Reactive Oxygen Species Scavenger Research Articles

Regulation of plum fruit cracking process during cold storage period by treatment of preharvest chitosan

Cracking fruit is a serious quality change phenomenon in the storage and transportation of postharvest plum fruit. To reduce the cracking rate of plum fruit during cold storage, the 'Guofeng No.7' plum was sprayed with chitosan with 1.5% concentration 30d from preharvest. The postharvest plum fruit was stored at (0±0.5) °C and (85-90) % relative humidity. The results showed that chitosan treatment could reduce the reactive oxygen species (ROS) level of plum fruit, effectively delaying the fruit cracking. Compared with the control, chitosan treated fruits inhibited the increase of free radical content such as O2-· and H2O2 and delayed the increase of membrane permeability and the accumulation of MDA (from 71.9 mmol/g to 53.5 mmol/g). It also regulates lipoxygenase (LOX), peroxidase (POD), superoxide dismutase (SOD), catalase (CAT) (enzymatic activity from 34.15 g/min to 42.21 g/min) and ascorbate peroxidase (APX) activity and gene expression during fruit cracking to maintain membrane integrity and intracellular compartmentalization, thereby increasing the crack tolerance of plum fruit during cold storage. These results indicate that preharvest chitosan treatment can inhibit the metabolism of active oxygen species, increase the activity of ROS scavenging enzymes and gene expression, and delay the postharvest cracking of plum fruit.

Bioinspired nanozyme-reinforced hydrogels with free radical scavenging capability for treating temporomandibular joint osteoarthritis

Temporomandibular joint osteoarthritis (TMJ-OA) is usually caused by increased friction at the joint interface, excessive release of inflammatory factors and catabolic enzymes, and free radical accumulation, which can lead to accelerated degradation and damage of cartilage. In this study, we develop a biological metabolism-inspired injectable hydrogel crosslinking by hydrazide modified hyaluronic acid (HA-HYD), aldehyde modified hyaluronic acid (HA-ALD), and ε-polylysine coated catalase-mimic nanozyme (mesoporous manganese cobalt oxide). Herein, this nanozyme-reinforced hydrogel with outstanding and durable reactive oxygen species (ROS) depletion capability and biocompatibility can alleviate the oxidative stress microenvironment, improve cell viability and proliferation, as well as up-regulate chondrogenic related gene expression and cartilage matrix formation of chondrocytes in vitro. Intra-articular administration of this engineered hydrogel can effectively scavenge endogenous over-expressed ROS to ameliorate the harsh microenvironment in the cavity of TMJ-OA. The nanozyme-reinforced hydrogel reduced proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and enhance anti-inflammatory cytokines (IL-10) expression, induced polarization of synovial macrophages towards M2 phenotype, alleviated structural damage to the cartilage and subchondral bone of the condyle, thus reducing cartilage matrix destruction and protect cartilage in osteoarthritis. In summary, the bioinspired nanozyme-reinforced hydrogels might be used as a promising ROS scavenger for treatment of TMJ-OA.

Physiological and molecular mechanisms of melatonin to alleviate benzoic acid-induced autotoxicity stress in Prunus persica

Autotoxicity stress is well known as a critical factor in the replant problem that hinders the sustainable development of agriculture. Benzoic acid (BA) is identified as a major autotoxin in peach replant problem, and causes serious growth inhibition of peach plants. Melatonin is a multi-functional molecule that plays a key role in alleviating stress-induced damage in plants. However, the functions and the inherent molecular mechanisms of melatonin under autotoxicity stress remains largely elusive. Here, we found that application of melatonin significantly enhanced BA tolerance in peach seedlings. Exogenous melatonin mitigated the negative impact of BA stress on peach root growth. Melatonin pretreatment boosted flavonoid biosynthesis and increased soluble sugar content of peach plants under BA stress. In addition, melatonin also promoted the reactive oxygen species scavenging by enhancing the antioxidant capacity. Consistent with these alterations, transcriptome analysis demonstrated that up-regulations of flavonoid biosynthesis, starch and sucrose metabolism, and antioxidant-related genes were observed when melatonin applied under BA stress. Furthermore, we also observed that an induction in genes involved in xenobiotic transmembrane transport, cell wall organization or biogenesis, and α-linolenic acid metabolism, which might contribute to the melatonin-mediated BA tolerance. Collectively, our findings reveal that melatonin confers BA tolerance of peach seedlings, primarily attributed to increased flavonoid and soluble sugar levels, enhanced antioxidant capacities, and extensive transcriptome reprograming. This opens new avenues for utilizing melatonin to alleviate peach replant problem.

Myricanol prevents aging-related sarcopenia by rescuing mitochondrial dysfunction via targeting peroxiredoxin 5.

Aging is a process that represents the accumulation of changes in organism overtime. In biological level, accumulations of molecular and cellular damage in aging lead to an increasing risk of diseases like sarcopenia. Sarcopenia reduces mobility, leads to fall-related injuries, and diminishes life quality. Thus, it is meaningful to find out novel therapeutic strategies for sarcopenia intervention that may help the elderly maintain their functional ability. Oxidative damage-induced dysfunctional mitochondria are considered as a culprit of muscle wasting during aging. Herein, we aimed to demonstrate whether myricanol (MY) protects aged mice against muscle wasting through alleviating oxidative damage in mitochondria and identify the direct protein target and its underlying mechanism. We discovered that MY protects aged mice against the loss of muscle mass and strength through scavenging reactive oxygen species accumulation to rebuild the redox homeostasis. Taking advantage of biophysical assays, peroxiredoxin 5 was discovered and validated as the direct target of MY. Through activating peroxiredoxin 5, MY reduced reactive oxygen species accumulation and damaged mitochondrial DNA in C2C12 myotubes. Our findings provide an insight for therapy against sarcopenia through alleviating oxidative damage-induced dysfunctional mitochondria by targeting peroxiredoxin 5, which may contribute an insight for healthy aging.

Hispidin Increases Cell Apoptosis and Ferroptosis in Prostate Cancer Cells Through Phosphatidylinositol-3-Kinase and Mitogen-activated Protein Kinase Signaling Pathway.

Chemotherapy is mainly used in the clinical treatment of prostate cancer. Different anticancer mechanisms can induce cell death in various cancers. Reactive oxygen species (ROS) play crucial roles in cell proliferation, differentiation, apoptosis, and signal transduction. It is widely accepted that ROS accumulation is closely related to chemical drug-induced cancer cell death. We utilized the MTT assay to detect changes in cell proliferation. Additionally, colony formation and wound healing assay were conducted to investigate the effect of hispidin on cell colony formation and migration ability. Fluorescence microscopy was used to detect intracellular and mitochondrial ROS levels, while western blot was used for detection of cell apoptosis. Hispidin treatment significantly decreased viability of PC3 and DU145 cancer cells but exhibited no cytotoxicity in WPMY-1 cells. Furthermore, hispidin treatment inhibited cell migration and colony formation and triggered cellular and mitochondrial ROS accumulation, leading to mitochondrial dysfunction and mitochondrion-dependent apoptosis. Moreover, hispidin treatment induced ferroptosis in PC3 cells. Scavenging of ROS with N-acetyl cysteine significantly inhibited hispidin-induced apoptosis by altering the expression of apoptosis-related proteins, such as cleaved caspase-3, 9, Bax, and Bcl2. Furthermore, hispidin treatment dramatically up-regulated MAPK (involving p38, ERK, and JNK proteins) and NF-kB signaling pathways while down-regulating AKT phosphorylation. Hispidin treatment also inhibited ferroptosis signaling pathways (involving P53, Nrf-2, and HO-1 proteins) in PC3 cells. In addition, inhibiting these signaling pathways via treatment with specific inhibitors significantly reversed hispidin-induced apoptosis, cellular ROS levels, mitochondrial dysfunction, and ferroptosis. Hispidin may represent a potential candidate for treating prostate cancer.

Peroxiredoxin I and II as novel therapeutic molecular targets in cervical cancer treatment through regulation of endoplasmic reticulum stress induced by bleomycin

Cervical cancer, significantly affecting women worldwide, often involves treatment with bleomycin, an anticancer agent targeting breast, ovarian, and cervical cancers by generating reactive oxygen species (ROS) to induce cancer cell death. The Peroxiredoxin (PRDX) family, particularly PRDX1 and 2, plays a vital role in maintaining cellular balance by scavenging ROS, thus mitigating the damaging effects of bleomycin-induced mitochondrial and cellular oxidative stress. This process reduces endoplasmic reticulum (ER) stress and prevents cell apoptosis. However, reducing PRDX1 and 2 levels reverses their protective effect, increasing apoptosis. This research highlights the importance of PRDX1 and 2 in cervical cancer treatments with bleomycin, showing their potential to enhance treatment efficacy by managing ROS and ER stress and suggesting a therapeutic strategy for improving outcomes in cervical cancer treatment.

Oral administration of probiotic spore ghosts for efficient attenuation of radiation-induced intestinal injury

Radiation-induced intestinal injury is the most common side effect during radiotherapy of abdominal or pelvic solid tumors, significantly impacting patients’ quality of life and even resulting in poor prognosis. Until now, oral application of conventional formulations for intestinal radioprotection remains challenging with no preferred method available to mitigate radiation toxicity in small intestine. Our previous study revealed that nanomaterials derived from spore coat of probiotics exhibit superior anti-inflammatory effect and even prevent the progression of cancer. The aim of this work is to determine the radioprotective effect of spore coat (denoted as spore ghosts, SGs) from three clinically approved probiotics (B.coagulans, B.subtilis and B.licheniformis). All the three SGs exhibit outstanding reactive oxygen species (ROS) scavenging ability and excellent anti-inflammatory effect. Moreover, these SGs can reverse the balance of intestinal flora by inhibiting harmful bacteria and increasing the abundance of Lactobacillus. Consequently, administration of SGs significantly reduce radiation-induced intestinal injury by alleviating diarrhea, preventing X-ray induced apoptosis of small intestinal epithelial cells and promoting restoration of barrier integrity in a prophylactic study. Notably, SGs markedly improve weight gain and survival of mice received total abdominal X-ray radiation. This work may provide promising radioprotectants for efficiently attenuating radiation-induced gastrointestinal syndrome and promote the development of new intestinal predilection.

Serum albumin-embedding copper nanoclusters inhibit Alzheimer’s β-amyloid fibrillogenesis and neuroinflammation

Increasing evidence suggests that the accumulations of reactive oxygen species (ROS), β-amyloid (Aβ), and neuroinflammation are crucial pathological hallmarks for the onset of Alzheimer’s disease (AD), yet there are few effective treatment strategies. Therefore, design of nanomaterials capable of simultaneously elimination of ROS and inhibition of Aβ aggregation and neuroinflammation is urgently needed for AD treatment. Herein, we designed human serum albumin (HSA)-embedded ultrasmall copper nanoclusters (CuNCs@HSA) via an HSA-mediated fabrication strategy. The as-prepared CuNCs@HSA exhibited outstanding multiple enzyme-like properties, including superoxide dismutase (>5000 U/mg), catalase, and glutathione peroxidase activities as well as hydroxyl radicals scavenging ability. Besides, CuNCs@HSA prominently inhibited Aβ fibrillization, and its inhibitory potency was 2.5-fold higher than native HSA. Moreover, CuNCs@HSA could significantly increase the viability of Aβ-treated cells from 60 % to over 96 % at 40 μg/mL and mitigate Aβ-induced oxidative stresses. The secretion of neuroinflammatory cytokines by lipopolysaccharide-induced BV-2 cells, including tumor necrosis factor-α and interleukin-6, was alleviated by CuNCs@HSA. In vivo studies manifested that CuNCs@HSA effectively suppressed the formation of plaques in transgenic C. elegans, reduced ROS levels, and extended C. elegans lifespan by 5 d. This work, using HSA as a template to mediate the fabrication of copper nanoclusters with robust ROS scavenging capability, exhibited promising potentials in inhibiting Aβ aggregation and neuroinflammation for AD treatment.

Integrated insulin-iron nanoparticles: a multi-modal approach for receptor-specific bioimaging, reactive oxygen species scavenging, and wound healing

Metallic nanoparticles have emerged as a promising option for various biological applications, owing to their distinct characteristics such as small size, optical properties, and ability to exhibit luminescence. In this study, we have successfully employed a one-pot method to synthesize multifunctional insulin-protected iron [Fe(II)] nanoparticles denoted as [IFe(II)NPs]. The formation of IFe(II)NPs is confirmed by the presence of FTIR bonds at 447.47 and 798.28 cm−1, corresponding to Fe–O and Fe–N bonds, respectively. Detailed analysis of the HR-TEM-EDS-SAED data reveals that the particles are spherical in shape, partially amorphous in nature, and have a diameter of 28.6 ± 5.2 nm. Additionally, Metal Ion Binding (MIB) and Protein Data Bank (PDB) analyses affirm the binding of iron ions to the insulin hexamer. Our findings underscore the potential of IFe(II)NPs as a promising new platform for a variety of biomedical applications due to their high signal-to-noise ratio, and minimal background fluorescence. The particles are highly luminescent, biocompatible, and have a significant quantum yield (0.632). Exemplar applications covered in this paper include insulin receptor recognition and protection against reactive oxygen species (ROS), harmful molecules known to inflict damage on cells and DNA. The IFe(II)NPs effectively mitigate ROS-induced inflammation, which is a hinderance to wound recovery, thereby facilitating enhanced wound recovery.Graphical abstract

Increased oxidative stress alters coronary microvascular tone in exercising swine with multiple comorbidities

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Dutch Cardiovascular Alliance Background/Objectives We have previously shown, in female swine that the combination of three cardiovascular risk factors (diabetes mellitus (DM), hypercholestolemia (HC) and chronic kidney disease (CKD)) induces systemic inflammation, oxidative stress, coronary endothelial dysfunction and impaired myocardial perfusion due to impaired nitric oxide (NO) bioavailability. In the present study we hypothesized that the reduced bioavailability of nitric oxide (NO) is the result of increased production of reactive oxygen species (ROS) and ROS scavenging will restore myocardial oxygen balance thereby improving myocardial perfusion. Methods 12 female swine, with DM (streptozotocin 3x50mg/kg iv), CKD (renal embolization), and HC (high fat, high sugar, high salt diet) and 9 female healthy swine on normal pig chow (Normal) were included. The effect of ROS scavenging on the coronary microvascular tone control was studied in vivo, at rest and during graded treadmill exercise before and after infusion of the ROS scavengers (MPG+Tempol). Additionally, vasodilation to bradykinin was studied in the presence of MPG and TEMPOL and after subsequent addition to catalase, in isolated left ventricle small coronary arteries, in vitro using wire-myography. Results 6 months of DM+HC+CKD resulted in hyperglycemia (18.0±1.3 vs 8.4±0.9mmol/L), hypercholesterolemia (13.4±2.1 vs 1.7±0.1mmol/l), renal dysfunction (plasma creatinine: 166±9 vs 119±3µmol/l), and systemic inflammation (TNFα: 63±8 vs 41±4pg/ml, all P<0.05) associated with impaired endothelium-dependent vasodilator response to bradykinin in vitro. Furthermore, myocardial oxidative stress was increased in DM+HC+CKD animals (8-isoprostane 13±1 vs 10±1pg/ml) and total antioxidant capacity was reduced (0.67±0.02 vs 0.72±0.01nmol Trolox eq./mg protein, both P<0.05). Surprisingly, in vivo ROS scavenging resulted in an even further increase in myocardial oxygen extraction in DM+HC+CKD while it had no effect in Normal, indicating the involvement of a vasodilator ROS (most likely H2O2) in the control of coronary microvascular tone. This was supported by increased activity of catalase in the myocardium of DM+HC+CKD animals (44±3 vs 31±4nmol/min/ml, both P<0.05) and the vascular relaxation response to bradykinin when catalase was added on top of the ROS scavenging in vitro. Conclusion In swine exposed for 6 months to multiple comorbidities, impaired myocardial perfusion is mediated by a loss of NO bioavailability due to increased oxidative stress which was partially compensated by increased H2O2-mediated coronary vasodilation.

A MYB-related transcription factor regulates effector gene expression in an oomycete pathogen.

Phytophthora pathogens possess hundreds of effector genes that exhibit diverse expression patterns during infection, yet how the expression of effector genes is precisely regulated remains largely elusive. Previous studies have identified a few potential conserved transcription factor binding sites (TFBSs) in the promoters of Phytophthora effector genes. Here, we report a MYB-related protein, PsMyb37, in Phytophthora sojae, the major causal agent of root and stem rot in soybean. Yeast one-hybrid and electrophoretic mobility shift assays showed that PsMyb37 binds to the TACATGTA motif, the most prevalent TFBS in effector gene promoters. The knockout mutant of PsMyb37 exhibited significantly reduced virulence on soybean and was more sensitive to oxidative stress. Consistently, transcriptome analysis showed that numerous effector genes associated with suppressing plant immunity or scavenging reactive oxygen species were down-regulated in the PsMyb37 knockout mutant during infection compared to the wild-type P. sojae. Several promoters of effector genes were confirmed to drive the expression of luciferase in a reporter assay. These results demonstrate that a MYB-related transcription factor contributes to the expression of effector genes in P. sojae.

Synthesis of organic-inorganic hybrid nanocomposites modified by catalase-like catalytic sites for the controlling of kiwifruit bacterial canker.

Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. Actinidiae (Psa), is one of the most important diseases in kiwifruit, creating huge economic losses to kiwifruit-growing countries around the world. Metal-based nanomaterials offer a promising alternative strategy to combat plant diseases induced by bacterial infection. However, it is still challenging to design highly active nanomaterials for controlling kiwifruit bacterial canker. Here, a novel multifunctional nanocomposite (ZnO@PDA-Mn) is designed that integrates the antibacterial activity of zinc oxide nanoparticles (ZnO NPs) with the plant reactive oxygen species scavenging ability of catalase (CAT) enzyme-like active sites through introducing manganese modified polydopamine (PDA) coating. The results reveal that ZnO@PDA-Mn nanocomposites can efficiently catalyze the conversion of H2O2 to O2 and H2O to achieve excellent CAT-like activity. In vitro experiments demonstrate that ZnO@PDA-Mn nanocomposites maintain the antibacterial activity of ZnO NPs and induce significant damage to bacterial cell membranes. Importantly, ZnO@PDA-Mn nanocomposites display outstanding curative and protective efficiencies of 47.7% and 53.8% at a dose of 200 μg mL-1 against Psa in vivo, which are superior to those of zinc thiozole (20.6% and 8.8%) and ZnO (38.7% and 33.8%). The nanocomposites offer improved in vivo control efficacy through direct bactericidal effects and decreasing oxidative damage in plants induced by bacterial infection. Our research underscores the potential of nanocomposites containing CAT-like active sites in plant protection, offering a promising strategy for sustainable disease management in agriculture.

Alleviating chromium-induced oxidative stress in Vigna radiata through exogenous trehalose application: insights into growth, photosynthetic efficiency, mineral nutrient uptake, and reactive oxygen species scavenging enzyme activity enhancement

Trehalose serves as a crucial osmolyte and plays a significant role in stress tolerance. The influence of exogenously added trehalose (1 and 5 mM) in alleviating the chromium (Cr; 0.5 mM) stress-induced decline in growth, photosynthesis, mineral uptake, antioxidant system and nitrate reductase activity in Vigna radiata was studied. Chromium (Cr) significantly declined shoot height (39.33%), shoot fresh weight (35.54%), shoot dry weight (36.79%), total chlorophylls (50.70%), carotenoids (29.96%), photosynthesis (33.97%), net intercellular CO2 (26.86%), transpiration rate (36.77%), the content of N (35.04%), P (35.77%), K (31.33%), S (23.91%), Mg (32.74%), and Ca (29.67%). However, the application of trehalose considerably alleviated the decline. Application of trehalose at both concentrations significantly reduced hydrogen peroxide accumulation, lipid peroxidation and electrolyte leakage, which were increased due to Cr stress. Application of trehalose significantly mitigated the Cr-induced oxidative damage by up-regulating the activity of reactive oxygen species (ROS) scavenging enzymes, including superoxide dismutase (182.03%), catalase (125.40%), ascorbate peroxidase (72.86%), and glutathione reductase (68.39%). Besides this, applied trehalose proved effective in enhancing ascorbate (24.29%) and reducing glutathione content (34.40%). In addition, also alleviated the decline in ascorbate by Cr stress to significant levels. The activity of nitrate reductase enhanced significantly (28.52%) due to trehalose activity and declined due to Cr stress (34.15%). Exogenous application of trehalose significantly improved the content of osmolytes, including proline, glycine betaine, sugars and total phenols under normal and Cr stress conditions. Furthermore, Trehalose significantly increased the content of key mineral elements and alleviated the decline induced by Cr to considerable levels.

Microenvironment‐Adaptive Metallo‐Polymeric Nanodecoys via Subcomponent Coordination for Bacterial Biofilm Eradication and Immunomodulation

AbstractBiofilm‐associated infections pose complex challenges that require addressing the multifaceted requirements of biofilm disruption, bacterial killing, and immunomodulation. In this study, microenvironment‐adaptive metallo‐polymeric nanodecoys (MPNs) are synthesized through one‐pot subcomponent coordination in aqueous solution, effectively eradicating bacterial biofilms and modulating immune response. Within the acidic microenvironment of biofilms, the positively charged MPNs demonstrated the ability to interact with and eliminate bacteria while facilitating a Fenton‐like reaction for efficient eradication of bacterial biofilms. As the local microenvironment shifted from a neutral to a basic state during subsequent tissue healing processes, the MPNs adaptively harness the multiple properties to bind pathogen‐associated molecular patterns, scavenge reactive oxygen species, thereby modulating the immune response, alleviating inflammation, and promoting tissue healing. This study presents an efficient strategy for preparing enzyme‐mimicking materials that closely resemble natural metalloenzymes, and the MPNs offer an efficient alternative to current antibiotic treatments for biofilm‐associated infections.

Overexpression of VaBAM3 from Vitis amurensis enhances seedling cold tolerance by promoting soluble sugar accumulation and reactive oxygen scavenging.

The VaBAM3 cloned from Vitis amurensis can enhance the cold tolerance of overexpressed plants, but VaBAM3 knock out by CRISPR/Cas9 system weakened grape callus cold tolerance. In grape production, extreme cold conditions can seriously threaten plant survival and fruit quality. Regulation of starch content by β-amylase (BAM, EC: 3.2.1.2) contributes to cold tolerance in plants. In this study, we cloned the VaBAM3 gene from an extremely cold-tolerant grape, Vitis amurensis, and overexpressed it in tomato and Arabidopsis plants, as well as in grape callus for functional characterization. After exposure to cold stress, leaf wilting in the VaBAM3-overexpressing tomato plants was slightly less pronounced than that in wild-type tomato plants, and these plants were characterized by a significant accumulation of autophagosomes. Additionally, the VaBAM3-overexpressing Arabidopsis plants had a higher freezing tolerance than the wild-type counterparts. Under cold stress conditions, the activities of total amylase, BAM, peroxidase, superoxide dismutase, and catalase in VaBAM3-overexpressing plants were significantly higher than those in the corresponding wild-type plants. Furthermore, sucrose, glucose, and fructose contents in these lines were similarly significantly higher, whereas starch contents were reduced in comparison to the levels in the wild-type plants. Furthermore, we detected high CBF and COR gene expression levels in cold-stressed VaBAM3-overexpressing plants. Compared with those in VaBAM3-overexpressing grape callus, the aforementioned indicators tended to change in the opposite direction in grape callus with silenced VaBAM3. Collectively, our findings indicate that heterologous overexpression of VaBAM3 enhanced cold tolerance of plants by promoting the accumulation of soluble sugars and scavenging of excessive reactive oxygen species. These findings provide a theoretical basis for the cultivation of cold-resistant grape and support creation of germplasm resources for this purpose.

Prdx1 regulates macrophage polarization by maintaining mitochondrial homeostasis

In order to investigate the role of Prdx1 in macrophage polarization, mouse leukemia cells of monocyte macrophage (RAW264.7) were treated with lipopolysaccharides (LPS)+ interferon gamma (IFNγ) or IL-4 to induce type 1 macrophage (M1) and type 1 macrophage (M2) macrophages, respectively. The Prdx1 gene knockout cells (Prdx1-/-) were used for the study. Flow cytometry was conducted to detect M1/M2 macrophage markers, and ELISA kits were used to measure M1/M2 cytokine levels. Inducible nitric-oxide synthase (iNOS) activity, arginase-1 (Arg-1) activity, and oxidative damage were also assessed. The Seahorse XFe24 Extracellular Flux Analyzer was employed to measure extracellular acidification rate and oxygen consumption rate. The mitochondrial membrane potential was analyzed using the mitochondrial membrane potential dye (JC-1) fluorescent probe, and mitochondrial superoxide was detected through fluorescence staining. Additionally, the impact of adding a mitochondrial reactive oxygen species (ROS) scavenger on RAW264.7 macrophage polarization was examined. The results demonstrated an increase in ROS, hydrogen peroxide, and 8-hydroxy-2 deoxyguanosine (8-OHDG). Cytotoxicity and mitochondrial toxic effects, including mitochondrial superoxide accumulation, decreased adenosine-triphosphate (ATP) production, reduced mitochondrial membrane potential, and decreased mitochondrial DNA copy number, were observed. Furthermore, down-regulation of translocase of inner mitochondrial membrane 23 (TIM23) mitochondrial protein and mitochondrial stress protein heat shock protein 60 (HSP60) was noted. The extra cellular acidification rate (ECAR) in M1 macrophage polarization in RAW264.7 cells was increased, while oxygen consumption rate (OCR) in M2 macrophages was reduced. These findings indicate that Prdx1 knockout in RAW264.7 cells can inhibit M2 macrophage polarization but promote M1 macrophage polarization by impairing mitochondrial function and reducing oxidative phosphorylation.

Methyl jasmonate elicitation improves the growth performance and biosynthesis of antioxidant metabolites in Portulaca oleracea through ROS modulation

The application of elicitors is regarded as one of the most efficient strategies for augmenting secondary metabolite contents in medicinal plants. There are numerous reports documenting the impact of methyl jasmonate (meJA) on plant growth and biosynthesis of secondary metabolites. However, the underlying physiological response of the plants towards meJA elicitation is understudied. Thus, the current study focused on evaluating the influence of meJA on growth performance, reactive oxygen species (ROS)/antioxidants crosstalk, and expression of bioactive metabolites in Portulaca oleracea. The seeds of P. oleracea were sown, and the plants were cultivated in pots in nursery settings. P. oleracea plants were sprayed with meJA (ranging from 0.1 to 1.0 mM) on the 35th day after sowing (DAS). The plants were harvested on the 60th DAS. The P. oleracea plants elicited with 1.0 mM meJA exhibited the highest plant height (PH), number of leaves (LN), root length (RL), fresh (FW-P), and dry weights of whole plants (DW-P). The highest increase in total anthocyanin (TAC), total chlorophyll (Total Chl), and total carotenoid (CAR) were observed in plants elicited with 0.4 mM meJA. Meanwhile, the highest increase in total phenolic content (TPC) occurred in plants elicited with 0.6 mM meJA, whereas the highest increase in total flavonoid (TFC) and ascorbic acid content (AsA) was noted in plants elicited with 0.8 mM meJA. The lowest decrease in the stress indicators, malondialdehyde (MDA) and hydrogen peroxide (H2O2) was observed in plants elicited with 0.6 mM meJA. Pearson's analysis and Partial Least Squares Regression (PLSR) were employed in exploring the relationships among all essential parameters. It was found that the antioxidant metabolites and enzymes, particularly the total soluble sugar (TSS), proline, chlorophyll a/chlorophyll b ratio (Chl a/Chl b), and superoxide dismutase (SOD) served as the most essential factors in influencing the growth performance of P. oleracea by modulating the total antioxidant activity (Total AOX) and acting as ROS scavengers. Moreover, meJA elicitation led to the distinct expression of various bioactive compounds, amplifying the medicinal properties of P. oleracea. Overall, this research indicates that meJA enhances growth performance and boosts the production of metabolites possessing medicinal values in P. oleracea.

Preparation of high antioxidant nanolignin and its application in cosmetics

Lignin, as a natural polyphenol, displays anti-oxidant activity by trapping and binding free radicals through its free phenolic hydroxyl groups. However, the most accessible form, industrial lignins, generally has low phenolic hydroxyl content, which severely limits their application value and scenarios. Herein, we showed that potassium-glycerate deep eutectic solvent (PG-DES) treatment can be combined with laccase oxidation to afford prepared high antioxidant lignin nanoparticles (HA-LNPs) with notably improved anti-oxidant activities benefiting from both the enhanced phenolic hydroxyl content 170.8 % and reduced average particle size (59.0 nm). At concentrations as low as 60 μg/mL, HA-LNPs showed favorable effects in promoting collagen formation. When HA-LNPs were used as an active ingredient in the anti-aging mask formulation, the reactive oxygen species (ROS) scavenging activity of mask samples containing 0.4 % HA-LNPs reached 37.2 %. The data suggest great promise of HA-LNPs as a natural antioxidant for formulating in anti-aging skin care products.

Construction of janus mesenchymal stem cell-hitchhiked melanin nanoparticles to modulate the Th17/Treg balance for rheumatoid arthritis therapy

Rheumatoid arthritis (RA) is a common chronic inflammatory disease capable of causing the disability. Although various antioxidant strategies have been attempted for prevention and treatment of RA through scavenging the free radicals, the therapeutic effect is limited. Recently, it is reported that the unremitting course of RA intensely correlates with the persistence of immunologic memory, in which the imbalance of T helper 17 (Th17) cells/regulatory T (Treg) cells plays an important role. Herein, we constructed Janus mesenchymal stem cell (MSC)-hitchhiked melanin nanoparticles (MSCFM) for RA therapy, where one half of MSC kept intact for chemotactically migrating towards the RA inflammatory sites and efficiently restoring the Th17/Treg balance based on the property of MSCs, while the other half hitchhiked the iron-doped melanin (FM) nanoparticles (NPs) and release them to scavenge free radicals for maintaining the durability of Th17/Treg balance. In vitro studies indicated MSCFM could migrate towards CXCL12 inflammatory cytokine, scavenge reactive oxygen and nitrogen species, inhibit Th17 cell proliferation and induce Treg cell production. Further in vivo studies corroborated that intravenously injected MSCFM could target the RA site of collagen-induced arthritis mouse model and alleviate the pathological progression of RA. MSCFM holds great potential as an anti-inflammatory agent for RA management.

Aβ42 and ROS dual-targeted multifunctional nanocomposite for combination therapy of Alzheimer’s disease

Amyloid-β (Aβ) readily misfolds into neurotoxic aggregates, generating high levels of reactive oxygen species (ROS), leading to progressive oxidative damage and ultimately cell death. Therefore, simultaneous inhibition of Aβ aggregation and scavenging of ROS may be a promising therapeutic strategy to alleviate Alzheimer’s disease pathology. Based on the previously developed antibody 1F12 that targets all forms of Aβ42, we developed an Aβ42 and ROS dual-targeting nanocomposite using biodegradable mesoporous silica nanoparticles as carriers to load ultra-small cerium oxide nanocrystals (bMSNs@Ce-1F12). By modifying the brain-targeted rabies virus glycoprotein 29 (RVG29-bMSNs@Ce-1F12), this intelligent nanocomposite can efficiently target brain Aβ-rich regions. Combined with peripheral and central nervous system treatments, RVG29-bMSNs@Ce-1F12 can significantly alleviate AD symptoms by inhibiting Aβ42 misfolding, accelerating Aβ42 clearance, and scavenging ROS. Furthermore, this synergistic effect of ROS scavenging and Aβ clearance exhibited by this Aβ42 and ROS dual-targeted strategy also reduced the burden of hyperphosphorylated tau, alleviated glial cell activation, and ultimately improved cognitive function in APP/PS1 mice. Our findings indicate that RVG29-bMSNs@Ce-1F12 is a promising nanodrug that can facilitate multi-target treatment of AD.