreased Acyl-CoA synthetase long-chain family member 4 and increased glutathione peroxidase 4, to minimize lipoperoxidation. Additionally, the carbon monoxide release upon the ONOO- reaction with PCOD585 further inhibited the neuronal Iron-dependent ferroptosis associated with ischemia-reperfusion. Such a synergistic neuroprotective mechanism of PCOD585 yields as potent a neuroprotective effect as Edaravone. Additionally, PCOD585 penetrates the blood-brain barrier and reduces the degradation of zonula occludens-1 by inhibiting matrix metalloproteinase-9, thereby protecting the integrity of the blood-brain barrier. Our study provides a new perspective for developing multi-functional compounds to treat ischemic stroke.

Glutathione‐induced hydrogen sulfide enhances drought tolerance in sweet pepper (Capsicum annuum L.)

AbstractGlutathione (GSH) has been studied for its potential to enhance stress tolerance in plant systems, but the role of hydrogen sulfide (H2S) in GSH‐induced water stress tolerance in sweet pepper (Capsicum annuum L.) is still under investigation. This study explores how H2S and GSH modulate water stress tolerance in pepper plants, addressing a research gap. The joint effect of sodium hydrosulfide (NaHS), a donor of H2S, and GSH on water stress tolerance was determined through pre‐treatment with the H2S scavenger 0.1 mM hypotaurine (HT). Pepper seedlings were sprayed with 1.0 mM GSH or GSH + 0.2 mM NaHS once a week, with soil moisture content set at 80% and 40% for full irrigation and water stress conditions for a duration of 2 weeks. The results showed that water stress significantly reduced total plant dry weight, chlorophyll a and b content, Fv/Fm, leaf water potential, and relative water content by 50%, 56%, 33%, 27%, 52%, and 34%, while increasing hydrogen peroxide (H2O2), proline, and H2S levels by 152%, 134%, and77%, respectively. Treatment with GSH and NaHS reduced water stress‐induced H2O2 production and improved plant growth, photosynthetic traits, proline, and the activity of L‐cysteine desulfhydrase (L‐DES), leading to the generation of H2S content. GSH reduced NADPH oxidase (NOX), superoxide dismutase (SOD), and H2O2 but increased glutathione peroxidase (GPX) activities. The interaction of NaHS and GSH led to further reductions in NOX, SOD, and H2O2 values but increased GPX activity. The combined GSH and NaHS treatment increased nitric oxide (NO) production but decreased the activity of S‐nitrosoglutathione reductase (GSNOR), potentially accelerating S‐nitrosylation. Hypotaurine negated the positive impacts of GSH on water stress tolerance by reducing H2S concentration in pepper plants, but this was corrected by the concurrent application of NaHS and GSH + HT. Therefore, water stress tolerance requires H2S.

Lipid Dysregulation Induced by Gasoline and Diesel Exhaust Exposure and the Interaction with Age.

Limited knowledge exists regarding gasoline and diesel exhaust effects on lipid metabolism. This study collected gasoline and diesel exhaust under actual driving conditions and conducted inhalation exposure on male young and middle-aged C57BL/6J mice for 4 h/day for 5 days to simulate commuting exposure intensity. Additionally, PM2.5 from actual roadways, representing gasoline and diesel vehicles, was generated for exposure to human umbilical vein endothelial cells (HUVECs) and normal liver cells (LO2) for 24, 48, and 72 h to further investigate exhaust particle toxicity. Results showed that diesel exhaust reduced total cholesterol and low-density lipoprotein cholesterol levels in young mice, indicating disrupted lipid metabolism. Aspartate aminotransferase and alanine aminotransferase levels increased by 53.7% and 21.7%, respectively, suggesting potential liver injury. Diesel exhaust exposure decreased superoxide dismutase and increased glutathione peroxidase levels. Cell viability decreased, and reactive oxygen species levels increased in HUVECs and LO2 following exposure to exhaust particles, with dose- and time-dependent effects. Diesel exhaust particles exhibited more severe inhibition of cell proliferation and oxidative damage compared to gasoline exhaust particles. These findings provide novel evidence of the risk of disrupted lipid metabolism due to gasoline and diesel exhaust, emphasizing the toxicity of diesel exhaust.

Curcumin mitigates ochratoxin A-induced oxidative stress and alters gene expression inbroiler chicken liver and kidney.

The study aimed to evaluate the effect of curcumin (CURC) supplementation on broiler chickens exposed to ochratoxin A (OTA), by examining biochemical parameters and the expression of glutathione redox system genes and their regulation. OTA reduced glutathione content in the liver while increasing glutathione peroxidase activity. CURC showed no significant effects. Kidney parameters remained mostly unaffected. Gene expression analysis revealed OTA-induced upregulation of KEAP1, NRF2, AHR, GPx4 and GSR genes in the liver. CURC supplementation led to the upregulation of GPx4and AHR genes with OTA+CURC treatment, resulting in the downregulation of GPx4, KEAP1, NRF2 and AHR genes compared to OTA treatment alone. In the kidney, GPx4 was downregulated, andNRF2and AHR were upregulated as an effect of OTA, while CURC upregulated the NRF2 gene only. OTA+CURC treatment led to the downregulation of GPx4, GSS and AHR genes compared to the control and downregulation of NRF2 and AHR genes compared to OTA. The results suggested that CURC is partly effective against OTA-induced oxidative stress and that the effect of OTA and CURC on the antioxidant response is regulated through the KEAP1-NRF2-ARE and AHR pathways.

Antioxidant Effects of Selenium Nanoparticles Prepared from Eruca Sativa Extract on Ketoconazole –Induced Testicular Oxidative Damage in Male Rats

Background: Recent studies have shown that the anti-fertility effects of Ketoconazole can be minimized by taking an antioxidant nanoparticles based-plant extract in combination with the medication or by taking it after medication. One of the effective methods to improve its medicinal properties and decrease the toxicities of Selenium is by formulating it as nanoparticles. However, this is still a challenging strategy. Objectives: The aim of this study was to analyze the impact of nano selenium, which was prepared from Eruca Sativa extract, on testicular oxidative stress parameters in rats that were treated with ketoconazole. The study will focus on the evaluation of glutathione peroxidase, superoxide dismutase, and malondialdehyde as indicators of oxidative stress. Methods: In this study, a 1% w/v solution of plant extract was added to a solution of 10mM sodium selenite in different ratios, and placed on a magnetic stirrer in the dark for 12 hours at a temperature 50Cº and pH9. The solution was then left for 48 hours, and the optimal fabricated selenium nanoparticles were selected for further characterization. forty-eight rats were divided into six groups with eight animals in each. Group A was the negative control, while Group B was given oral Ketoconazole at a dose of 50mg/kg for fourteen days. Group BC, BD, BE1 and BE2 were given oral Ketoconazole at a dose of 50 mg/kg for fourteen days, followed by 200mg/kg Eruca Sativa, 0.5mg/kg oral sodium selenite, 0.25mg/kg oral nano selenium and 0.5mg/kg oral nano selenium for 28 days, respectively. Finally, the animals were euthanized and their testicle anti-oxidant parameters were evaluated. Results: Significant increases in glutathione peroxidase and superoxide dismutase ( p value < 0.001), and a decrease in malondialdehyde levels ( p value < 0.001) were observed in groups treated with nanoparticles compared to control group. Conclusion: Nano forms of prepared by Eruca sativa extract exhibit significant antioxidant effects on testicular tissues, while being available for several metabolic, biological, and physiological functions.

Protective Role of Dioscin against Doxorubicin-Induced Chronic Cardiotoxicity: Insights from Nrf2-GPX4 Axis-Mediated Cardiac Ferroptosis.

Recent evidence suggests that ferroptosis, an iron-facilitated cell death with excessive lipid peroxidation, is a critical mechanism underlying doxorubicin (DOX)-induced cardiotoxicity (DIC). Although dioscin has been reported to improve acute DIC, direct evidence is lacking to clarify the role of dioscin in chronic DIC and its potential mechanism in cardiac ferroptosis. In this study, we used chronic DIC rat models and H9c2 cells to investigate the potential of dioscin to mitigate DIC by inhibiting ferroptosis. Our results suggest that dioscin significantly improves chronic DIC-induced cardiac dysfunction. Meanwhile, it significantly inhibited DOX-induced ferroptosis by reducing Fe2+ and lipid peroxidation accumulation, maintaining mitochondrial integrity, increasing glutathione peroxidase 4 (GPX4) expression, and decreasing acyl-CoA synthetase long-chain family 4 (ACSL4) expression. Through transcriptomic analysis and subsequent validation, we found that the anti-ferroptotic effects of dioscin are achieved by regulating the nuclear factor-erythroid 2-related factor 2 (Nrf2)/GPX4 axis and Nrf2 downstream iron metabolism genes. Dioscin further downregulates nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) and upregulates expression of frataxin (FXN) and ATP-binding cassette B8 (ABCB8) to limit mitochondrial Fe2+ and lipid peroxide accumulation. However, Nrf2 inhibition diminishes the anti-ferroptotic effects of dioscin, leading to decreased GPX4 expression and increased lipid peroxidation. This study is a compelling demonstration that dioscin can effectively reduce DIC by inhibiting ferroptosis, which is dependent on the Nrf2/GPX4 pathway modulation.

The Potential of Bioactive Fish Collagen Oligopeptides against Hydrogen Peroxide-Induced NIH/3T3 and HUVEC Damage: The Involvement of the Mitochondria.

Extensive in vivo investigations have demonstrated the antioxidant properties of fish collagen oligopeptides (FCOPs). One of the main causes of aging and chronic non-communicable diseases is oxidative stress. Therefore, FCOPs have a broad range of applications in illness prevention and delaying aging from the standpoint of the "food is medicine" theory. However, the mechanisms that underpin the antioxidant activity of FCOPs are not completely understood. The specific objective of this essay was to investigate the antioxidant effect of FCOPs and its possible mechanism at the cellular level. Mouse embryonic fibroblasts NIH/3T3 and human vein endothelial cells (HUVECs) were exposed to 200 µM hydrogen peroxide containing different concentrations of FCOPs for 4 h and were supplemented with different concentrations of FCOPs for 24 h. Normal growth medium without FCOPs was applied for control cells. An array of assays was used to evaluate the implications of FCOPs on cellular oxidative stress status, cellular homeostasis, inflammatory levels, and mitochondrial function. We found that FCOPs exerted a protective effect by inhibiting reactive oxygen species (ROS) production, enhancing superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS) activities and cell viability, inhibiting cell cycle arrest in the G1 phase, suppressing interleukin-1β (IL-1β), IL-6, matrix metalloproteinase-3 (MMP-3) and intercellular adhesion molecule-1(ICAM-1) secretion, downregulating nuclear factor-kappa B (NF-κB) activity, protecting mitochondrial membrane potential, and increasing ATP synthesis and NAD+ activities in both cells. FCOPs had a stronger antioxidant impact on NIH/3T3 than on HUVECs, simultaneously increasing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) content in NIH/3T3. These findings indicate that FCOPs have antioxidant effects on different tissue cells damaged by oxidative stress. FCOPs were therefore found to promote cellular homeostasis, inhibit inflammation, and protect mitochondria. Meanwhile, better health outcomes will be achieved by thoroughly investigating the effective dose and intervention time of FCOPs, as the absorption efficiency of FCOPs varies in different tissue cells.

Time-restricted feeding prevents ionizing radiation-induced hematopoietic stem cell damage by inhibiting NOX-4/ROS/p38 MAPK pathway

Ionizing radiation (IR)-induced damage to the hematopoietic system is a prominent symptom following exposure to total body irradiation (TBI). The exploration of strategies aimed at to mitigating radiation-induced hematopoietic damage assumes paramount importance. Time-restricted feeding (TRF) has garnered attention for its beneficial effects in various diseases. In this study, we evaluated the preventive effects of TRF on TBI-induced hematopoietic damage. The results suggested that TRF significantly enhanced the proportion and function of hematopoietic stem cells in mice exposed to 4 Gy TBI. These effects might be attributed to the inhibition of the NOX-4/ROS/p38 MAPK pathway in hematopoietic stem cells. TRF also influenced the expression of nuclear factor erythroid2-related factor 2 and increased glutathione peroxidase activity, thereby promoting the clearance of reactive oxygen species. Furthermore, TRF alleviated aberrations in plasma metabolism by inhibiting the mammalian target of rapamycin. These findings suggest that TRF may represent a novel approach to preventing hematopoietic radiation damage.

Effects of Foliar Selenium Application on Oxidative Damage and Photosynthetic Properties of Greenhouse Tomato under Drought Stress.

Both drought stress and exogenous selenium (Se) cause changes in plant physiological characteristics, which are key factors affecting crop yield. Although Se is known to be drought-resistant for crops, its internal physiological regulatory mechanisms are not clear. This study analyzed the effects of selenium application (SeA) on antioxidant enzyme activities, osmoregulatory substance contents, and photosynthetic characteristics of greenhouse tomatoes under drought stress and related physiological mechanisms. The results showed that drought stress induced oxidative damage in cells and significantly increased the content of the membrane lipidation product malondialdehyde (MDA) and the osmoregulatory substance proline (p < 0.001) compared with the adequate water supply. The proline content of severe drought stress (W1) was 9.7 times higher than that of the adequate water supply (W3), and foliar SeA increased glutathione peroxidase (GSH-PX) activity, and SeA induced different enzymatic reactions in cells under different drought stresses; catalase (CAT) was induced under severe drought stress (p < 0.01) and was significantly increased by 32.1% compared with the clear water control, CAT. Peroxidase (POD) was induced under adequate water supply conditions (p < 0.01), which was significantly increased by 15.2%, and SeA attenuated cell membrane lipidation, which reduced MDA content by an average of 21.5% compared with the clear water control, and also promoted photosynthesis in the crop. Meanwhile, through the entropy weighting method analysis (TOPSIS) of the indexes, the highest comprehensive evaluation score was obtained for the S5W3, followed by the S2.5W3 treatment. Therefore, this study emphasized the importance of SeA to reduce oxidative damage and enhance photosynthesis under drought stress.

ED-71 ameliorates bone regeneration in type 2 diabetes by reducing ferroptosis in osteoblasts via the HIF1α pathway

Eldecalcitol (ED-71), a novel active form of vitamin D, shows potential in treating osteoporosis. However, its underlying mechanisms of action remain to be determined. This study aimed to investigate the effect of ED-71 on bone regeneration and to illustrate its mode of action. The in-vitro model was developed using rat primary osteoblasts cultured under high-glucose conditions, and these cells were treated with ED-71. Additionally, an in vivo model of cranial bone defects was established in type 2 diabetic rats, and ED-71 was administered by gavage. The results demonstrated that ED-71 prevented osteoblast cell death, enhanced rat primary osteoblasts' osteogenic capacity, and attenuated the overexpression of hypoxia-inducible factor 1α (HIF1α) induced by high glucose levels. Furthermore, ED-71 increased glutathione peroxidase 4 (GPX4) levels and inhibited ferroptosis in response to hyperglycemic stimulation. Notably, interference with the HIF1α activator and ferroptosis activator Erastin significantly reduced the therapeutic effects of edetate osteolysis. These findings were further tested in vivo experiments. These results suggest that ED-71 activates the HIF1α pathway in vivo and in vitro, effectively relieving the ferroptosis induced by high glucose. Significantly, ED-71 may improve osteogenic disorders caused by diabetes.

Lemon extract reduces the hepatic oxidative stress and persulfidation levels by upregulating the Nrf2 and Trx1 expression in old rats.

Citrus flavanones are recognized as promising bioactives within the concept of healthy aging. Thus, the present study investigated the effects of a nutritionally relevant dose of lemon extract (LE) on liver redox regulation and persulfidation levels in 24-month-old Wistar rats. LE (40 mg/kg b.m.) was administered orally once daily for 4 weeks. Control groups received either vehicle (sunflower oil) or remained intact. The applied methodology considered qPCR, Western blot, protein persulfidation levels evaluation, histochemistry in line with immunofluorescence, liver biochemical assays (glutathione, total -SH groups and malonaldehyde; MDA), liver enzymes in serum and in silico analysis to explore the potential interaction/binding between the proteins studied in the paper. Our results showed that LE increased glutathione peroxidase (GPx), reductase (GR), glutamate-cysteine ligase catalytic and modifier subunit, respectively, as well as Nrf2 gene expressions, but decreased the expression of superoxide dismutase 2 (SOD2). Upon LE application, protein expression showed upregulation of NRF2, SOD2, GPx, GR, and thioredoxin 1 (Trx1). LE significantly decreased the protein persulfidation levels and concentration of MDA, a marker of oxidative damage in the cell. Histological analysis showed a normal liver histoarchitecture without pathological changes, aligning with the normal serum level of hepatic enzymes. Obtained results showed that LE, by modulating hepatic redox regulators Nrf2 and Trx1, diminishes oxidative stress and alters the persulfidation levels, suggesting a considerable beneficial antioxidant potential of lemon flavanones in the old-aged liver.

The SH-SY5Y Human Cell Line: Hawthorne Berry (Crataegus spp.) Protects against 6-OHDA Induced Neurotoxicity In Vitro Model of Parkinson's Disease

Aim: We purposed to study the neuroprotective effects of Hawthorn berry (crataegus spp.) extract, which is familiar to have antioxidant and anti-inflammatory features, opposite the neurotoxicity led to by 6-OHDA in SH-SY5Y cells. Method: SH-SY5Y cells were treated with Hawthorn berry (25-50-75 and 100 μg/mL) for two hours ago 6-OHDA administration. Cells were exposed to 200 µM 6-OHDA for 24 hours to mimic the in vitro Parkinson's disease model. After one day, cell viability was measured by lactate dehydrogenase and 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis. Oxidative stress was evaluated with tumor necrosis factor-α, interleukin-1β, superoxide dismutase, catalase, glutathione, glutathione peroxidase, myeloperoxidase, and malondialdehyde assays. Results: It was found that the viability rate of Hawthorn berry increased depending on the concentration and the cell viability was 94% at the highest concentration (p&amp;lt;0.001). Also, 6-OHDA raised lactate dehydrogenase leakage in SH-SY5Y cells (p&amp;lt;0.001). While 6-OHDA exacerbated oxidative stress by enhancing tumor necrosis factor-α, interleukin-1β, myeloperoxidase, and malondialdehyde (p&amp;lt;0.001), pretreatment with Hawthorn berry alleviated these toxic effects of 6-OHDA through antioxidant capacity by increasing glutathione peroxidase, superoxide dismutase, catalase and glutathione (p&amp;lt;0.05), (p&amp;lt;0.001). In line with all findings, Hawthorn berry attenuated neuronal cell demise in a dose-dependent manner. Conclusion: Considering its neuroprotective role as well as its effects on oxidative stress, Hawthorn berry could be a potential natural bio-medicine to prevent the development of Parkinson's disease.

Propolis Protects GC-1spg Spermatogonial Cells against Tert-Butyl Hydroperoxide-Induced Oxidative Damage.

Propolis is a natural resin produced by honeybees with plenty of pharmacologic properties, including antioxidant activity. Oxidative stress disrupts germ cell development and sperm function, with demonstrated harmful effects on male reproduction. Several natural antioxidants have been shown to reduce oxidative damage and increase sperm fertility potential; however, little is known about the effects of propolis. This work evaluated the role of propolis in protecting spermatogonial cells from oxidative damage. Propolis' phytochemical composition and antioxidant potential were determined, and mouse GC-1spg spermatogonial cells were treated with 0.1-500 µg/mL propolis (12-48 h) in the presence or absence of an oxidant stimulus (tert-butyl hydroperoxide, TBHP, 0.005-3.6 µg/mL, 12 h). Cytotoxicity was assessed by MTT assays and proliferation by Ki-67 immunocytochemistry. Apoptosis, reactive oxygen species (ROS), and antioxidant defenses were evaluated colorimetrically. Propolis presented high phenolic and flavonoid content and moderate antioxidant activity, increasing the viability of GC-1spg cells and counteracting TBHP's effects on viability and proliferation. Additionally, propolis reduced ROS levels in GC-1spg, regardless of the presence of TBHP. Propolis decreased caspase-3 and increased glutathione peroxidase activity in TBHP-treated GC-1spg cells. The present study shows the protective action of propolis against oxidative damage in spermatogonia, opening the possibility of exploiting its benefits to male fertility.

Preparation of antioxidant peptides from yak skin gelatin and their protective effect on myocardial ischemia reperfusion injury.

We herein report a study on the antioxidant peptides that show potential in alleviating myocardial ischemia reperfusion injury (MI/RI). Yak skin gelatin fraction Ac (YSG-Ac), obtained through ultrafiltration and gel filtration with Sephadex G-15, exhibits a favorable nutrient composition, high foaming capacity and stability, and resistance against gastrointestinal digestion. LC-MS/MS analysis reveals that YSG-Ac contains 26 peptide segments with sequence lengths of 8 to 12 amino acids. Online screening suggests that the antioxidant capacity of YSG-Ac is mainly attributed to the presence of hydrophobic and antioxidant amino acids. In vitro, our results demonstrate the MI/RI protective effects of YSG-Ac by effectively repairing H2O2-induced oxidative damage in H9c2 cells, which is achieved by inhibiting malondialdehyde (MDA) levels, and increasing glutathione peroxidase (GSH-pX) and superoxide dismutase (SOD) activity. In vivo, our results further confirm the effectiveness of YSG-Ac in narrowing the area of myocardial infarction, decreasing MDA levels, increasing SOD activity, and reducing the content of lactate dehydrogenase (LDH) in a mouse MI/RI model. Molecular docking analysis indicates that PGADGQPGAK with xanthine dehydrogenase (XDH) and GAAGPTGPIGS with tumor necrosis factor-alpha (TNF-α) exhibit strong bonding capability, and other related targets also show certain binding ability toward YSG-Ac. This suggests that YSG-Ac can regulate MI/RI through multiple targets and pathways. Overall, our findings highlight the potential of YSG-Ac as a functional food ingredient with antioxidant and MI/RI protective characteristics.

Oxidative stability in meat (pectoralis major) of broiler orally supplemented with essential oils of allium sativum, Curcuma longa, Zingiber officinale, and Cinnamomum zeylanicum.

Lipid oxidation is a normal process in living muscles, but is escalated postmortem due to the loss of inherent antioxidant defense, which causes quality deterioration of meat. This study investigates the effects of essential oil (EO) supplementation to the drinking water of broiler chicken on physical properties, antioxidants, and lipid oxidation in Pectoralis major during frozen storage. Two hundred day-old chicks of arbo acre were allocated to five groups; control (T1) and the groups supplemented with: Allium sativum (T2), Curcuma longa (T3), Zingiber officinale (T4) and Cinnamomum zeylanicum (T5) at the level of 300ml/L into drinking water throughout a 49-d study. Thereafter, birds were slaughtered and breast meat excised for assessments during a 28-d storage period at 4 °C using standard procedure. The results show that cooking loss of Pectoralis major from T1 birds was not significantly (P > 0.05) different from that of T4, and were significantly higher than those of T2, T3, and T5 birds. Meat from T5 birds showed the lowest drip loss. The results for total antioxidant activity are not similar among sampling days. In general, control group showed inferior values, but T2 and T4 had greater values on days 0 and 28. The rate of lipid peroxidation increased with time; however, EOs administration markedly reduced the peroxidation rates compared to controls. The catalase activity of breast meat was significantly declined from day 14, but was enhanced as an effect of EO consumption especially in group T5 at 21 and 28 d. Supplementation of garlic, turmeric, and cinnamon EOs to broiler chickens increased glutathione peroxidase in breast meat on days 21 and 28, while turmeric EO enhanced superoxide dismutase up to 7 d. In conclusion, EOs are valuable supplements for broiler chickens and potent in enhancing meat quality and prolonging the shelf life.

Noni (Morinda Citrifolia) Ethanol Extract Lowered Blood Glucose Levels, Increased Glutathione Peroxidase Activity, And Decreased Malondialdehyde in White Rats Model of Diabetes

Diabetes mellitus can increase oxidative stress and damage cells. Noni fruit has antibacterial, antifungal, antitumor, analgesic, hypotensive, and anti-inflammatory benefits, can boost immunity, and has antioxidant content. Noni contains phenolic compounds (anthraquinones, acuities, asperulosides, and scopoletin), organic acids (capric and caprylic acids), and alkaloids (xeronine). The effect of noni ethanol extract can significantly reduce blood glucose (P&lt;0.05) of the T2 group (177.00±137.78) and T3 (159.40±86.53) when compared to the C+ group (511.00±131.45). The T1 group (387.40±170.06) had no significant difference (P&gt;0.05) when compared to the C+ group (511.00±131.45), but there was a decrease in the average yield at T1 (387.40±170.06). Serum malondialdehyde (MDA) examination showed a significant decrease (p&lt;0.05) in T1 (1188.32±93.41), while in T2 (1385.35±38.65) and T3 (1460.32±42.51) was not significant (p&lt;0.05). Examination of serum glutathione peroxidase (GPX) showed a significant decrease in T1 (119.97±37.45), there was a decrease in GPX levels, while in the T2 group (236.14±6.05) and T3 (185.24±43.07), there was no decrease. Noni ethanol extract can lower blood glucose levels, reduce Malondialdehyde levels, and prevent increased activity of the enzyme glutathione peroxidase. Flavonoid compounds in noni ethanol extract can avoid increased blood glucose and reduce free radicals formed due to hyperglycemia conditions.

Impact of heat stress on blood physiological parameters, body temperature, respiratory frequency, antioxidant status, carcass quality, production performance, and egg quality of Japanese quails

The study was performed with three experiments. The first experiment studied respiratory rate (RR), body temperature (BT), blood physiological parameters (BPP), serum antioxidant enzyme activities (SAEA), and meat quality of 240 quails under three temperatures (38 °C, 25 °C, and environmental temperature 30 °C) and two bodyweights (heavy and lighter). Heat stress (HS) increased RR and BT of quails but had no effect on BPP; superoxide dismutase (SOD) activity was decreased in group 38 °C (P&lt;0.05), and a trend of increasing glutathione peroxidase (GSH-Px) was also observed in group 38 °C (P=0.06); meat quality was not affected by HS except yellow index of meat color was increased (P&lt;0.05). The second experiment was conducted with 168 quails (experiment 1) to record reproductive performance and egg quality. HS negatively affected feed intake, egg weight, egg height, albumen height, yolk weight, yolk color, and Haugh unit (P&lt;0.05). The third experiment was performed to evaluate the effect of HS on growth and reproductive performance, and SAEA of the first generation (G1) from 84 quails (experiment 2). Feed intake, weight gain, and feed conversion ratio in the 38 °C H – G1 quail line were not significantly different from other groups. The higher egg weight and egg production were discovered in heat-stressed G1 groups. The lowest value of SOD and GSH-Px was reported in the 38 °C H – G1 quail line but no different in catalase (P&gt;0.05). The 38 °C – G1 quail groups adapted to HS from G0 by expanding feed intake at the growing phase, improving egg weight and egg production, and maintaining the low SAEA.

Long-term spermidine therapy potentially protects the heart against estrogen deprivation in female rats via suppressing cardiac mitochondrial dysfunction, inflammation, oxidative stress, and apoptosis

Abstract Background Postmenopausal women have been associated with a higher risk of cardiovascular diseases (CVDs). Several pathophysiological mechanisms, including cardiac mitochondrial dysfunction, oxidative stress, inflammation, and cardiomyocyte apoptosis, played a key role in the development of postmenopausal CVDs. Long-term estrogen supplementation is widely used to treat postmenopausal symptoms, but it has been linked to an increased risk of breast cancer and cardiac complications. Spermidine is a natural organic compound which has been shown to exert cardioprotection under several pathological conditions. However, the benefits of spermidine against impaired cardiac function due to estrogen-deprivation are unknown. Purpose To investigate the effects of therapeutic intervention with spermidine on cardiac mitochondrial function, oxidative stress, inflammation, and programmed cardiomyocyte death in rats with estrogen deprivation. Methods Fifteen female Wistar rats underwent ovariectomy (OVX) to induce estrogen deprivation. After 12 weeks, all OVX-operated rats were randomly divided into three interventional groups as follows: 1) vehicle or OV (n = 5), 2) spermidine or OS (20 mg/kg/day, p.o., n = 5), and 3) estradiol or OE (50 µg/kg/day, s.c., n = 5) for an additional 8 weeks. At the end of the experiment, echocardiography for the heart’s function was performed. Then, all the rats were sacrificed, and their hearts were dissected for mitochondrial and molecular analysis, including the protein expressions of inflammation, oxidative stress, and apoptosis. Results Treatment with either spermidine or estrogen provided a similar cardioprotective efficacy against OVX-induced estrogen deprivation in reducing mitochondrial membrane potential depolarization and cardiac inflammation, as shown by increased red to green fluorescence and lowered p-NFkB to NFkB ratios, respectively (Fig. 1A, B). Spermidine and estrogen also exerted anti-oxidative stress via increasing glutathione peroxidase (GPX4) and anti-apoptosis via decreasing the cleaved caspase-3 to procaspase-3 ratio following OVX-induced estrogen deficiency (Fig. 1C, D). All of the beneficial effects of spermidine and estrogen led to an improved left ventricular ejection fraction (89% for OS and OE vs. 76% for OV). Conclusion Long-term treatment with spermidine rescued cardiac mitochondrial dysfunction, inflammation, oxidative stress, and apoptosis, resulting in the restoration of left ventricular function with the same efficacy as estrogen treatment. These findings suggest that spermidine could be a novel therapeutic strategy to alleviate the adverse cardiac complications associated with postmenopausal women.