Reactive Oxygen Species Scavenger Research Articles

How to Cope With Stress in the Desert-The Date Palm Approach.

Increasing desertification constitutes a global environmental problem, mainly driven by climate change and inappropriate land-use that limits agriculture, forestry and human colonization. The selection of suitable plant species to mitigate desertification is particularly challenging, as it usually requires simultaneous counteraction against a whole set of unfavourable environmental conditions, including heat, drought, high tropospheric ozone and salinity. It therefore seems useful to identify the survival strategies of plants native in desert environments. Date palm constitutes a plant species native in desert environments and cultivated worldwide in arid regions that have been studied intensively for stress defence during the last decade. The present review summarizes the current state of biochemical stress defence mechanisms including avoidance, osmotic and metabolic adjustments and reactive oxygen species scavenging, addresses whole-plant regulations and trade-off between stress compensation/defence and growth of date palms. The review advances our knowledge about how this typical desert species copes with both individual and multiple environmental stresses at the cellular to the whole-plant level, and identifies areas of future research required to fully understand the strategies of this plant species to survive in the desert, thereby contributing to efforts for the mitigation of climate change and desertification.

Glucose and pH dual-responsive hydrogels with antibacterial, reactive oxygen species scavenging, and angiogenesis properties for promoting the healing of infected diabetic foot ulcers

The healing process of diabetic foot ulcers is challenging due to the presence of a complex and severe inflammatory microenvironment, characterized by hyperglycemia, low pH, susceptibility to infection, vascular dysfunction, and over-expression of reactive oxygen species (ROS), which can potentially lead to amputation or even mortality. Herein, a glucose and pH dual-responsive hydrogel was designed and prepared by crosslinking phenylboronic acid-grafted quaternary chitosan (QF, 4 wt%) with dopamine-grafted oxidized hyaluronic acid (OD, 5 wt%) through phenylboronation, schiff-base reaction, and other techniques. The multifunctional QO/@PV@AB7 hydrogel was prepared by incorporating pravastatin-loaded chitosan nanoparticles (CSNPs@PV, 2 mg/mL) and antimicrobial peptide AMP-AB7 loaded silica nanoparticles (SiO2NPs@AB7, 0.5 mg/mL). The results demonstrate that the QO/@PV@AB7 hydrogel exhibits good responsiveness to acidic conditions and high glucose levels, while effectively scavenging various types of ROS. Moreover, it exerted protective effects against oxidative stress on cells, enhanced HUVECs viability, and promoted angiogenesis. Notably, the QO/@PV@AB7 hydrogel displayed potent antibacterial activity against methicillin-resistant Staphylococcus aureus (MRSA) and Escherichia coli. Additionally, in an MRSA-infected rat model of diabetic foot wounds, administration of the QO/@PV@AB7 hydrogel led to increased secretion of pro-angiogenic factors such as vascular endothelial nitric oxide synthase (eNOS), vascular endothelial-generating factor (VEGF), and endothelial cell adhesion molecule (CD31). Furthermore, the hydrogel significantly reduced the levels of inflammatory factors such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), while simultaneously increasing the levels of anti-inflammatory cytokines such as interleukin-10 (IL-10). The findings suggest that multifunctional hydrogels incorporating PV@CSNPs and SiO2NPs@AB7 demonstrate promising potential as a therapeutic approach for the treatment of diabetic foot. Statement of SignificanceHere, a glucose and pH dual-responsive QO/@PV@AB7 hydrogel with antimicrobial and angiogenesis-promoting properties was developed for the treatment of infected wounds in diabetic feet. Our findings demonstrate that the proposed hydrogel exhibits good responsiveness, effectively scavenges various types of reactive oxygen species (DPPH, O2-, -OH, and ABTS+), provides protection against oxidative stress, enhances HUVECs cell viability, and promotes angiogenesis. Notably, it also demonstrates potent antibacterial activity against methicillin-resistant Staphylococcus aureus (MRSA) and Escherichia coli. Additionally, in vivo experiments demonstrated that the hydrogel exhibited accelerated wound healing in MRSA-infected diabetic foot ulcers, with a reduction of four days compared to the control group.

Caveolin-1 ameliorates hepatic injury in non-alcoholic fatty liver disease by inhibiting ferroptosis via the NOX4/ROS/GPX4 pathway

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease globally, with a complex and contentious pathogenesis. Caveolin-1 (CAV1) is an important regulator of liver function and can mitigate liver injury by scavenging reactive oxygen species (ROS). Evidence suggests that NOX4 is a source of ROS production, that oxidative stress and ferroptosis are closely related, and that both are involved in the onset and progression of NAFLD. However, whether CAV1 attenuates liver injury in NAFLD caused by high-fat diet via the NOX4/ROS/GPX4 pathway remains unclear. An in vivo fatty liver model was established by feeding mice with a high-fat diet for 16 weeks. In addition, an in vitro fatty liver model was established by incubating AML-12 cells with free fatty acids for 24 h using an in vitro culture method. In our study, it was observed that a high-fat diet induces mitochondrial damage and worsens oxidative stress in NAFLD. This diet also hinders GPX4 expression, leading to an escalation of ferroptosis and lipid accumulation. To counteract these effects, intraperitoneal administration of CSD peptide in mice attenuated the high-fat diet-induced liver mitochondrial damage and ferroptosis. Likewise, overexpression of CAV1 resulted in an increase in GPX4 expression and a reduction in levels of ROS-mediated iron metamorphosis, thus mitigating the progression of the disease. However, the effects of CAV1 on GPX4-mediated ferroptosis and lipid deposition could be reversed by CAV1 small interfering RNA (SiRNA). Finally, NOX4 inhibitor (GLX351322) treatment increased CAV1 siRNA-mediated GPX4 expression and decreased the level of ROS-mediated ferroptosis. These findings suggest a potential mechanism underlying the protective role of CAV1 against high-fat diet-induced hepatotoxicity in NAFLD, shedding new light on the interplay between CAV1, GPX4, and ferroptosis in liver pathology

Nanozyme-enhanced injectable hyaluronic acid-based hydrogel for the treatment of osteoarthritis

The progression of osteoarthritis (OA) is dramatically accelerated by excessive reactive oxygen species (ROS)-induced apoptosis of chondrocytes and the inflammatory response of synovial macrophages. In this study, we developed an injectable hydrogel with a catalase-mimicking nanozyme activity as a therapeutic agent for OA. In vitro experiments confirmed that the HA and peroxide-mimetic nanoenzyme-enhanced hydrogel, containing ε-polylysine/Mn1.8Co1.2O4 (ε-PLE/MnCoO) nanoparticles, continuously eliminated ROS and inflammatory cytokines while promoting the polarization of inflammatory macrophages (M1 phenotype) towards anti-inflammatory macrophages (M2 phenotype) in dysfunctional microenvironments. When used for intraarticular injections in OA models, the nanoenzyme-enhanced hydrogel effectively reduced oxidative stress by scavenging ROS and regulating the immune microenvironment. It resulted in a subsequent reduction in the expression of inflammatory factors, including MMP-13, TNF-α, IL-1β, and iNOS in both the synovium and joint fluid. Moreover, cartilage repair was enhanced by the promotion of COL-2 and SOX-9 expression in the cartilage tissue, whereas osteophyte formation in OA was reduced. This study introduced an innovative treatment strategy for the clinical management of OA, demonstrating its significant potential for application in treating OA.

Tile: Construction of a specific nanoprobe for scavenging ROS in hypobaric hypoxia induced brain injury of mice

The prevention and treatment of hypobaric hypoxia brain injury (HHBI) remains an unprecedented challenge due to the complex oxidative stress response at the damage site. In this study, RuCO phthalocyanine compound (RuPc) and bovine serum albumin (BSA) were self-assembled to obtain RuPc-BSA nanoparticles for HHBI therapy. As a nanoprobe carrying and storing carbon monoxide (CO), RuPc-BSA delivers CO to pathologically damaged areas of the brain. CO specifically attaches itself to the heme functional groups on mitochondria and restricts the source of reactive oxygen species (ROS) generation. RuPc-BSA nanoparticles have been demonstrated in vitro to exhibit amazing stability as well as remarkable scavenging activity on hydroxyl radical, superoxide anion, and hydrogen peroxide. In vivo experiments showed that ROS levels in the brain of HHBI rats pretreated with RuPc-BSA decreased significantly, and neuronal function and oxidative stress levels were alleviated. Western blot and qRT-RCR results indicated that RuPc-BSA restricted the protein levels of Keap1, whereas enhanced the gene and protein levels of Nrf2. This study demonstrated that RuPc-BSA can ameliorate HHBI of mice by scavenging ROS partly via activating Keap1/Nrf2 signaling pathway.

NIR stimulated epigallocatechin gallate loaded polydopamine with enhanced antibacterial and ROS scavenging abilities for improved infectious wound healing

Infectious wound healing is complicated with and limited by infection and oxidative stress at the wound site. In recent years, various evidences suggest that nanozymes with multiple enzymatic activities have enabled the development of novel strategies for infectious wound healing. In this study, epigallocatechin gallate loaded polydopamine (P@E) was developed to act as a potent reactive oxygen species (ROS) scavenger for scavenging ROS, alleviating inflammatory responses, and promoting infectious wound healing. Combining with near infrared (NIR) irradiation, P@E presented excellent antibacterial ability of Escherichia coli (E. coli, 93.6%) and methicillin-resistant Staphylococcus aureus (MRSA, 87.6%). Specifically, P@E+NIR exhibited the most potent antioxidant, anti-inflammatory and cell proliferation behaviors through down-regulating intracellular ROS levels (81.9% and 94.3% for NIH3T3 and RAW264.7 respectively) and inducible nitric oxide synthase (iNOS) expression level (55.7%), and up-regulating the expression levels of arginase-1 (Arg-1, 71.4%), heat shock protein 70 (HSP70, 48.6%) and platelet endothelial cell adhesion molecule (CD31, 35.3%) compared to control group. Meanwhile, it also efficiently induced M2 directional polarization of lipopolysaccharide induced murine macrophages to achieve anti-inflammation, indicated by the down-regulation of CD86 (86.2%), and up-regulation of CD206 (85.6%). Significantly, it was also observed that P@E+NIR presented the excellent behaviors of inhibiting wound infection, alleviating wound inflammation, as well as promoting skin tissue repairing. Altogether, it has developed the strategy of using P@E combining with NIR irradiation for the synergistic enhanced healing of infectious skin wound, which can serve as a promising therapeutic strategy for its clinical treatment.

Vanadium doped ZIF-L derived V-NC peroxidase-like nanozymes for tanwenic acid sensing

Transition metal-relied nitrogen doping carbon nanozyme has attracted great attention owning to their high potential to replace natural enzymes. In this study, we prepared novel vanadium doped ZIF-L derived N-doped carbon nanozyme (V-NC) via facilely pyrolysis strategy. The cross-shaped morphology endows V-NC with unique V-Nx active sites, hierarchical pore character and large specific surface area, leading to its good peroxidase-mimetic activity. The steady-state kinetics trials revealed the low Km values of V-NC for TMB and H2O2, demonstrating its good affinity to TMB and H2O2. Mechanism research revealed that the excellent peroxidase-like activity of V-NC resulted from co-participation of •OH and O2•−, which were confirmed by reactive oxygen species (ROS) scavenging experiments and EPR trials. Under optimized operational conditions, and by virtue of the antioxidant properties of tannic acid (TA), a colorimetric sensing programme in terms of the peroxidase-imitating function of V-NC was developed for sensitive detection of TA in the 0.1–2.5 µM linear range with low detection limit of 19.8 nM and the relative standard deviation (RSD, n = 3) of below 5 %. This contribution renders a novel idea for designing and developing high activity N-doped carbon nanozyme, and provides an accurate and feasible assay for the analysis of TA in real samples.

Tripartite interactions between grapevine, viruses, and arbuscular mycorrhizal fungi provide insights into modulation of oxidative stress responses

Arbuscular mycorrhizal fungi (AMF) can be beneficial for plants exposed to abiotic and biotic stressors. Although widely present in agroecosystems, AMF influence on crop responses to virus infection is underexplored, particularly in woody plant species such as grapevine. Here, a two-year greenhouse experiment was set up to test the hypothesis that AMF alleviate virus-induced oxidative stress in grapevine. The ‘Merlot’ cultivar was infected with three grapevine-associated viruses and subsequently colonized with two AMF inocula, containing one or three species, respectively. Five and fifteen months after AMF inoculation, lipid peroxidation - LPO as an indicator of oxidative stress and indicators of antioxidative response (proline, ascorbate - AsA, superoxide dismutase - SOD, ascorbate- APX and guaiacol peroxidases - GPOD, polyphenol oxidase - PPO, glutathione reductase - GR) were analysed. Expression of genes coding for a stilbene synthase (STS1), an enhanced disease susceptibility (EDS1) and a lipoxygenase (LOX) were determined in the second harvesting. AMF induced reduction of AsA and SOD over both years, which, combined with not AMF-triggered APX and GR, suggests decreased activation of the ascorbate-glutathione cycle. In the mature phase of the AM symbiosis establishment GPOD emerged as an important mechanism for scavenging H2O2 accumulation. These results, together with reduction in STS1 and increase in EDS1 gene expression, suggest more efficient reactive oxygen species scavenging in plants inoculated with AMF. Composition of AMF inocula was important for proline accumulation. Overall, our study improves the knowledge on ubiquitous grapevine-virus-AMF systems in the field, highlighting that established functional AM symbiosis could reduce virus-induced stress.

Gastrointestinal Self-Adaptive and Nutrient Self-Sufficient Akkermansia muciniphila-Gelatin Porous Microgels for Synergistic Therapy of Ulcerative Colitis.

To realize effective and long-term synergistic therapy of ulcerative colitis (UC) with probiotics, we developed gastrointestinal self-adaptive and nutrient self-sufficient Akkermansia muciniphila (AKK)-gelatin porous microgels (AKK@GPMGs). In AKK@GPMGs, AKK was covered with sequential layers of proanthocyanidins (PAs), mucin (MUC), and phosphatidylcholine (PC) to obtain AKK@PAs-MUC-PC (AKK@PMP), and then encapsulated within the methacrylate-modified gelatin porous microgels. AKK@GPMGs provide sufficient mucus as a nutrition source for AKK and boost resistance to stomach acid by 30.49-fold, and colonization in the intestines is enhanced by 83.46 times. The microgels can be dissociated by matrix metalloproteinase at the inflammatory sites of the intestine, and release AKK@PMP, which acts as "band-aid" that adheres to the inflamed colon for a long time and offers improved synergistic therapy for UC. Compared to uncoated AKK, AKK@GPMGs increase reactive oxygen species scavenging capacity by 26.47 times, improve the intestinal mucus layer thickness by 5.63 times, increase the goblet cells abundance by 3.93 times, reduce intestinal permeability by 5.60 times and significantly enhance beneficial gut microbiota while repressing harmful microbiota. These results indicate that AKK@GPMGs can restore mucus layer and tight junction integrity, reduce inflammation and oxidative stress, and regulate gut microbiota homeostasis to effectively treat intestinal inflammation.

Targeting the Main Sources of Reactive Oxygen Species Production: Possible Therapeutic Implications in Chronic Pain.

Humans have long been combating chronic pain. In clinical practice, opioids are firstchoice analgesics, but long-term use of these drugs can lead to serious adverse reactions. Finding new, safe and effective pain relievers that are useful treatments for chronic pain is an urgent medical need. Based on accumulating evidence from numerous studies, excess reactive oxygen species (ROS) contribute to the development and maintenance of chronic pain. Some antioxidants are potentially beneficial analgesics in the clinic, but ROS-dependent pathways are completely inhibited only by scavenging ROS directly targeting cellular or subcellular sites. Unfortunately, current antioxidant treatments do not achieve this effect. Furthermore, some antioxidants interfere with physiological redox signaling pathways and fail to reverse oxidative damage. Therefore, the key upstream processes and mechanisms of ROS production that lead to chronic pain in vivo must be identified to discover potential therapeutic targets related to the pathways that control ROS production in vivo. In this review, we summarize the sites and pathways involved in analgesia based on the three main mechanisms by which ROS are generated in vivo, discuss the preclinical evidence for the therapeutic potential of targeting these pathways in chronic pain, note the shortcomings of current research and highlight possible future research directions to provide new targets and evidence for the development of clinical analgesics.

Drug-Loaded Mesoporous Polydopamine Nanoparticles in Chitosan Hydrogels Enable Myocardial Infarction Repair through ROS Scavenging and Inhibition of Apoptosis.

In this study, we synthesized mesoporous polydopamine nanoparticles (MPDA NPs) using an emulsion-induced interface assembly strategy and loaded epigallocatechin gallate (EGCG) into MPDA NPs via electrostatic attraction to form EGCG@MPDA NPs. In the post myocardial infarction (MI) environment, these interventions specifically aimed to eliminate reactive oxygen species (ROS) and facilitate the repair of MI. We further combined them with a thermosensitive chitosan (CS) hydrogel to construct an injectable composite hydrogel (EGCG@MPDA/CS hydrogel). Utilizing in vitro experiments, the EGCG@MPDA/CS hydrogel exhibited excellent ROS-scavenging ability of H9C2 cells under the oxidative stress environment and also could inhibit their apoptosis. The EGCG@MPDA/CS hydrogel significantly promoted left ventricular ejection fraction (LVEF) in infarcted rat models post injection for 28 days compared to the PBS group (51.25 ± 1.73% vs 29.31 ± 0.78%, P < 0.05). In comparison to the PBS group, histological analysis revealed a substantial increase in left ventricular (LV) wall thickness in the EGCG@MPDA/CS hydrogel group (from 0.58 ± 0.03 to 1.39 ± 1.11 mm, P < 0.05). This work presents a novel approach to enhance MI repair by employing the EGCG@MPDA/CS hydrogel. This hydrogel effectively reduces local oxidative stress by ROS and stimulates the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway.

The homeostasis of ions and reactive oxygen species in root and shoot play crucial roles in the tolerance of alfalfa to salt alkali stress

High pH saline-alkali stress, mainly NaHCO3, limited the development of animal husbandry in Songnen Plain. Ion imbalance and reactive oxygen species (ROS) metabolism disorder caused by saline-alkali stress inhibited plant growth. In this study, we compared the differences in ion absorption, transport and ROS metabolism between saline-tolerant alfalfa (ZD) and saline-sensitive alfalfa (ZM) under NaHCO3 stress using physiology and transcripomics techniques. WGCNA analysis identified key genes associated with NaHCO3 stress-induced changes. NaHCO3 stress inhibited the absorption of K+ and Mg2+, but activated Ca2+ signal. Furthermore, ZD maintained higher K+, Mg2+ and Ca2+ contents and the K+/Na+ ratio than ZM, this is mainly related to the higher expression of proteins or channel-encoding genes involved in ion absorption and transport in ZD. Antioxidant enzyme systems can be activated in response to NaHCO3 stress. Peroxidase (EC 1.11.1.6), catalase (EC 1.11.1.7) and glutathione transferase (EC 2.5.1.18) activities were higher in ZD than ZM, and most genes encoding the relevant enzymes also demonstrated a stronger up-regulation trend in ZD. Although NaHCO3 stress inhibited Trx-Prx pathway, ZD related enzymes and their genes were also inhibited less than ZM. WGCNA results identified many genes involved in ion absorption, transport and antioxidant systems that play an important role in NaHCO3 stress adaptation. Collectively, ZD has the stronger ion homeostasis regulation and ROS scavenging ability, so it's more resistant to NaHCO3. The results provide theoretical guidance for further understanding of the molecular mechanism of NaHCO3 resistance and provide potential genes for research to improve saline-alkali tolerance in alfalfa.

2D MXene Nanosheets with ROS Scavenging Ability Effectively Delay Osteoarthritis Progression.

MXenes nanosheets with high conductivity, hydrophilicity, and excellent reactive oxygen species (ROS) scavenging ability have shown promise in treating various degenerative diseases correlated with abnormal ROS accumulation. Herein, the therapeutic potential of Ti3C2Tx nanosheets, which is the most widely investigated MXene material, in delaying osteoarthritis (OA) progression is demonstrated. In vitro experiments indicate the strong ROS scavenging capacity of Ti3C2Tx nanosheets and their acceptable biocompatibility. Ti3C2Tx nanosheets effectively protect chondrocytes from cell death induced by oxidative stress. In addition, Ti3C2Tx nanosheets demonstrate a prominent anti-inflammatory effect and the ability to restore homeostasis between anabolic activities and catabolic activities in chondrocytes. Furthermore, RNA sequencing reveals the potential mechanism underlying the Ti3C2Tx nanosheet-mediated therapeutic effect. Finally, the in vivo curative effect of Ti3C2Tx nanosheets is verified using a rat OA model. Histological staining and immunohistochemical analyses indicate that Ti3C2Tx nanosheets effectively ameliorate OA progression. Conclusively, the in vitro and in vivo experiments suggest that Ti3C2Tx nanosheets could be a promising and effective option for OA treatment.

Isovalerylspiramycin I suppresses small cell lung cancer proliferation via ATR/CHK1 mediated DNA damage response and PERK/eIF2α/ATF4/CHOP mediated ER stress

Small cell lung cancer (SCLC) urgently needs new therapeutic approaches. We found that the antibiotic-derived compound Isovalerylspiramycin I (ISP-I) has potent anti-tumor activity against SCLC cell lines H1048 and DMS53 both in vitro and in vivo. ISP-I induced apoptosis, G2/M phase cell cycle arrest, and mitochondrial respiratory chain dysfunction in both cell lines. Comprehensive RNA sequencing revealed that the anti-SCLC effects of ISP-I were primarily attributed to ATR/CHK1-mediated DNA damage response and PERK/eIF2α/ATF4/CHOP-mediated ER stress. Importantly, the induction of DNA damage, ER stress, and apoptosis by ISP-I was mitigated by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC), underscoring the critical role of ROS in the anti-SCLC mechanism of ISP-I. Moreover, ISP-I treatment induced immunogenic cell death (ICD) in SCLC cells, as evidenced by increased adenosine triphosphate (ATP) secretion, elevated release of high-mobility group box 1 (HMGB1), and enhanced exposure of calreticulin (CRT) on the cell surface. Additionally, network pharmacology analysis, combined with cellular thermal shift assay (CETSA) and cycloheximide (CHX) chase experiments, demonstrated that ISP-I acted as a ligand for apurinic/apyrimidinic endonuclease 1 (APEX1) and promoted its degradation, leading to the accumulation of ROS. In conclusion, our findings elucidate the multifaceted mechanisms underlying the anti-cancer effects of ISP-I, highlighting its potential as a promising therapeutic candidate for SCLC treatment.

Mn–Ce Symbiosis: Nanozymes with Multiple Active Sites Facilitate Scavenging of Reactive Oxygen Species (ROS) Based on Electron Transfer and Confinement Anchoring

Mn–Ce Symbiosis: Nanozymes with Multiple Active Sites Facilitate Scavenging of Reactive Oxygen Species (ROS) Based on Electron Transfer and Confinement Anchoring

Ursolic acid, a natural endogenous compound, inhibits browning in fresh-cut apples

Enzymatic browning occurs rapidly in fresh-cut apples and can lead to economic losses. Although various methods have been developed to prevent this browning, physical methods are costly, and chemical methods are controversial, suggesting the potential usefulness of an endogenous natural browning inhibitor. In this study, the effects of ursolic acid (UA), a natural endogenous compound, on apple browning were investigated. It was found that UA inhibited the activity of polyphenol oxidase through Cu2+ chelation. Molecular docking indicated that the inhibition was reversible and mixed-type. Moreover, UA treatment promoted the scavenging of reactive oxygen species in fresh-cut apple and reduced the proliferation of microorganisms on the apple surface. Similar effects were observed on the browning of chestnut, eggplant, potatoes, and pears. In conclusion, the findings demonstrate the efficacy of UA on inhibiting browning in fresh-cut apple, together with an analysis of the mechanism involved.

Polydopamine-coated chondroitin sulfate methacryloyl multifunctional microspheres for wound treatment

The disappearance of the protective barrier after skin injury leads to the overproduction of reactive oxygen species (ROS) in response to various stimuli. Oxidative stress is one of the most important causes of delayed wound healing, leading to negative outcomes, such as excessive inflammatory response and impaired angiogenesis. In this study, we used microfluidic technology to integrate Prussian blue nanozymes and vascular endothelial growth factor and constructed multifunctional microspheres that improved local oxidative stress. In order to enhance the adhesion of the microspheres on the wound surface and prolong the release of the drug, we coated them with dopamine, ensuring uniform encapsulation on their surface. The microspheres adhered well to the wound surface and promoted wound healing by scavenging ROS, reducing the inflammatory response, and promoting angiogenesis. This strategy of integrating nanozymes and growth factors can have a synergistic effect, which is significant for wound healing.

Reactive oxygen species-inducing itraconazole and its anti-biofilm activity against resistant Candida parapsilosis sensu lato biofilm cells isolated from patients with recalcitrant onychomycosis.

Candida parapsilosis was introduced as the second most responsible for nail involvement. The colonization of biotic and abiotic surfaces by Candida spp.can result in the formation of biofilms, which possess a high level of resistance to typical antifungal agents. Since Candida spp. can produce biofilm mass on the surface of the nails, dermatologists should consider appropriate antifungals to eliminate both the planktonic and biofilm cells. The aim of this research was to determine the antifungal efficacy of itraconazole against C. parapsilosis sensu lato biofilm formations, in addition to its static effects. Ten C. parapsilosis sensu lato isolates were enrolled in this study. The use of itraconazole results in the accumulation of reactive oxygen species (ROS) during treatment. In order to verify the correlation between ROS and itraconazole-induced cell death, the viability of cells was analyzed by administering the ROS scavenger Ascorbic acid. The apoptotic features of itraconazole were analyzed using the Annexin V-FITC method. Based on current data, it was found that the generation of intracellular stresses by itraconazole is not observed in cells upon ROS inhibition, emphasizing the importance of intracellular ROS in the apoptotic mechanism of itraconazole. Targeting the oxidative defense system is a powerful point to use ROS-inducing antifungals as a superior choice for more effective therapies in case of recalcitrant onychomycosis.

Non-thermal atmospheric pressure plasma induces selective cancer cell apoptosis by modulating redox homeostasis

BackgroundAnticancer treatments aim to selectively target cancer cells without harming normal cells. While non-thermal atmospheric pressure plasma (NTAPP) has shown anticancer potential across various studies, the mechanisms behind its selective action on cancer cells remain inadequately understood. This study explores the mechanism of NTAPP-induced selective cell death and assesses its application in cancer therapy.MethodsWe treated HT1080 fibrosarcoma cells with NTAPP and assessed the intracellular levels of mitochondria-derived reactive oxygen species (ROS), mitochondrial function, and cell death mechanisms. We employed N-acetylcysteine to investigate ROS’s role in NTAPP-induced cell death. Additionally, single-cell RNA sequencing was used to compare gene expression in NTAPP-treated HT1080 cells and human normal fibroblasts (NF). Western blotting and immunofluorescence staining examined the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), a key antioxidant gene transcription factor. We also evaluated autophagy activity through fluorescence staining and transmission electron microscopy.ResultsNTAPP treatment increased ROS levels and induced mitochondrial dysfunction, leading to apoptosis in HT1080 cells. The involvement of ROS in selective cancer cell death was confirmed by N-acetylcysteine treatment. Distinct gene expression patterns were observed between NTAPP-treated NF and HT1080 cells, with NF showing upregulated antioxidant gene expression. Notably, NRF2 expression and nuclear translocation increased in NF but not in HT1080 cells. Furthermore, autophagy activity was significantly higher in normal cells compared to cancer cells.ConclusionsOur study demonstrates that NTAPP induces selective cell death in fibrosarcoma cells through the downregulation of the NRF2-induced ROS scavenger system and inhibition of autophagy. These findings suggest NTAPP’s potential as a cancer therapy that minimizes damage to normal cells while effectively targeting cancer cells.

Morphological, physiological, and transcriptomic analyses indicate that cell wall properties and antioxidant processes are potential targets for improving the aluminium tolerance of broad beans

Aluminium (Al) stress is the second-leading abiotic stress on crops. An improved understanding of the response mechanisms of plants to Al stress will provide scientific guidance for enhancing the crops’ tolerance to Al stress. In this study, Al stress (50–200 μM AlCl3) caused visible damage to broad bean (Vicia faba L.) roots rather than shoots, which was attributed to Al accumulation and distribution in different tissues. Root transcriptomic analysis revealed that Al stress altered cell wall properties by downregulating lignin synthesis and several xyloglucan endotransglucosylase/hydrolase-, expansin- and peroxidase (POD)-encoding genes, which likely weakened cell extensibility to inhibit root growth. Additionally, Al stress impeded reactive oxygen species scavenging pathways involving POD activity and flavonoid biosynthesis, leading to oxidative damage characterised by malondialdehyde accumulation. These results indicate that optimising cell wall properties and/or enhancing antioxidant processes are crucial for alleviating Al toxicity to broad beans. Interestingly, exogenous application (500 and 1000 μM) of the flavonoid apigenin effectively alleviated Al toxicity in broad bean roots by partially improving the total antioxidant capacity of the roots. This study contributes to understanding the interaction between plants and Al and provides new strategies to alleviate Al toxicity in crops.