Effective removal of chromium,copper,and nickel heavy metal ions from industrial electroplating wastewater by in situ oxidative adsorption using sodium hypochlorite as oxidant and sodium trititanate nanorod as adsorbent

Sodium hypochlorite and synthesized sodium trititanate nanorods(Na_(2)Ti_(3)O_(7),186 nm×1270 nm)were used as the oxidant and adsorbents for in situ oxidative adsorption treatment of actual electroplating wastewater containing Cr(Ⅵ)(2.6-5.2 mg·L^(-1)),Cu^(2+)(2.7-5.4 mg·L^(-1)),and Ni^(2+)(0.2705-0.541 mg·L^(-1))ions at pH of 8.8-9.1 and 20-60℃.The as-synthesized sodium trititanate nanorods were characterized by XRD,HRTEM,N2 adsorption/desorption,SEM,EDX,and zeta potential techniques.The concentrations of heavy metal ions in wastewater were analyzed by ICP technique.After in situ oxidative adsorption treatment under the concentrations of 25 g·L^(-1) for sodium hypochlorite and 125 mg·L^(-1) for sodium trititanate nanorods at 60℃ for 5 h,the heavy metal ion concentrations could be reduced from initial value of 2.6 to final value of 1.92 mg·L^(-1) for Cr(Ⅵ),3.6 to 0.17 mg·L^(-1) for Cu^(2+),and from 0.2705 to 0.097 mg·L^(-1) for Ni^(2+),respectively.Cr(Ⅵ),Cu^(2+) and Ni^(2+) ions could be effectively removed by the in situ oxidative adsorption method.The in situ oxidative adsorption processes of Cr(Ⅵ),Cu^(2+) and Ni^(2+) ions are satisfactorily simulated by the pseudo-second order adsorption kinetics and Langmuir adsorption isotherm,respectively.Adsorption thermodynamics analyses reveal that the oxidative adsorption processes of Cr(Ⅵ),Cu^(2+) and Ni^(2+) ions are spontaneous and endothermic.The oxidation degree of metalcontained complexes influences the values of thermodynamics functions.

Supplementation of vitamin E or a botanical extract as antioxidants to improve growth performance and health of growing pigs housed under thermoneutral or heat-stressed conditions

Background Heat stress has severe negative consequences on performance and health of pigs,leading to significant economic losses.The objective of this study was to investigate the effects of supplemental vitamin E and a botanical extract in feed or drinking water on growth performance,intestinal health,and oxidative and immune status in grow-ing pigs housed under heat stress conditions.Methods Duplicate experiments were conducted,each using 64 crossbred pigs with an initial body weight of 50.7±3.8 and 43.9±3.6 kg and age of 13-week and 12-week,respectively.Pigs(n=128)were housed individually and assigned within weight blocks and sex to a 2×4 factorial arrangement consisting of 2 environments(thermo-neutral(21.2℃)or heat-stressed(30.9℃))and 4 supplementation treatments(control diet;control+100 IU/L of D-α-tocopherol in water;control+200 IU/kg of DL-α-tocopheryl-acetate in feed;or control+400 mg/kg of a botanical extract in feed).Results Heat stress for 28 d reduced(P≤0.001)final body weight,average daily gain,and average daily feed intake(-7.4 kg,-26.7%,and-25.4%,respectively)but no effects of supplementation were detected(P>0.05).Serum vitamin E increased(P<0.001)with vitamin E supplementation in water and in feed(1.64 vs.3.59 and 1.64 vs.3.24),but not for the botanical extract(1.64 vs.1.67 mg/kg)and was greater when supplemented in water vs.feed(P=0.002).Liver vitamin E increased(P<0.001)with vitamin E supplementations in water(3.9 vs.31.8)and feed(3.9 vs.18.0),but not with the botanical extract(3.9 vs.4.9 mg/kg).Serum malondialdehyde was reduced with heat stress on d 2,but increased on d 28(interaction,P<0.001),and was greater(P<0.05)for antioxidant supplementation compared to control.Cellular proliferation was reduced(P=0.037)in the jejunum under heat stress,but increased in the ileum when vitamin E was supplemented in feed and water under heat stress(interaction,P=0.04).Tumor necrosis factor-αin jejunum and ileum mucosa decreased by heat stress(P<0.05)and was reduced by vitamin E sup-plementations under heat stress(interaction,P<0.001).Conclusions The addition of the antioxidants in feed or in drinking water did not alleviate the negative impact of heat stress on feed intake and growth rate of growing pigs.

Effect of antioxidants on the efficiency of jet milling and the powder characteristics of Sm2Co17 permanent magnets

This study investigated the effect of antioxidants on the grinding efficiency,magnetic powder characteristics,microstructure,and magnetic properties of 2:17 type SmCo permanent magnet materials.The results show that adding antioxidants helps improve the dispersion among magnetic powders,leading to a 33.3%decrease in jet milling time and a 15.8%increase in magnet powder production yield.Additionally,adding antioxidants enhances the oxidation resistance of the magnetic powders.After being stored in a constant temperature air environment at 25C for 48 h,the O content in the powder decreased by 33%compared to samples without antioxidants.While in the magnet body,the O content decreased from 0.21 wt.%to 0.14 wt.%,which helps increase the effective Sm content and domain wall pinning uniformity in the magnet.Excellent magnetic properties were obtained in the magnet with added antioxidants:B_(r)=11.6 kGs,SF=79.6%,H_(cj)=16.8 kOe,and(BH)_(max)=32.5 MGOe.

The extraction of effective components and an antioxidant activity study of Tulipa edulis

Plant extracts from natural sources are an excellent choice for food additives and natural antioxidants.In this study,the active components of Tulipa edulis were extracted and analysed,and their antioxidant capacity was measured.Then,the crude extract mixture was separated and purified using a Sephadex LH-20 gel,and the antioxidant activity of the purified products was determined.Human umbilical vein endothelial human umbilical vein endothelial cells(HUVEC)cells were treated with 35 mmol/L glucose to construct a model of oxidative stress.Then,the cells were treated with the active component to observe whether the products of T.edulis could have a good protective effect on HUVEC cells induced by glucose.Transcriptome analysis was also performed on HUVEC cells after same treatment to explore the possible mechanism of the component F2 protecting HUVEC cells from oxidative stress induced by high glucose.The results showed that component F2 obtained from T.edulis has strong antioxidant activity.Moreover,F2 can play a strong antioxidant protective role in HUVEC cells.Meanwhile,the gene expression of heme oxygenase 1(HO-1),γ-glutamyl cysteine ligase catalytic subunit(GCLC)and NAD(P)H quinone oxidoreductase-1(NQO1)in HUVEC cells was up-regulated after treated with F2.This study provides reference value for the further development and application of T.edulis and the d evelopment of functional food.

Silicon Mitigates Aluminum Toxicity of Tartary Buckwheat by Regulating Antioxidant Systems

Aluminum (Al) toxicity is a considerable factor limiting crop yield and biomass in acidic soil. Tartary buckwheatgrowing in acidic soil may suffer from Al poisoning. Here, we investigated the influence of Al stress on the growthof tartary buckwheat seedling roots, and the alleviation of Al stress by silicon (Si), as has been demonstrated inmany crops. Under Al stress, root growth (total root length, primary root length, root tips, root surface area, androot volume) was significantly inhibited, and Al and malondialdehyde (MDA) accumulated in the root tips. At thesame time, catalase (CAT) and ascorbate peroxidase activities, polyphenols, flavonoids, and 1,1-diphenyl-2-picrylhydrazyl(DPPH) and 2,2′-azinobis-(3-ethylbenzthiazoline-6-sulphonate) (ABTS) free-radical scavenging abilitywere significantly decreased. After the application of Si, root growth, Al accumulation, and oxidative damage wereimproved. Compared to Al-treated seedlings, the contents of ·O2− and MDA decreased by 29.39% and 25.22%,respectively. This was associated with Si-induced increases in peroxidase and CAT enzyme activity, flavonoidcompounds, and free-radical scavenging (DPPH and ABTS). The application of Si therefore has positive effectson Al toxicity in tartary buckwheat roots by reducing Al accumulation in the roots and maintaining oxidationhomeostasis.

Enhancement of the Antigenotoxic and Antioxidant Actions of Eugenol from Spice Clove and the Stabilizer Gum Arabic on Colorectal Carcinogenesis

Spices are defined as any aromatic condiment of plant origin used to alter the flavor and aroma of foods. Besides flavor and aroma, many spices have antioxidant activity, mainly related to the presence in cloves of phenolic compounds, such as flavonoids, terpenoids and eugenol. In turn, the most common uses of gum arabic are in the form of powder for addition to soft drink syrups, cuisine and baked goods, specifically to stabilize the texture of products, increase the viscosity of liquids and promote the leavening of baked products (e.g., cakes). Both eugenol, extracted from cloves, and gum arabic, extracted from the hardened sap of two species of the Acacia tree, are dietary constituents routinely consumed virtually throughout the world. Both of them are also widely used medicinally to inhibit oxidative stress and genotoxicity. The prevention arm of the study included groups: Ia, IIa, IIIa, Iva, V, VI, VII, VIII. Once a week for 20 weeks, the controls received saline s.c. while the experimental groups received DMH at 20 mg/kg s.c. During the same period and for an additional 9 weeks, the animals received either water, 10% GA, EUG, or 10% GA + EUG by gavage. The treatment arm of the study included groups Ib, IIb, IIIb e IVb, IX, X, XI, XII). Once a week for 20 weeks, the controls received saline s.c. while the experimental groups received DMH at 20 mg/kg s.c. During the subsequent 9 weeks, the animals received either water, 10% GA, EUG or 10% GA + EUG by gavage. The novelty of this study is the investigation of their use alone and together for the prevention and treatment of experimental colorectal carcinogenesis induced by dimethylhydrazine. Our results show that the combined use of 10% gum arabic and eugenol was effective, with antioxidant action in the colon, as well as reducing oxidative stress in all colon segments and preventing and treating genotoxicity in all colon segments. Furthermore, their joint administration reduced the number of aberrant crypts and the number of aberrant crypt foci (ACF) in the distal segment and entire colon, as well as the number of ACF with at least 5 crypts in the entire colon. Thus, our results also demonstrate the synergistic effects of 10% gum arabic together with eugenol (from cloves), with antioxidant, antigenotoxic and anticarcinogenic actions (prevention and treatment) at the doses and durations studied, in the colon of rats submitted to colorectal carcinogenesis induced by dimethylhydrazine.

Significance of oxidative stress and antioxidant capacity tests as biomarkers of premature ovarian insufficiency: A case control study

BACKGROUND Premature ovarian insufficiency(POI)is a condition that causes secondary amenorrhea owing to ovarian hypofunction at an early stage.Early follicular depletion results in intractable infertility,thereby considerably reducing the quality of life of females.Given the continuum in weakened ovarian function,progressing from incipient ovarian failure(IOF)to transitional ovarian failure and further to POI,it is necessary to develop biomarkers for predicting POI.The oxidative stress states in IOF and POI were comprehensively evaluated via oxidative stress[diacron-reactive oxygen metabolites(d-ROMs)]test and anti-oxidant capacity[biological antioxidant potential(BAP)].METHODS Females presenting with secondary amenorrhea over 4 mo and a follicle stimulating hormone level of>40 mIU/mL were categorized into the POI group.Females presenting with a normal menstrual cycle and a follicle stimulating hormone level of>10.2 mIU/mL were categorized into the IOF group.Healthy females without ovarian hypofunction were categorized into the control group.Among females aged<40 years who visited our hospital from January 2021 to June 2022,we recruited 11 patients into both POI and IOF groups.For the potential antioxidant capacity,the relative oxidative stress index(BAP/d-ROMs×100)was calculated,and the oxidative stress defense system was comprehensively evaluated.RESULTS d-ROMs were significantly higher in the POI and IOF groups than in the control group,(478.2±58.7 U.CARR,434.5±60.6 U.CARR,and 341.1±35.1 U.CARR,respectively)(U.CARR is equivalent to 0.08 mg/dL of hydrogen peroxide).However,no significant difference was found between the POI and IOF groups.Regarding BAP,no significant difference was found between the control,IOF,and POI groups(2078.5±157.4μmol/L,2116.2±240.2μmol/L,and 2029.0±186.4μmol/L,respectively).The oxidative stress index was significantly higher in the POI and IOF groups than in the control group(23.7±3.3,20.7±3.6,and 16.5±2.1,respectively).However,no significant difference was found between the POI and IOF groups.CONCLUSION High levels of oxidative stress suggest that evaluating the oxidative stress state may be a useful indicator for the early detection of POI.

Oxidative leaching behavior of metalliferous black shale in acidic solution using persulfate as oxidant

The oxidative dissolution of metalliferous black shale in sulfuric acid solution using sodium persulfate as an oxidant was investigated. The effects of leaching factors including leaching temperature, leaching time, stirring speed, initial concentration of sodium persulfate and sulfuric acid and particle size on the leaching rate were studied as well. The leaching kinetics of molybdenum, nickel and iron from metalliferous black shale shows that the leaching rate is controlled by a chemical reaction through a layer on the unreacted shrinking core. The leaching process follows the kinetics model 1-（1-a）^1/3=kt with apparent activation energies of 34.50, 43.14 and 71.79 kJ/mol for Mo, Ni and Fe, respectively. The reaction orders in sodium persulfate are 0.80, 1.01 and 0.75 for molybdenum, nickel and iron, respectively, while in sulfuric acid, these orders are 0.45, 0.75 and 0.50 for molybdenum, nickel and iron, respectively. In addition, the reaction mechanism for the dissolution of the metalliferous black shale was discussed.

Research on Oxidative Stress Induced by Tenuazonic Acid from Alternaria augustiovoide and Changes in Antioxidant Enzyme Activities in Leaves of Echinochloa crus-galli

[Objective] The aim of the study was to determine whether phytotoxicity of TeA against Echinochloa crus-galli leaves was correlated with oxidative stress caused by generation of reactive oxygen and the changes of antioxidant enzymes activity.[Method] The changes of malondialdehyde（MDA）content,hydrogen peroxide（H2O2）,and activities of superoxide dismutase（SOD）,glutathione reductase（GR）and catalase（CAT）were studied by leaf segment method in vitro.[Result] After the treatment of 500 μmol/L TeA,the content of MDA and H2O2 increased by 247.86% and 67.00%,respectively,indicating that the accumulation of MDA and H2O2 in E.crus-galli leaves was due to the reactive oxygen burst induced by TeA.TeA induced a significant increase in activities of SOD,GR and CAT.At 500 μmol/L TeA,activities of SOD,GR and CAT increased more than one fold compared with the control.[Conclusion] TeA could not only cause oxidative stress in leaves of E.crus-galli through the induction of reactive oxygen,but also induce the increasing of antioxidant enzyme activity.

Effect of Chromium on Oxidative Damage and Antioxidant Capacity of Ctenopharyngodon idellus

[Objective] This study aimed to investigate the effect of chromium on ox- idative damage and antioxidant capacity of Ctenopharyngodon idellus （grass carp）. [Method] The grass carps were treated with hexavalent chromium （Cr^6＋） solution at concentrations of 0, 7.23, 14.47, 28.94 mg/L, and then the content of malondialde- hyde （MDA）, the level of total antioxidative capacity （T-AOC） and the activity of gtu- tathione-S-transferase （GST） in the hepatopancreas of grass carp were determined after 96 hours in different treatment groups. [Result] The content of MDA presented increasing trend with the increase of exposure Cr^6＋ concentrations. The activity of T-AOC increased firstly, then decreased with the increasing Cr^6＋ exposure concentra- tions, showing that the level of T-AOC was induced in tow and medium concentrat ions （7.23 and 14.47 mg/L）, but inhibited in high concentrations （28.94 mg/L）. Among the exposure groups, the level of T-AOC in medium concentration group （14.47 mg/L） was significantly higher than the control （P〈0.05）. Except the low concentration groups （7.23 mg/L） of which the GST activity was slightly induced, the GST activities of the other groups all showed downward trend with increasing Cr^6＋ levels, and the activity of GST in 28.94 mg/L group was significantly lower than the control group （P〈0.05）. [Conclusion] Cr^6＋ could cause large oxidative damage in the hepatopancreas of grass carp, thus poisoning it, and Cr^6＋ may further damage the organizational structure and physiological function of grass carp.

Hypidone hydrochloride(YL-0919)ameliorates functional deficits after traumatic brain injury in mice by activating the sigma-1 receptor for antioxidation

Traumatic brain injury involves complex pathophysiological mechanisms,among which oxidative stress significantly contributes to the occurrence of secondary injury.In this study,we evaluated hypidone hydrochloride(YL-0919),a self-developed antidepressant with selective sigma-1 receptor agonist properties,and its associated mechanisms and targets in traumatic brain injury.Behavioral experiments to assess functional deficits were followed by assessment of neuronal damage through histological analyses and examination of blood-brain barrier permeability and brain edema.Next,we investigated the antioxidative effects of YL-0919 by assessing the levels of traditional markers of oxidative stress in vivo in mice and in vitro in HT22 cells.Finally,the targeted action of YL-0919 was verified by employing a sigma-1 receptor antagonist(BD-1047).Our findings demonstrated that YL-0919 markedly improved deficits in motor function and spatial cognition on day 3 post traumatic brain injury,while also decreasing neuronal mortality and reversing blood-brain barrier disruption and brain edema.Furthermore,YL-0919 effectively combated oxidative stress both in vivo and in vitro.The protective effects of YL-0919 were partially inhibited by BD-1047.These results indicated that YL-0919 relieved impairments in motor and spatial cognition by restraining oxidative stress,a neuroprotective effect that was partially reversed by the sigma-1 receptor antagonist BD-1047.YL-0919 may have potential as a new treatment for traumatic brain injury.

The emerging role of nitric oxide in the synaptic dysfunction of vascular dementia

With an increase in global aging,the number of people affected by cerebrovascular diseases is also increasing,and the incidence of vascular dementia-closely related to cerebrovascular risk-is increasing at an epidemic rate.However,few therapeutic options exist that can markedly improve the cognitive impairment and prognosis of vascular dementia patients.Similarly in Alzheimer’s disease and other neurological disorders,synaptic dysfunction is recognized as the main reason for cognitive decline.Nitric oxide is one of the ubiquitous gaseous cellular messengers involved in multiple physiological and pathological processes of the central nervous system.Recently,nitric oxide has been implicated in regulating synaptic plasticity and plays an important role in the pathogenesis of vascular dementia.This review introduces in detail the emerging role of nitric oxide in physiological and pathological states of vascular dementia and summarizes the diverse effects of nitric oxide on different aspects of synaptic dysfunction,neuroinflammation,oxidative stress,and blood-brain barrier dysfunction that underlie the progress of vascular dementia.Additionally,we propose that targeting the nitric oxide-sGC-cGMP pathway using certain specific approaches may provide a novel therapeutic strategy for vascular dementia.

Acquired sensorineural hearing loss,oxidative stress,and microRNAs

Hearing loss is the third leading cause of human disability.Age-related hearing loss,one type of acquired sensorineural hearing loss,is largely responsible for this escalating global health burden.Noise-induced,ototoxic,and idiopathic sudden sensorineural are other less common types of acquired hearing loss.The etiology of these conditions is complex and multi-fa ctorial involving an interplay of genetic and environmental factors.Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss.Short non-coding RNA sequences known as microRNAs(miRNAs)have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response.Sensory hair cell death is a central histopathological finding in sensorineural hearing loss.As these cells do not regenerate in humans,it underlies the irreversibility of human age-related hearing loss.Ovid EMBASE,Ovid MEDLINE,Web of Science Core Collection,and ClinicalTrials.gov databases over the period August 1,2018 to July 31,2023 were searched with"hearing loss,""hypoxamiRs,""hypoxia,""microRNAs,""ischemia,"and"oxidative stress"text words for English language primary study publications or registered clinical trials.Registe red clinical trials known to the senior author we re also assessed.A total of 222studies were thus identified.After excluding duplicates,editorials,retra ctions,secondary research studies,and non-English language articles,39 primary studies and clinical trials underwent full-text screening.This resulted in 11 animal,in vitro,and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review.MiRNAs miR-34a and miR-29b levels increase with age in mice.These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferato r-activated receptor gamma coactivator-1-alpha(SIRT1/P GC-1α),SIRT1p53,and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis.Furthermore,hypoxia and oxidative stress had a similar adve rse apoptotic effect,which was inhibited by resve ratrol and a myocardial inhibitorassociated transcript,a miR-29b competing endogenous mRNA.Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice-an effect that was corrected by inner ear stem cell-derived exosomes.There is ongoing work seeking to determine if these findings can be effectively translated to humans.

Tale of mitochondria and mitochondria-associated ER membrane in patient-derived neuronal models of Wolfram syndrome

Mitochondria and mitochondria-associated endoplasmic reticulum membrane in neurodegenerative diseases:Mitochondria generate most of the chemical energy needed to power the biochemical reactions of cells,and thus are often referred to as the"powerhouse"of the cell.Nevertheless,this organelle is also involved in a pleth,ora of different cellular functions such as calcium(Ca^(2+))homeostasis,apoptosis,oxidative stress,and several metabolic pathways including oxidative phosphorylation,tricarboxylic acid cycle,andβ-oxidation of fatty acids.

Metabolic reprogramming: a new option for the treatment of spinal cord injury

Spinal cord injuries impose a notably economic burden on society,mainly because of the severe after-effects they cause.Despite the ongoing development of various therapies for spinal cord injuries,their effectiveness remains unsatisfactory.However,a deeper understanding of metabolism has opened up a new therapeutic opportunity in the form of metabolic reprogramming.In this review,we explore the metabolic changes that occur during spinal cord injuries,their consequences,and the therapeutic tools available for metabolic reprogramming.Normal spinal cord metabolism is characterized by independent cellular metabolism and intercellular metabolic coupling.However,spinal cord injury results in metabolic disorders that include disturbances in glucose metabolism,lipid metabolism,and mitochondrial dysfunction.These metabolic disturbances lead to corresponding pathological changes,including the failure of axonal regeneration,the accumulation of scarring,and the activation of microglia.To rescue spinal cord injury at the metabolic level,potential metabolic reprogramming approaches have emerged,including replenishing metabolic substrates,reconstituting metabolic couplings,and targeting mitochondrial therapies to alter cell fate.The available evidence suggests that metabolic reprogramming holds great promise as a next-generation approach for the treatment of spinal cord injury.To further advance the metabolic treatment of the spinal cord injury,future efforts should focus on a deeper understanding of neurometabolism,the development of more advanced metabolomics technologies,and the design of highly effective metabolic interventions.

Potential role and therapeutic implications of glutathione peroxidase 4 in the treatment of Alzheimer's disease

Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinical trials are required to validate the therapeutic effects of strategies targeting glutathione peroxidase 4 in the treatment of Alzheimer's disease.

PI3K/AKT signaling and neuroprotection in ischemic stroke:molecular mechanisms and therapeutic perspectives

It has been reported that the PI3K/AKT signaling pathway plays a key role in the pathogenesis of ischemic stroke.As a result,the development of drugs targeting the PI3K/AKT signaling pathway has attracted increasing attention from researchers.This article reviews the pathological mechanisms and advancements in research related to the signaling pathways in ischemic stroke,with a focus on the PI3K/AKT signaling pathway.The key findings include the following:(1)The complex pathological mechanisms of ischemic stroke can be categorized into five major types:excitatory amino acid toxicity,Ca^(2+)overload,inflammatory response,oxidative stress,and apoptosis.(2)The PI3K/AKT-mediated signaling pathway is closely associated with the occurrence and progression of ischemic stroke,which primarily involves the NF-κB,NRF2,BCL-2,mTOR,and endothelial NOS signaling pathways.(3)Natural products,including flavonoids,quinones,alkaloids,phenylpropanoids,phenols,terpenoids,and iridoids,show great potential as candidate substances for the development of innovative anti-stroke medications.(4)Recently,novel therapeutic techniques,such as electroacupuncture and mesenchymal stem cell therapy,have demonstrated the potential to improve stroke outcomes by activating the PI3K/AKT signaling pathway,providing new possibilities for the treatment and rehabilitation of patients with ischemic stroke.Future investigations should focus on the direct regulatory mechanisms of drugs targeting the PI3K/AKT signaling pathway and their clinical translation to develop innovative treatment strategies for ischemic stroke.

Lipid droplets in the nervous system:involvement in cell metabolic homeostasis

Lipid droplets serve as primary storage organelles for neutral lipids in neurons,glial cells,and other cells in the nervous system.Lipid droplet formation begins with the synthesis of neutral lipids in the endoplasmic reticulum.Previously,lipid droplets were recognized for their role in maintaining lipid metabolism and energy homeostasis;however,recent research has shown that lipid droplets are highly adaptive organelles with diverse functions in the nervous system.In addition to their role in regulating cell metabolism,lipid droplets play a protective role in various cellular stress responses.Furthermore,lipid droplets exhibit specific functions in neurons and glial cells.Dysregulation of lipid droplet formation leads to cellular dysfunction,metabolic abnormalities,and nervous system diseases.This review aims to provide an overview of the role of lipid droplets in the nervous system,covering topics such as biogenesis,cellular specificity,and functions.Additionally,it will explore the association between lipid droplets and neurodegenerative disorders.Understanding the involvement of lipid droplets in cell metabolic homeostasis related to the nervous system is crucial to determine the underlying causes and in exploring potential therapeutic approaches for these diseases.

Neuroprotective potential for mitigating ischemia-reperfusion-induced damage

Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient's condition;this phenomenon is known as cerebral ischemia-reperfusion injury.Current studies have elucidated the neuroprotective role of the sirtuin protein family(Sirtuins)in modulating cerebral ischemia-reperfusion injury.However,the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional exploration.In this review,the origin and research progress of Sirtuins are summarized,suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury,including inflammation,oxidative stress,blood-brain barrier damage,apoptosis,pyroptosis,and autophagy.The therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways,such as nuclear factor-kappa B signaling,oxidative stress mediated by adenosine monophosphate-activated protein kinase,and the forkhead box O.This review also summarizes the potential of endogenous substances,such as RNA and hormones,drugs,dietary supplements,and emerging therapies that regulate Sirtuins expression.This review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk factors.While Sirtuins show promise as a potential target for the treatment of cerebral ischemiareperfusion injury,most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans,potentially influencing the efficacy of Sirtuinstargeting drug therapies.Overall,this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury.

Ultra‑Transparent and Multifunctional IZVO Mesh Electrodes for Next‑Generation Flexible Optoelectronics

Mechanically durable transparent electrodes are essential for achieving long-term stability in flexible optoelectronic devices.Furthermore,they are crucial for applications in the fields of energy,display,healthcare,and soft robotics.Conducting meshes represent a promising alternative to traditional,brittle,metal oxide conductors due to their high electrical conductivity,optical transparency,and enhanced mechanical flexibility.In this paper,we present a simple method for fabricating an ultra-transparent conducting metal oxide mesh electrode using selfcracking-assisted templates.Using this method,we produced an electrode with ultra-transparency(97.39%),high conductance(Rs=21.24Ωsq^(−1)),elevated work function(5.16 eV),and good mechanical stability.We also evaluated the effectiveness of the fabricated electrodes by integrating them into organic photovoltaics,organic light-emitting diodes,and flexible transparent memristor devices for neuromorphic computing,resulting in exceptional device performance.In addition,the unique porous structure of the vanadium-doped indium zinc oxide mesh electrodes provided excellent flexibility,rendering them a promising option for application in flexible optoelectronics.