Alleviation Of Oxidative Stress Research Articles

Augmenting hematoma-scavenging capacity of innate immune cells by CDNF reduces brain injury and promotes functional recovery after intracerebral hemorrhage

During intracerebral hemorrhage (ICH), hematoma formation at the site of blood vessel damage results in local mechanical injury. Subsequently, erythrocytes lyse to release hemoglobin and heme, which act as neurotoxins and induce inflammation and secondary brain injury, resulting in severe neurological deficits. Accelerating hematoma resorption and mitigating hematoma-induced brain edema by modulating immune cells has potential as a novel therapeutic strategy for functional recovery after ICH. Here, we show that intracerebroventricular administration of recombinant human cerebral dopamine neurotrophic factor (rhCDNF) accelerates hemorrhagic lesion resolution, reduces peri-focal edema, and improves neurological outcomes in an animal model of collagenase-induced ICH. We demonstrate that CDNF acts on microglia/macrophages in the hemorrhagic striatum by promoting scavenger receptor expression, enhancing erythrophagocytosis and increasing anti-inflammatory mediators while suppressing the production of pro-inflammatory cytokines. Administration of rhCDNF results in upregulation of the Nrf2-HO-1 pathway, but alleviation of oxidative stress and unfolded protein responses in the perihematomal area. Finally, we demonstrate that intravenous delivery of rhCDNF has beneficial effects in an animal model of ICH and that systemic application promotes scavenging by the brain’s myeloid cells for the treatment of ICH.

Molecular Mechanisms of Oxidative Stress Relief by CAPE in ARPE-19 Cells.

Caffeic acid phenylethyl ester (CAPE) is an antioxidative agent originally derived from propolis. Oxidative stress is a significant pathogenic factor in most retinal diseases. Our previous study revealed that CAPE suppresses mitochondrial ROS production in ARPE-19 cells by regulating UCP2. The present study explores the ability of CAPE to provide longer-term protection to RPE cells and the underlying signal pathways involved. ARPE-19 cells were given CAPE pretreatment followed by t-BHP stimulation. We used in situ live cell staining with CellROX and MitoSOX to measure ROS accumulation; Annexin V-FITC/PI assay to evaluate cell apoptosis; ZO-1 immunostaining to observe tight junction integrity in the cells; RNA-seq to analyze changes in gene expression; q-PCR to validate the RNA-seq data; and Western Blot to examine MAPK signal pathway activation. CAPE significantly reduced both cellular and mitochondria ROS overproduction, restored the loss of ZO-1 expression, and inhibited apoptosis induced by t-BHP stimulation. We also demonstrated that CAPE reverses the overexpression of immediate early genes (IEGs) and activation of the p38-MAPK/CREB signal pathway. Either genetic or chemical deletion of UCP2 largely abolished the protective effects of CAPE. CAPE restrained ROS generation and preserved the tight junction structure of ARPE-19 cells against oxidative stress-induced apoptosis. These effects were mediated via UCP2 regulation of p38/MAPK-CREB-IEGs pathway.

Modulation of Morpho-Physiological and Metabolic Profiles of Lettuce Subjected to Salt Stress and Treated with Two Vegetal-Derived Biostimulants.

Salinity in water and soil is a critical issue for food production. Using biostimulants provides an effective strategy to protect crops from salinity-derived yield losses. The research supports the effectiveness of protein hydrolysate (PH) biostimulants based on their source material. A greenhouse experiment was performed on lettuce plants under control (0 mM NaCl) and high salinity conditions (30 mM NaCl) using the Trainer (T) and Vegamin (V) PH biostimulants. The recorded data included yield parameters, mineral contents, auxiliary pigments, and polyphenolics. The plant sample material was further analyzed to uncover the unique metabolomic trace of the two biostimulants. The results showed an increased yield (8.9/4.6%, T/V) and higher photosynthetic performance (14%) compared to control and salinity treatments. Increased yield in salinity condition by T compared to V was deemed significant due to the positive modulation in stress-protecting molecules having an oxidative stress relief effect such as lutein (39.9% 0 × T vs. 30 × V), β-carotene (23.4% vs. V overall), and flavonoids (27.7% vs. V). The effects of PH biostimulants on the physio-chemical and metabolic performance of lettuce plants are formulation dependent. However, they increased plant growth under stress conditions, which can prove profitable.

Glutamine-Based Metabolism Normalization and Oxidative Stress Alleviation by Self-Assembled Bilirubin/V9302 Nanoparticles for Psoriasis Treatment.

Psoriasis is an immune-mediated chronic inflammatory skin disorder characterized by epidermal hyperplasia and infiltration of inflammatory cells. Even though the pathogenesis remains unclear, T helper 17 (Th17) cells-mediated inflammation and keratinocyte-involved proliferation are considered to play key roles during the occurrence and the development of psoriasis. Therefore, suppressing the infiltration/function of Th17 and the abnormal hyperplasia of keratinocytes can be a rational strategy for ameliorating and treating psoriasis. In this study, a self-assembly nanoparticle (BVn) is developed with bilirubin (an endogenous antioxidant) and V9302 (a blocker of ASCT2, an amino acid transporter mediating glutamine influx for providing energy and activating mammalian target of rapamycin [mTOR] pathway) to intervene the local metabolism and alleviate oxidative stress for psoriasis treatment. BVn effectively suppresses inflammatory keratinocyte proliferation and scavenges excess reactive oxygen species (ROS). In the in vivo psoriasis mouse model, BVn shows increased permeation and delayed retention in the psoriatic lesion and reverses the psoriasis-related symptoms, evidenced by the normalized keratinocyte condition and decreased Th17 infiltration/activation. Mechanism study indicates that BVn not only cut off the energy supply but also suppressed cell proliferation or lymph cell expansion by deactivating mTOR pathway, besides alleviated oxidative stress. BVn-based glutamine metabolism modulation strategy offers a promising strategy for psoriasis therapy.

Exosomes from Adipose-Derived Stem Cells Alleviate Dexamethasone-Induced Bone Loss by Regulating the Nrf2/HO-1 Axis.

The widespread use of therapeutic glucocorticoids has increased the incidences of glucocorticoid-induced osteoporosis (GIOP). Oxidative stress and mitochondrial dysfunction are major causes of GIOP; therefore, alleviation of excess oxidative stress in osteoblasts is a potential therapeutic strategy for osteoporosis. Exosomes derived from ADSCs (ADSCs-Exos), as novel cell-free therapeutics, can modulate various biological processes, such as immunomodulation, reduce oxidative damage, and promote tissue repair as well as regeneration. In this study, ADSCs-Exos restored the viability and osteogenic potential of MC3T3-E1 cells by attenuating apoptosis, oxidative damage, intracellular ROS generation, and mitochondrial dysfunction. Moreover, after pretreatment with ADSCs-Exos, Nrf2 expressions were upregulated in Dex-stimulated osteoblasts. Inhibitory assays showed that silencing Nrf2 partially eliminated the protective effects of ADSCs-Exos. The rat model assays confirmed that ADSCs-Exos alleviated the Dex-induced increase in oxidation levels, restored bone mass of the distal femur, and increased the expressions of Nrf2 and osteogenic markers in bone tissues. Thus, ADSCs-Exos alleviated apoptosis and oxidative stress by regulating Nrf2/HO-1 expressions after Dex and prevented the development of GIOP in vivo.

Jian Pi Sheng Sui Gao (JPSSG) alleviation of skeletal myoblast cell apoptosis, oxidative stress, and mitochondrial dysfunction to improve cancer-related fatigue in an AMPK-SIRT1- and HIF-1-dependent manner.

Jian Pi Sheng Sui Gao (JPSSG), a Chinese traditional herbal paste, possesses certain efficacy in patients with cancer-related fatigue (CRF); however, its related mechanism remains unclear. Hence, network pharmacology analysis, followed by in vivo and in vitro experiments were conducted in this study with the aim to evaluate the effect of JPSSG on CRF and clarify its potential mechanism. Network pharmacology analysis was performed. Subsequently, 12 mice were injected with CT26 cells to establish CRF mouse models and randomly divided into a model group (n=6) and JPSSG group (n=6); meanwhile, another 6 normal mice served as a control group. Then, 3.0 g/kg JPSSG was given to mice in JPSSG group for 15 days, while mice in the n control and model groups received phosphate-buffered saline (PBS) of the same volume for 15 days. For the in vitro experiment, CT26 conditioned medium (CM) was established; meanwhile, the mitochondrial damage model was constructed through C2C12 myotubes stimulated with H2O2. C2C12 myotubes were divided into 5 groups: control group (without treatment), CM group, CM + JPSSG group, H2O2 group, and H2O2 + JGSSP group. Network pharmacology analysis identified 87 bioactive compounds and 132 JPSSG-CRF interaction targets. Moreover, according to the Kyoto Encyclopedia of Genes and Genomes enrichment analysis and the subsequent in vivo and in vitro experiments, JPSSG activated adenosine 5'-monophosphate-activated protein kinase-silent-information-regulator factor 2-related-enzyme 1 (AMPK-SIRT1) and hypoxia-inducible factor-1 (HIF-1) signaling pathways during CRF. Moreover, the in vivo experiment showed that JPSSG attenuated CRF in mice, reflected by increased distance traveled, mobile time in open field test, and swimming time in exhaustive swimming test, and decreased absolute rest time and tail suspension test in the JPSSG group (vs. model group). Furthermore, JPSSG upregulated gastrocnemius weight, adenosine triphosphate (ATP), superoxide dismutase (SOD), and the cross-sectional area of the gastrocnemius. With regard to in vitro study, JPSSG elevated cell viability, B-cell lymphoma-2, ATP, SOD, and mitochondrial membrane potential, while it decreased apoptosis rate, cleaved-caspase3, malondialdehyde, and reactive oxygen species in C2C12 myotubes. JPSSG ameliorates CRF via alleviating skeletal myoblast cell apoptosis, oxidative stress, and mitochondrial dysfunction in an AMPK-SIRT1- and HIF-1-dependent manner.

Lansoprazole attenuates cyclophosphamide-induced cardiopulmonary injury by modulating redox-sensitive pathways and inflammation.

Cyclophosphamide (CPA) is a classical chemotherapeutic drug widely used as an anticancer and immunosuppressive agent. However, it is frequently associated with significant toxicities to the normal cells of different organs, including the lung and heart. Lansoprazole (LPZ), a proton pump inhibitor (PPI), possesses antioxidant and anti-inflammatory properties. The current study investigated how LPZ protects against CPA-induced cardiac and pulmonary damage, focusing on PPARγ, Nrf2, HO-1, cytoglobin, PI3K/AKT, and NF-κB signaling. Animals were randomly assigned into four groups: normal control group (received vehicle), LPZ only group (Rats received LPZ at a dose of 50mg/kg/day P.O. for 10days), CPA group (CPA was administered (200mg/kg) as a single i.p. injection on the 7th day), and cotreatment group (LPZ plus CPA). Histopathological and biochemical analyses were conducted. Our results revealed that LPZ treatment revoked CPA-induced heart and lung histopathological alterations. Also, LPZ potently mitigated CPA-induced cardiac and pulmonary oxidative stress through the activation of PPARγ, Nrf2/HO-1, cytoglobin, and PI3K/AKT signaling pathways. Also, LPZ effectively suppressed inflammatory response as evidenced by down-regulating the inflammatory strategic controller NF-κB, MPO, and pro-inflammatory cytokines. The present findings could provide a mechanistic basis for understanding LPZ's role in CPA-induced cardiopulmonary injury through the alleviation of oxidative stress and inflammatory burden.

Genome-centered metagenomics illuminates adaptations of core members to a partial Nitritation-Anammox bioreactor under periodic microaeration.

The partial nitritation-anaerobic ammonium oxidation (anammox; PN-A) process has been considered a sustainable method for wastewater ammonium removal, with recent attempts to treat low-strength wastewater. However, how microbes adapt to the alternate microaerobic-anoxic operation of the process when treating low ammonium concentrations remains poorly understood. In this study, we applied a metagenomic approach to determine the genomic contents of core members in a PN-A reactor treating inorganic ammonium wastewater at loading as low as 0.0192 kg-N/m3/day. The metabolic traits of metagenome-assembled genomes from 18 core species were analyzed. Taxonomically diverse ammonia oxidizers, including two Nitrosomonas species, a comammox Nitrospira species, a novel Chloroflexota-related species, and two anammox bacteria, Ca. Brocadia and Ca. Jettenia, accounted for the PN-A reactions. The characteristics of a series of genes encoding class II ribonucleotide reductase, high-affinity bd-type terminal oxidase, and diverse antioxidant enzymes revealed that comammox Nitrospira has a superior adaptation ability over the competitors, which may confer the privileged partnership with anammox bacteria in the PN-A reactor. This finding is supported by the long-term monitoring experiment, showing the predominance of the comammox Nitrospira in the ammonia-oxidizing community. Metagenomic analysis of seven heterotrophs suggested that nitrate reduction is a common capability in potentially using endogenous carbohydrates and peptides to enhance nitrogen removals. The prevalence of class II ribonucleotide reductase and antioxidant enzymes genes may grant the adaptation to cyclically microaerobic/anoxic environments. The predominant heterotroph is affiliated with Chloroflexota; its genome encodes complete pathways for synthesizing vitamin B6 and methionine. By contrast, other than the two growth factors, Nitrospira and anammox bacteria are complementary to produce various vitamins and amino acids. Besides, the novel Chloroflexota-related ammonia oxidizer lacks corresponding genes for detoxifying the reactive oxygen species and thus requires the aid of co-existing members to alleviate oxidative stress. The analysis results forecast the exchanges of substrates and nutrients as well as the collective alleviation of oxidative stress among the core populations. The new findings of the genomic features and predicted microbial interplay shed light on microbial adaptation to intermittent microaeration specific to the PN-A reactor, which may aid in improving its application to low-strength ammonium wastewater.

Metabolomics analysis reveals amelioration effects of yellowhorn tea extract on hyperlipidemia, inflammation, and oxidative stress in high-fat diet-fed mice.

Yellowhorn tea (YT) is traditionally used as a lipid-lowering beverage in Mongolian minorities. However, the pharmacological effects of YT extract and its specific metabolic changes in hyperlipidemia models are not fully understood. The aim of this study was to identify biomarkers using untargeted metabolomics techniques and to investigate the mechanisms underlying the changes in metabolic pathways associated with lipid lowering, anti-inflammation and anti-oxidant in hyperlipidemic mice. A high-fat diet (HFD)-induced hyperlipidemic mouse model was established. YT extract was administered as oral gavage at 0.15, 0.3, and 0.6 g/kg doses for 10 weeks. HFD-induced hyperlipidemia and the therapeutic effect of YT extract were evaluated based on histopathology and by assessing blood lipid levels. Liver inflammatory factors and oxidative stress indices were determined using enzyme-linked immunosorbent assays. Liver metabolites were evaluated using untargeted metabolomics. Biochemical and histological examinations showed that YT extract significantly reduced body-weight gain (p < 0.01) and fat deposition in tissues. YT extract significantly reduced the levels of serum and liver triglyceride and total cholesterol; inflammatory factors [interleukin (IL)-6, IL-1β, and tumor necrosis factor-α]; malondialdehyde; and leptin (p < 0.05) in hyperlipidemic mice. YT extract also significantly increased the levels of oxidative stress indicators (superoxide dismutase, catalase, and glutathione peroxidase) and adiponectin. Metabolomics studies revealed several endogenous molecules were altered by the high-fat diet and recovery following intervention with YT extract. The metabolites that were significantly different in the liver after YT intake included citicoline, acetylcholine, pyridoxine, and NAD. Pathway analysis indicated that YT extract ameliorated HFD-induced hyperlipidemia in mice via three major metabolic pathways, namely, glycerophospholipid metabolism, vitamin B6 metabolism, and nicotinate and nicotinamide metabolism. This study demonstrates YT extract has profound effects on the alleviation of HFD-induced hyperlipidemia, inflammation and oxidative stress.

CaFe-layered double hydroxide corn straw biochar reduced heavy metal uptake by Brassica campestris L. and Ipomoea aquatic F.: Rhizosphere effects and oxidative stress alleviation

In the present study, CaFe-layered double hydroxide corn straw biochar (CaFe-LDH@CSB) was applied to the rhizosphere soil of both pakchoi (Brassica campestris L. ssp. Chinensis Makino, B. campestris L.) and water spinach (Ipomoea aquatic F., I. aquatic F.) to explore and clarify the potential mechanism by which CaFe-LDH@CSB helps vegetables reduce heavy metal (HM) uptake and alleviate oxidative stress. Pot experiments were conducted with CaFe-LDH@CSB applied at four levels: control (CK), T1 (5 g kg−1), T2 (10 g kg−1) and T3 (20 g kg−1). The results indicated that the application of CaFe-LDH@CSB significantly increased pH and decreased the acid-soluble forms of Cd, Pb, Zn and Cu in the rhizosphere soil of both B. campestris L. and I. aquatic F.; decreases of 39.4%, 18.0%, 10.0% and 33.3% in B. campestris L. and of 26.6%, 49.1%, 13.2% and 36.8% in I. aquatic F., respectively, were observed at the T3 level. Moreover, CaFe-LDH@CSB application reduced HM uptake by B. campestris L. and decreased HM-induced oxidative stress through the regulation of soil physicochemical properties and microbial abundance. For B. campestris L., variations in Sordariomycetes helped alleviate the accumulation of HMs in the aerial part, while GSH and –SH from the nonenzymatic system played an important role in scavenging H2O2 in leaves, thus helping B. campestris L. alleviate HM-induced oxidative stress. For I. aquatica F., variations in Vicinamibacteria and Mortierellomycetes helped alleviate the accumulation of HMs in plants, while GSH and PCs from nonenzymatic systems played an important role in removing ·O2− in leaves, thereby helping I. aquatica F. alleviate HM-induced oxidation stress. Our study indicated that the application of CaFe-LDH@CSB improved the rhizosphere soil environment and rebuilt the soil microbial community, helping B. campestris L. and I. aquatica F. alleviate HM-induced oxidative stress and promoting the growth of both vegetables.

Vitamin D Supplementation in Alleviation of Oxidative Stress among Type 2 Diabetics

Globally diabetes mellitus (T2DM) is a burning issue. Prediction of global estimation that the proportion of diabetes with adult will increase 69% for the year 2030. Hans Selye, the Canadian physiologist, was the first scientist to study the effects of psychological stress on the human body in 1936.Diabetic patients are in a state of high oxidative stress which leading to impaired glucose homeostasis, insulin insufficiency, and other complications.: A randomized controlled trial was conducted to see the effect of the vitamin D supplementation on oxidative stress in vitamin D deficientT2DM patients. In this study, a total of 124 T2DM patients were randomly enrolled, among them Treatment group 61 and placebo 63. In treatment group received 20,000IU vitamin D every 5thDay for three months in addition to regular treatment. Analysis of fasting plasma glucose (FPG), Vitamin D 25(OH)2, malondialdehyde (MDA) and superoxide dismutase (SOD) have been estimated both at the time of study recruitment, at 6th weeks and after 12-weeks of vitamin D supplementation (endline). Present study showed after vitamin D supplementation, baseline mean FBG gradually significantly (P&lt;0.001) decreased at the end line in treatment group as compared to placebo. All biochemical indices by P- trend like FBG, vitamin D, MDA and SOD were significantly different (P&lt;0.05). Whenever, consider between groups vitamin D increased (P&lt;0.05) and FBG decreased significantly (P&lt;0.05) in treatment group as compared to placebo. However, no significant impact on socio-demography variables, vitamin D and Stress-related characteristics between treatment and control groups after vitamin D supplementation as those variables are somewhat independent (p&gt;0.05) both at baseline and end line. The results were considered significant at P&lt;0.05. The statistical calculations were done using SPSS version 26 software. A strong positive co-relation between diabetes and oxidative stress were observed in this study and showed beneficial impact of vitamin D supplementation to reduce oxidative stress those who were vitamin D deficient.

Resistance mechanisms and remediation potential of hexavalent chromium in Pseudomonas sp. strain AN-B15

The understanding of bacterial resistance to hexavalent chromium [Cr(VI)] are crucial for the enhancement of Cr(VI)-polluted soil bioremediation. However, the mechanisms related to plant-associated bacteria remain largely unclear. In this study, we investigate the resistance mechanisms and remediation potential of Cr(VI) in a plant-associated strain, AN-B15. The results manifested that AN-B15 efficiently reduced Cr(VI) to soluble organo-Cr(III). Specifically, 84.3 % and 56.5 % of Cr(VI) was removed after 48 h in strain-inoculated solutions supplemented with 10 and 20 mg/L Cr(VI) concentrations, respectively. Transcriptome analyses revealed that multiple metabolic systems are responsible for Cr(VI) resistance at the transcriptional level. In response to Cr(VI) exposure, strain AN-B15 up-regulated the genes involved in central metabolism, providing the reducing power by which enzymes (ChrR and azoR) transformed Cr(VI) to Cr(III) in the cytoplasm. Genes involved in the alleviation of oxidative stress and DNA repair were significantly up-regulated to neutralize Cr(VI)-induced toxicity. Additionally, genes involved in organosulfur metabolism and certain ion transporters were up-regulated to counteract the starvation of sulfur, molybdate, iron, and manganese induced by Cr(VI) stress. Furthermore, a hydroponic culture experiment showed that toxicity and uptake of Cr(VI) by plants under Cr(VI) stress were reduced by strain AN-B15. Specifically, strain AN-B15 inoculation increased the fresh weights of the wheat root and shoot by 55.5 % and 18.8 %, respectively, under Cr(VI) stress (5 mg/L). The elucidation of bacterial resistance to Cr(VI) has an important implication for exploiting microorganism for the effective remediation of Cr(VI)-polluted soils.

Enzyme a Biosynthesis System on Manifestation of Metabolic Stress and Glutathione System in the CNS under Aluminium Neurotoxicosis

Alzheimer’s-like disease was simulated in female adult Wistar CRL(WI) WUBR rats by 6-week intragastric administration of aluminium chloride at a dose of 200 mg/kg body mass. In the presence of developed oxidative stress (OS), we found a decrease in the activities of tricarboxylic acid cycle (TCA cycle) enzymes and an increase in the activities of pentose phosphate pathway (PPP) dehydrogenases as well as a reduction of SH-and SS-groups in proteins (P) along with the increased SH/SS ratio and glutathionylation with simultaneous decreases of glutathione (GSH) and the GSH/GSSG ratio and its redox potential in the brain hemispheres. The glutathione system enzymes were changed multidirectionally, with glutathione reductase remaining stable. Decreased activities of GSH biosynthesis enzymes and cysteine content were noticed. The intragastric administration of the CoA biosynthesis modulators D-panthenol (PL), D-pantethine or D-homopantothenate (HPA) at a dose of 200 mg/kg since the 5th week of the experiment caused either reduction or leveling of OS manifestations in blood plasma, an increase in acetyl cholinesterase, normalization of the activities of TCA cycle and PPP enzymes, P-SH level (not the SH/SS ratio) and a considerable reduction of S-glutathionylation as well as increases in GSH level, the GSH/GSSG ratio and redox potential in the hemispheres. The effect of CoA system modulators was manifested in activation of glutathione transferase, a decrease of glutathione peroxidase and less evident activation of GSH biosynthesis enzymes (PL) although they contributed to the elevation of cysteine content due to the reduced protein S-cysteinylation. The levels and the ratio of CoA/acetyl-CoA (except for PL) were not changed by toxicosis and the OS modulators. The feasibility of non-conenzyme effects was confirmed by the administration of HPA. The phenomenon of redox activity of the CoA biosynthesis modulators with clearly directional effects on the glutathione system and the TCA cycle and PPP enzymes during alleviation of OS and aluminium neurotoxicosis is discussed.

Thiol-Disulfide Exchange Coordinates the Release of Nitric Oxide and Dexamethasone for Synergistic Regulation of Intestinal Microenvironment in Colitis.

The cell-specific functions of nitric oxide (NO) in the intestinal microenvironment orchestrate its therapeutic effects in ulcerative colitis. While most biomaterials show promise by eliciting the characteristics of NO, the insufficient storage, burst release, and pro-inflammatory side effects of NO remain as challenges. Herein, we report the development of thiol-disulfide hybrid mesoporous organosilica nanoparticles (MONs) that improve the storage and sustained release of NO, broadening the therapeutic window of NO-based therapy against colitis. The tailored NO-storing nanomaterials coordinated the release of NO and the immunoregulator dexamethasone (Dex) in the intestinal microenvironment, specifically integrating the alleviation of oxidative stress in enterocytes and the reversal of NO-exacerbated macrophage activation. Mechanistically, such a synchronous operation was achieved by a self-motivated process wherein the thiyl radicals produced by NO release cleaved the disulfide bonds to degrade the matrix and release Dex via thiol-disulfide exchange. Specifically, the MON-mediated combination of NO and Dex greatly ameliorated intractable colitis compared with 5-aminosalicylic acid, even after delayed treatment. Together, our results reveal a key contribution of synergistic modulation of the intestinal microenvironment in NO-based colitis therapy and introduce thiol-disulfide hybrid nanotherapeutics for the management of inflammatory diseases and cancer.

External-loop split-type dynamic membrane photobioreactor for the treatment of high-strength pyridine wastewater: Improved photosynthetic oxygenation and mitigated membrane fouling

In order to avoid pyridine volatilization in the conventional aerobic system based on bubble aeration, an algal-bacterial symbiotic system based on photosynthetic oxygenation was developed. Nonetheless, pyridine at high concentration would inhibit algal growth and photosynthetic activity, and thus decrease oxygen production efficiency. An external-loop split-type dynamic membrane photobioreactor system was proposed for treating high-strength pyridine wastewater, which consisted of a pyridine degrading reactor (R 1-1 ), and an algal-bacterial dynamic membrane bioreactor (R 1-2 ) for the photosynthetic oxygenation. The results showed that pyridine could be effectively removed at the influent concentration as high as 500 mg·L -1 at the hydraulic retention time of 48 h. Preferable algal growth and photosynthetic activity were retained in R 1-2 , with Fv/Fm maintained at 0.502±0.013 at the influent pyridine concentration of 500 mg·L -1 . The decreased reactive oxygen species and malondialdehyde level as well as the relative low catalase and superoxide dismutase activities also revealed the alleviation of oxidative stress in algae. The mitigated membrane fouling was due to reduced protein/polysaccharide ratio in the extracellular polymeric substances in the mixed liquor and fouling layer in R 1-2 . Rhodobacter and Rhodococcus were the dominant genus in R 1-1 and R 1-2 , and Chlorella was enriched in R 1-2 , responsible for pyridine degradation and oxygen production. • ESDMPBR was developed to alleviate the inhibitory effects of pyridine to algae. • Pyridine removal, nitrogen removal and oxygen production were enhanced in ESDMPBR. • Membrane fouling could be alleviated at high PS concentration and low PN/PS ratio. • Mechanism for enhanced pyridine removal involved in ESDMPBR was proposed. • Algal-bacterial symbiotic system was promising in treating high-strength pyridine.

Effect of Acarbose and olive leaf extract (Oleuropein) on Glycemic index and Antioxidant Status in High Fructose and H2O2 Exposed Rats (Parts-II)

This study was carried out to investigate the effect of acarbose or combination of acarbose and Oleuropein (OLEU) on glycemic index and antioxidant status of male rats exposed to high fructose(40%) and 0.05% hydrogen peroxide H2O2 Thirty-two adult male rats were randomly divided into four equal groups: control group (CC); T1( HFr-H2O2) group were exposed to high fructose (40%) in drinking water and given orally 0.05% H2O2; T2: 30mg/kg of acarbose were given orally to HF-H2O2 treated rats, while combination of acarbose and Oleuropein (50mg/kg. B.W) were given orally to (HFr-H2O2) treated rats in group T3. Blood samples were taken at zero time and after two months of the experiment for measuring some parameters related to glycemic index and antioxidant status. The results declared an elevation in the glycemic index (insulin and glucose concentrations and insulin resistance (IR)) and malondialdehyde (MDA) and depression in glutathione (GSH) concentrations in T1 group at the end of experiment comparing to other treated groups. Antioxidant status and glycemic index were restored after acarbose or combination of acarbose and Oleuropein treatment characterized by significant depression of serum glucose, insulin concentrations and IR, and alleviation of oxidative stress clarified by depression of serum MDA with elevation in serum GSH concentration in groups T2 and T3. On conclusion, the current study documented the oxidative and hyperglycemic effect of fructose and H2O2 that can be ameliorating by oral administration of acarbose. Besides, combination of OLUE supplement with acarbose possessed additive effects.

Pingyin Rose Essential Oil Restores Intestinal Barrier Integrity in DSS-induced Mice Colitis Model

Rosa rugosa cv. Plena is a ‘drug homologous food’ in China with a long history. Pingyin rose essential oil (PREO) is a mixture of compounds extracted from blooming R. rugosa cv. Plena. With its elegant smell and excellent effects on oxidative stress and inflammation alleviation, PREO is wildly used in the food industry as a popular additive. We aimed to decipher if the PREO could alleviate and restore dextran sodium sulfate (DSS)-induced barrier integrity damages. The results showed that a 7-day PREO (15 μL/kg) treatment alleviated the colitis symptoms by improving disease activity index (DAI) scores through weight loss, occult blood, and colon shortening. The expression of tight junction proteins and the enzyme activities of superoxide dismutases (SOD), and catalase (CAT) increased while nitric oxide (NO), malondialdehyde (MDA), and myeloperoxidase (MPO) production decreased in PREO-treated BALB/c female mice. PREO treatment inhibited the expression of pro-inflammatory cytokines tumor necrosis factor (TNF-α), interleukin (IL)-1β, and IL-6. Further, PREO modulated the composition of the gut microbiota and Spearman’s correlation analysis revealed a positive effect. The transcriptome analysis and western blot results indicated that PREO might ameliorate intestinal barrier dysfunction in this study via the TLR4-NF-kB signaling pathway. We hypothesized that PREO has preventive potential against gut disorders and could serve as a functional food additive.

Coassembly of Fiber Hydrogel with Antibacterial Activity for Wound Healing.

Wound healing remains a critical challenge due to its vulnerability to bacterial infection and the complicated inflammatory microenvironment. Herein, we report a novel antibacterial hydrogel constructed only by gallic acid (GA) and phycocyanin (PC), which is expected for the treatment of bacteria-infected wounds. These GA/PC hydrogels (GP) was found to coassemble into fibrous networks with a diameter of around 2 μm mainly through noncovalent interactions of hydrogen bonds, van der Waals force, and π interaction. Notably, these GP hydrogels showed excellent rheological properties (i.e., storage modulus of more than 9.0 × 104 Pa) and outstanding biocompatibility and antibacterial activities. Thanks to the incorporation of GA and PC, the GP hydrogels enabled adherence to the moist wound tissue and achieved a sustained release of GA and PC into the wound skin, therefore effectively attenuating inflammation and accelerating wound healing both in normal mice and bacteria-infected mice through regulating the expression of the tight junction protein and the alleviation of oxidative stress. Considering these results, these GP hydrogels are demonstrated to be a promising candidate for bacteria-infected wound healing.

Mesenchymal stem cell-derived exosomes: The dawn of diabetic wound healing.

Chronic wound healing has long been an unmet medical need in the field of wound repair, with diabetes being one of the major etiologies. Diabetic chronic wounds (DCWs), especially diabetic foot ulcers, are one of the most threatening chronic complications of diabetes. Although the treatment strategies, drugs, and dressings for DCWs have made great progress, they remain ineffective in some patients with refractory wounds. Stem cell-based therapies have achieved specific efficacy in various fields, with mesenchymal stem cells (MSCs) being the most widely used. Although MSCs have achieved good feedback in preclinical studies and clinical trials in the treatment of cutaneous wounds or other situations, the potential safety concerns associated with allogeneic/autologous stem cells and unknown long-term health effects need further attention and supervision. Recent studies have reported that stem cells mainly exert their trauma repair effects through paracrine secretion, and exosomes play an important role in intercellular communication as their main bioactive component. MSC-derived exosomes (MSC-Exos) inherit the powerful inflammation and immune modulation, angiogenesis, cell proliferation and migration promotion, oxidative stress alleviation, collagen remodeling imbalances regulation of their parental cells, and can avoid the potential risks of direct stem cell transplantation to a large extent, thus demonstrating promising performance as novel "cell-free" therapies in chronic wounds. This review aimed to elucidate the potential mechanism and update the progress of MSC-Exos in DCW healing, thereby providing new therapeutic directions for DCWs that are difficult to be cured using conventional therapy.

Regulation of denitrification performance and microbial topology by lights: Insight into wavelength effects towards microbiota

The low efficiency of conventional complete denitrification, as well as the unstable nitrite supply for partial-denitrification coupled anammox (PD/A) restrict the efficient removal of nitrogen from industrial wastewaters. Herein, we proposed an optical strategy to bidirectionally regulate denitrification by introducing lights at different wavelengths, and the underlying mechanisms were elucidated accordingly. It turned out that yellow light at wavelength of 590 nm accelerated denitrification by 35.4%, while blue light delayed denitrification with stable nitrite accumulation above 86.9% and high nitrate removal (99.8%). Microbial physiology and viability further supported the positive effects of yellow light on microbial activity. Additionally, despite the sluggish denitrification aroused by blue light, negligible cellular damage was observed. Antioxidant capability divergence, microbial community shifting and metabolic flux redirection contributed to the wavelength-dependent effects. Halomonas and Pseudomonas were identified as high-credit taxonomic biomarkers of yellow and blue light. As revealed by metabolomics, pantothenate and CoA biosynthesis, glutamate metabolism and alkaloid biosynthesis presented high impact values. Co-analysis of metabolomics and metagenomics based on microbial topology further distinguished pivotal metabolic pathways and genes. Oxidative phosphorylation contributed to the divergent denitrification performance through electron transfer chains, whereas glutamate and glutathione metabolism contributed to oxidative stress alleviation and mediated the metabolic flux between peroxisome and nitrogen metabolism. This study shed a light on the application of optical strategy to regulate denitrification performance and achieve either complete denitrification or PD/A.