Reactive Oxygen Species Scavenger Research Articles

Elastic Nanofibrous Dressings with Mesenchymal Stem Cell-Recruiting and Protecting Characteristics for Promoting Diabetic Wound Healing.

Diabetic wounds that do not heal for a long time challenge global healthcare. Mesenchymal stem cell (MSC) therapy has positive significance in promoting diabetic wound healing. However, traditional MSC therapy involves exogenous MSCs, which brings many limitations and unsatisfactory treatment. Moreover, the maintenance of MSC viability and function is difficult because of the high level of reactive oxygen species (ROS) in diabetic wounds. Therefore, we developed a nanofibrous dressing to recruit and protect endogenous MSCs while avoiding the inherent disadvantages of exogenous MSCs. Ceria nanoparticles capable of ROS scavenging are integrated into the nanofibrous dressings, together with Apt19S, a DNA aptamer with affinity and selectivity for MSCs. In addition, the homogenization and freeze-drying technology give the nanofibrous dressings good elasticity, which protects the wound from external pressure. Further experiments in diabetic mice show that the dressing has excellent endogenous MSC recruitment and anti-inflammatory properties, thereby synergistically promoting diabetic wound healing. This study is expected to explore an efficient method of stem cell therapy, providing a new way to construct high-performance wound dressings.

Artificial Mitochondria Nanoarchitectonics via a Supramolecular Assembled Microreactor Covered by ATP Synthase

AbstractAbiotic stress tends to induce oxidative damage to enzymes and organelles that in turns hampers the phosphorylation process and decreases the adenosine triphosphate (ATP) productivity. Artificial assemblies can alleviate abiotic stress and simultaneously provide nutrients to diminish the oxidative damage. Here, we have integrated natural acid phosphatase (ACP) and ATP synthase with plasmonic Au clusters in a biomimetic microreactor. ACP immobilized on the Au clusters is harnessed to generate proton influx to drive ATP synthase and concurrently supply phosphate to improve phosphorus availability to combat phosphorus‐deficiency stress. In tandem with the reactive oxygen species (ROS) scavenging and the photothermal functionality of Au clusters, such an assembled microreactor exhibits an improved abiotic stress tolerance and achieves plasmon‐accelerated ATP synthesis. This innovative approach offers an effective route to enhance the stress resistance of ATP synthase‐based energy‐generating systems, opening an exciting potential of these systems for biomimicking applications.

Artificial Mitochondria Nanoarchitectonics via a Supramolecular Assembled Microreactor Covered by ATP Synthase.

Abiotic stress tends to induce oxidative damage to enzymes and organelles that in turns hampers the phosphorylation process and decreases the adenosine triphosphate (ATP) productivity. Artificial assemblies can alleviate abiotic stress and simultaneously provide nutrients to diminish the oxidative damage. Here, we have integrated natural acid phosphatase (ACP) and ATP synthase with plasmonic Au clusters in a biomimetic microreactor. ACP immobilized on the Au clusters is harnessed to generate proton influx to drive ATP synthase and concurrently supply phosphate to improve phosphorus availability to combat phosphorus-deficiency stress. In tandem with the reactive oxygen species (ROS) scavenging and the photothermal functionality of Au clusters, such an assembled microreactor exhibits an improved abiotic stress tolerance and achieves plasmon-accelerated ATP synthesis. This innovative approach offers an effective route to enhance the stress resistance of ATP synthase-based energy-generating systems, opening an exciting potential of these systems for biomimicking applications.

Curcumin loaded hydrogel with double ROS-scavenging effect regulates microglia polarization to promote poststroke rehabilitation

Cyclodextrins are used to include curcumin to form complex, which is subsequently loaded into a reactive oxygen species (ROS) responsive hydrogel (Cur gel). This gel exhibits a dual ROS scavenging effect. The gel can neutralize extracellular ROS to lead to a ROS-sensitive curcumin release. The released curcumin complex can eliminate intracellular ROS. Furthermore, the Cur gel effectively downregulates the expression of CD16 and IL-1β while upregulating CD206 and TGF-β in oxygen and glucose-deprived (OGD) BV2 cells. Additionally, it restores the expression of synaptophysin and PSD95 in OGD N2a cells. Upon injection into the stroke cavity, the Cur gel reduces CD16 expression and increases CD206 expression in the peri-infarct area of stroke mice, indicating an in vivo anti-inflammatory polarization of microglia. Colocalization studies using PSD95 and VGlut-1 stains, along with Golgi staining, reveal enhanced neuroplasticity. As a result, stroke mice treated with the Cur gel exhibit the most significant motor function recovery. Mechanistic investigations demonstrate that the released curcumin complex scavenges ROS and suppresses the activation of the ROS-NF-κB signaling pathway by inhibiting the translocation of p47-phox and p67-phox to lead to anti-inflammatory microglia polarization. Consequently, the Cur gel exhibits promising potential for promoting post-stroke rehabilitation in clinics.

Cost-effective and natural-inspired lotus root/GelMA scaffolds enhanced wound healing via ROS scavenging, angiogenesis and reepithelialization

Skin wounds, prevalent and fraught with complications, significantly impact individuals and society. Wound healing encounters numerous obstacles, such as excessive reactive oxygen species (ROS) production and impaired angiogenesis, thus promoting the development of chronic wound. Traditional clinical interventions like hemostasis, debridement, and surgery face considerable challenges, including the risk of secondary infections. While therapies designed to scavenge excess ROS and enhance proangiogenic properties have shown effectiveness in wound healing, their clinical adoption is hindered by high costs, complex manufacturing processes, and the potential for allergic reactions. Lotus root, distinguished by its natural micro and macro porous architecture, exhibits significant promise as a tissue engineering scaffold. This study introduced a novel scaffold based on hybridization of lotus root-inspired and Gelatin Methacryloyl (GelMA), verified with satisfactory physicochemical properties, biocompatibility, antioxidative capabilities and proangiogenic abilities. In vivo tests employing a full-thickness wound model revealed that these scaffolds notably enhanced micro vessel formation and collagen remodeling within the wound bed, thus accelerating the healing process. Given the straightforward accessibility of lotus roots and the cost-effective production of the scaffolds, the novel scaffolds with ROS scavenging, pro-angiogenesis and re-epithelialization abilities are anticipated to have clinical applicability for various chronic wounds.

Brassinosteroid improves resistance to phosphorus deficiency stress through regulating nutrient balance and reactive oxygen species scavenging in potato

Brassinosteroid (BR) plays a crucial role in plant growth, development and response to abiotic stress. However, the mechanism by which BR regulates the response of potato plants to phosphorus deficiency stress is still largely unknown. In this work, the effects of BR on the growth of potato plants under phosphorus deficient condition were investigated. Exogenous BR application mitigated the growth inhibition caused by phosphorus deficiency stress. Transcriptomic analyses revealed that BR application altered the expression of genes involved in mitogen-activated protein kinase (MAPK) signaling pathway, plant hormone signal transduction, and nitrogen and phosphorus metabolisms under phosphorus deficient condition. Further gene ontology (GO) analysis indicated a significant enrichment of genes associated with reactive oxygen species scavenging process. Ectopic expression of potato brassinosteroid synthesis gene StCYP85A1 in Arabidopsis improved the resistance of transgenic plants to phosphorus deficiency stress, as indicated by the increased germination greening ratio and root growth. Quantitative real time PCR and antioxidant enzyme activity analysis revealed that ectopic expression of StCYP85A1 altered the expression of genes related to nitrogen and phosphorus metabolism, and promoted antioxidant enzyme activity in transgenic plants. These findings indicated that BR improved the tolerance of potato plants to phosphorus deficiency stress by regulating nutrient homeostasis and reactive oxygen species scavenging.

Plumbagin's Antiproliferative Mechanism in Human Cancer Cells: A Copper-Dependent Cytotoxic Approach.

Cancer is a serious global health problem, causing the loss of millions of lives each year. Plumbagin, a compound derived from the medicinal plant Plumbago zeylanica, has shown promise in stopping the growth of tumor cells both in laboratory settings and in living organisms. Many plant-based compounds exert their effects through copper's ability to produce reactive oxygen species (ROS). This study aimed to understand how plumbagin, dependent on copper, induces cell death (apoptosis) in human cancer cells through various experiments. The results demonstrate that plumbagin hinders the growth of pancreatic cancer cells PNAC-1 and MIA PaCa-2 by utilizing the copper naturally present in the cells. Unlike metal chelators that remove iron and zinc (desferrioxamine mesylate and histidine), a specific copper chelator called neocuproine lessens the cell death caused by plumbagin. When ROS scavengers are used, plumbagin-induced apoptosis is inhibited, indicating that ROS plays a role in initiating cell death. The study also proves that plumbagin prevents copper from leaving cancer cells by suppressing the expression of specific genes (CTR1 and ATP7A). It is confirmed that plumbagin targets the nuclear copper, leading to signals that promote oxidative stress and, ultimately, cell death. These findings provide valuable insights into the potential of plumbagin as a substance to combat cancer, highlighting the importance of understanding how copper behaves within cancer cells.

Improving Treatment for Parkinson's Disease: Harnessing Photothermal and Phagocytosis-Driven Delivery of Levodopa Nanocarriers Across the Blood-Brain Barrier

Parkinson's disease (PD) poses a significant therapeutic challenge, mainly due to the limited ability of drugs to cross the blood-brain barrier (BBB) without undergoing metabolic transformations. Levodopa, a key component of dopamine replacement therapy, effectively enhances dopaminergic activity. However, it encounters obstacles from peripheral decarboxylase, hindering its passage through the BBB. Furthermore, levodopa metabolism generates reactive oxygen species (ROS), exacerbating neuronal damage. Systemic pulsatile dosing further disrupts natural physiological buffering mechanisms. In this investigation, we devised a ROS-responsive levodopa prodrug system capable of releasing the drug and reducing ROS levels in the central nervous system. The prodrug was incorporated within second near-infrared region (NIR-II) gold nanorods (AuNRs) and utilized angiopep-2 (ANG) for targeted delivery across the BBB. The processes of tight junction opening and endocytosis facilitated improved levodopa transport. ROS scavenging helped alleviate neuronal oxidative stress, leading to enhanced behavioral outcomes and reduced oxidative stress levels in a mouse model of PD. Following treatment, the PD mouse model exhibited enhanced flexibility, balance, and spontaneous exploratory activity. This approach successfully alleviated the motor impairments associated with the disease model. Consequently, our strategy, utilizing NIR-Ⅱ AuNRs and ANG-mediated BBB penetration, coupled with the responsive release of levodopa, offers a promising approach for dopamine supplementation and microenvironmental regulation. This system holds substantial potential as an efficient platform for delivering neuroprotective drugs and advancing PD therapy.

Melatonin-coated nanofiber cell sheets promote periodontal regeneration through ROS scavenging and preservation of stemness

Mesenchymal stem cell (MSC)-based cell sheet engineering holds great promise for periodontal tissue engineering and restoring damaged tissues. However, achieving optimal regenerative outcomes remains a challenge. This study introduces a novel approach that integrates melatonin-coated nanofiber fragments (mNFs) into dental follicle stem cell sheets (mNF-CSs) to enhance their regenerative potential. The mNF-CSs were engineered using electrospun poly-L-lactic acid (PLLA) nanofiber sheets fragmented into mNFs and coated with melatonin, a potent antioxidant and osteogenic agent. The mNF-CSs exhibited a homogenous morphology with sustained melatonin release over 21 days, providing a prolonged antioxidative effect critical for tissue regeneration. In vitro experiments demonstrated that mNF-CSs significantly reduced intracellular reactive oxygen species (ROS) levels and upregulated antioxidative proteins such as SOD1 and SOD2, resulting in improved cell viability, maintenance of stemness, and enhanced osteogenic differentiation potential of dental follicle stem cells (DFCs). In vivo studies using both a nude mouse and a rat periodontal defect model demonstrated that mNF-CSs promoted alveolar bone repair and periodontal tissue regeneration, with enhanced retention of MSCs at the defect site and increased expression of periodontal tissue-related markers. Transcriptome analysis revealed the upregulation of genes associated with biomineralization, odontogenesis, and autophagy pathways in mNF-CSs, suggesting their ability to modulate crucial cellular processes for tissue regeneration. Overall, mNF-CSs offer a promising strategy for enhancing periodontal tissue engineering applications, providing a platform for improving bone grafts and regenerative medicine strategies in the context of periodontal diseases.

Alendronate sodium induces G1 phase arrest and apoptosis in human umbilical vein endothelial cells by inhibiting ROS-mediated ERK1/2 signaling

Bisphosphonates are potent bone resorption inhibitors, among which alendronate sodium (ALN) is commonly prescribed for most osteoporosis patients, but long-term application of ALN can cause bisphosphonate-related osteonecrosis of jaw (BRONJ), the pathogenesis of which remains unclear. Previous studies have suggested that bisphosphonates cause jaw ischemia by affecting the biological behavior of vascular endothelial cells, leading to BRONJ. However, the impacts of ALN on vascular endothelial cells and its mechanism remain unclear. The purpose of this work is to assess the influence of ALN on human umbilical vein endothelial cells (HUVECs) and clarify the molecular pathways involved. We found that high concentration of ALN induced G1 phase arrest in HUVECs, demonstrated by downregulation of Cyclin D1 and Cyclin D3. Moreover, high concentration of ALN treatment showed pro-apoptotic effect on HUVECs, demonstrated by increased levels of the cleaved caspase-3, the cleaved PARP and Bax, along with decreased levels of anti-apoptotic protein Bcl-2. Further experiments showed that ERK1/2 phosphorylation was decreased. Additionally, ALN provoked the build-up of reactive oxygen species (ROS) in HUVECs, leading to ERK1/2 pathway suppression. N-acetyl-L-cysteine (NAC), a ROS scavenger, efficiently promoted the ERK1/2 phosphorylation and mitigated the G1 phase arrest and apoptosis triggered by ALN in HUVECs. PD0325901, an inhibitor of ERK1/2 that diminishes the ERK1/2 phosphorylation enhanced the ALN-induced G1 phase arrest and apoptosis in HUVECs. These findings show that ALN induces G1 phase arrest and apoptosis through ROS-mediated ERK1/2 pathway inhibition in HUVECs, providing novel insights into the pathogenic process, prevention and treatment of BRONJ in individuals receiving extended use of ALN.

A molybdenum sulfide based nitric oxide controlled release oral gel for rapid healing of oral mucosal ulcers

Oral mucosal ulcer is the most prevalent oral mucosal lesion, affecting over 25 % of general population. The current treatment regimens lack efficacy in addressing challenges such as wound bleeding, bacterial infection and inflammation on a continuous basis. Hence, a multi-functional oral gel (termed MPCST) with a long-acting duration is designed. It is based on a tannic acid-thioctic acid (TATA) supramolecular hydrogel which absorbs tissue exudate while exhibiting robust tissue adhesion properties. To form MPCST, TATA is loaded with MPCS, which are composed of polydopamine (PDA)-coated molybdenum disulfide (MoS2) nanoflakes (MoS2@PDA) with high photothermal conversion efficiency, nitric oxide (NO) precursor nitroprusside (SNP) and cerium oxide (CeO2) with high reactive oxygen species (ROS) scavenging rate. Upon exposure to 808 nm near-infrared (NIR) irradiation, MPCS rapidly heats up and releases NO to promote angiogenesis, while exhibiting strong ROS scavenging, antibacterial (including oral common Streptococcus mutans), and anti-inflammatory properties. Animal experiments show that the MPCST oral gel, composed of MPCS and TATA hydrogel, exhibits superior therapeutic efficacy compared to the commonly used dexamethasone patch.

Reactive oxygen-scavenging polydopamine nanoparticle coated 3D nanofibrous scaffolds for improved osteogenesis: Toward an aging in vivo bone regeneration model.

Tissue engineered scaffolds aimed at the repair of critical-sized bone defects lack adequate consideration for our aging society. Establishing an effective aged in vitro model that translates to animals is a significant unmet challenge. The in vivo aged environment is complex and highly nuanced, making it difficult to model in the context of bone repair. In this work, 3D nanofibrous scaffolds generated by the thermally-induced self-agglomeration (TISA) technique were functionalized with polydopamine nanoparticles (PD NPs) as a tool to improve drug binding capacity and scavenge reactive oxygen species (ROS), an excessive build-up that dampens the healing process in aged tissues. PD NPs were reduced by ascorbic acid (rPD) to further improve hydrogen peroxide (H2O2) scavenging capabilities, where we hypothesized that these functionalized scaffolds could rescue ROS-affected osteoblastic differentiation in vitro and improve new bone formation in an aged mouse model. rPDs demonstrated improved H2O2 scavenging activity compared to neat PD NPs, although both NP groups rescued the alkaline phosphatase activity (ALP) of MC3T3-E1 cells in presence of H2O2. Additionally, BMP2-induced osteogenic differentiation, both ALP and mineralization, was significantly improved in the presence of PD or rPD NPs on TISA scaffolds. While in vitro data showed favorable results aimed at improving osteogenic differentiation by PD or rPD NPs, in vivo studies did not note similar improvements in ectopic bone formation an aged model, suggesting that further nuance in material design is required to effectively translate to improved in vivo results in aged animal models.

Nano-Fe3O4: Enhancing the tolerance of Elymus nutans to Cd stress through regulating programmed cell death

Cadmium (Cd) poses a significant threat to plant growth and the environment. Nano-Fe3O4 is effective in alleviating Cd stress in plants. Elymus nutans Griseb. is an important fodder crop on the Qinghai-Tibetan Plateau (QTP). However, the potential mechanism by which nano-Fe3O4 alleviates Cd stress in E. nutans is not well understood. E. nutans were subjected to single Cd, single nano-Fe3O4, and co-treatment with nano-Fe3O4 and Cd, and the effects on morphology, Cd uptake, antioxidant enzyme activity, reactive oxygen species (ROS) levels and programmed cell death (PCD) were studied to clarify the regulatory mechanism of nano-Fe3O4. The results showed that Cd stress significantly decreased the germination percentage and biomass of E. nutans. The photosynthetic pigment content decreased significantly under Cd stress. Cd stress also caused oxidative stress and lipid peroxidation, accumulation of excessive ROS, resulting in PCD, but the effect of nano-Fe3O4 was different. Seed germination, seedling growth, and physiological processes were analyzed to elucidate the regulatory role of nano-Fe3O4 nanoparticles in promoting photosynthesis, reducing Cd accumulation, scavenging ROS, and regulating PCD, to promote seed germination and seedling growth in E. nutans. This report provides a scientific basis for improving the tolerance of Elymus to Cd stress by using nano-Fe3O4.

Mesoporous manganese-doped nano-antioxidant suppresses pyroptosis for effective ischemic stroke therapy

Pyroptosis mediates neuroinflammation following ischemic stroke and contributes to its development, indicating that targeting pyroptosis-related pathways could be a potential therapeutic strategy for stroke. In this study, a mesoporous manganese-doped cerium oxide (MMC) nano-antioxidant encapsulated with caspase-1 inhibitor VX765 is rationally designed and engineered to relieve ischemic stroke by integrating the suppression of pyroptosis activity with reactive oxygen species (ROS) scavenging capability. Through the surface modification of Angiopoietin-2 (Ang2), the nano-antioxidant can specifically bind to the low-density lipoprotein receptor-related protein, cross the blood–brain barrier, and ultimately aggregate in ischemic neuronal tissues. In mice subjected to middle cerebral artery occlusion/reperfusion, the nano-antioxidant alleviates oxidative stress, inhibits cell pyroptosis, reduces inflammatory cytokines, and regulates microglial polarization toward M2, ultimately mitigating neuroinflammation and reperfusion injury in brain tissue. Mechanistic studies reveal that the pyroptosis-associated NOD-like receptor signaling pathway, the inflammation-associated TNF signaling pathway, the neutrophil chemotaxis-associated Toll-like receptor signaling pathway, and the oxidative stress-associated NF-kappa B signaling pathway are involved in the antioxidant-mediated stroke therapy. Endowed with pyroptosis-reversing ability and nano-antioxidant activities, this engineered antioxidant presents a novel therapeutic paradigm for minimizing reperfusion injury and enhancing stroke treatment efficacy.

Multi-responsive sodium hyaluronate/tannic acid hydrogels with ROS scavenging ability promote the healing of diabetic wounds

Oxidative stress caused by excessive reactive oxygen species (ROS) accumulation significantly hinders wound healing in patients with diabetes. Scavenging ROS and reducing inflammation are crucial for rapid healing. In this work, a multi-responsive sodium hyaluronate (HA)/tannic acid (TA) hydrogel was developed based on boronate ester bonds. Sodium hyaluronate with 3-aminophenyl boronic acid modification (HA-APBA) was mixed and crosslinked with TA to form HA-APBA/TA hydrogels. These hydrogels are injectable, self-healing, and biocompatible. The HA-APBA/TA hydrogels could release free TA through the collapse of the structure at low pH, high H2O2 concentration, and high glucose concentration, thus possessing good ROS scavenging ability. In full-thickness skin wounds of db/db mice, the HA-APBA/TA hydrogels promoted wound healing, collagen deposition, and significant angiogenesis. Furthermore, they have been shown to effectively reduce the levels of inflammatory factors in wounds and lower the expression of CD86, a pro-inflammatory macrophage surface marker. This resulted in a more effective transition of wound healing from the inflammatory phase to the proliferative phase. This study provides an optional strategy for alleviating oxidative stress and controlling excessive inflammation, thereby promoting diabetic wound healing.

Loss of the DNA repair protein, polynucleotide kinase/phosphatase, activates the type 1 interferon response independent of ionizing radiation.

DNA damage has been implicated in the stimulation of the type 1 interferon (T1IFN) response. Here, we show that downregulation of the DNA repair protein, polynucleotide kinase/phosphatase (PNKP), in a variety of cell lines causes robust phosphorylation of STAT1, upregulation of interferon-stimulated genes and persistent accumulation of cytosolic DNA, all of which are indicators for the activation of the T1IFN response. Furthermore, this did not require damage induction by ionizing radiation. Instead, our data revealed that production of reactive oxygen species (ROS) synergises with PNKP loss to potentiate the T1IFN response, and that loss of PNKP significantly compromises mitochondrial DNA (mtDNA) integrity. Depletion of mtDNA or treatment of PNKP-depleted cells with ROS scavengers abrogated the T1IFN response, implicating mtDNA as a significant source of the cytosolic DNA required to potentiate the T1IFN response. The STING signalling pathway is responsible for the observed increase in the pro-inflammatory gene signature in PNKP-depleted cells. While the response was dependent on ZBP1, cGAS only contributed to the response in some cell lines. Our data have implications for cancer therapy, since PNKP inhibitors would have the potential to stimulate the immune response, and also to the neurological disorders associated with PNKP mutation.

Integrated transcriptomic and proteomic analysis unravels the response mechanisms of Saccharina japonica to heat stress

High temperature is a major abiotic stress that limits the growth and productivity of seaweed. Over the past decades, the cold-temperate seaweed Saccharina japonica has been domesticated and gradually adapted to subtropical regions with higher temperatures. However, there is limited knowledge regarding the molecular responses of S. japonica to heat stress. In this study, an integrated transcriptomic and proteomic analysis was performed to explore the molecular mechanism underlying the response to heat stress in S. japonica. A total of 6777 genes and 226 proteins were identified that exhibited differential expression in heat stress samples comparison to non-stress sample. GO analysis revealed that the GO molecular function (MF) terms related to unfolded protein binding/protein binding, and heat shock protein (HSP) binding/HSP90 binding were significantly enriched in the up-regulated DEGs/DEPs in S. japonica sporophytes under heat stress. Further analysis of the global gene and protein expression profiles unveiled the potential mechanisms in S. japonica to alleviate heat stress through up-regulation of the heat stress transcription factor-heat shock proteins-HSP70/HSP90 organising proteins (HSF-HSPs-HOPs) module, down-regulation of reactive oxygen species (ROS) generation and up-regulation of ROS scavenging. Our results provide novel insights into the heat stress acclimation mechanism in S. japonica, and would benefit future selection of heat-tolerant varieties.

CRISPR/Cas9-mediated genome editing of OsCS511 enhances cold tolerance in Oryza sativa L.

The frequency of climate change is increasing globally, which makes predictions challenging. Cold spells during the rice seedling stage can significantly reduce yield, prompting a constant need for cold-tolerant cultivars, which is a major breeding goal. However, the traditional crossbreeding of rice cultivars requires substantial time and effort. Recently, the application of CRISPR/Cas9 to reduce defects in elite cultivars has become a more cost-effective and time-efficient method for breeding cultivars than cross-breeding methods and can alleviate food insecurity. In the present study, CRISPR/Cas9-mediated genome editing was performed for OsCS511 a gene involved in cold susceptibility, identified using quantitative trait loci (QTL) mapping in Ilmi (Oryza sativa L. spp. Japonica cv. Ilmi). In Ilmi, CRISPR/Cas9 tool-edited OsCS511 homozygous lines were used in T0 and advanced generations in the field. CRISPR/Cas9 induced variations in the DNA sequence and plants with insertions or deletions compared to OsCS511 of Ilmi were selected as genome-edited lines. Agricultural traits, reactive oxygen species scavenging capacity, and stress-tolerance-related gene expression levels were evaluated under normal and cold stress conditions. Under normal conditions, all traits evaluated in the Ilmi and OsCS511 genome-edited lines exhibited similar results; however, when subjected to cold stress, the cold tolerance of OsCS511 genome-edited lines improved or reached the same level as that of Ilmi. OsCS511 genome-edited lines recovered and survived. From a breeding perspective, we suggest that CRISPR/Cas9 technology can precisely reduce defects in existing superior rice cultivars with high efficiency and speed.

Light-activated nanoclusters with tunable ROS for wound infection treatment

Infected wounds pose a significant clinical challenge due to bacterial resistance, recurrent infections, and impaired healing. Reactive oxygen species (ROS)-based strategies have shown promise in eradicating bacterial infections. However, the excess ROS in the infection site after treatments may cause irreversible damage to healthy tissues. To address this issue, we developed bovine serum albumin-iridium oxide nanoclusters (BSA-IrOx NCs) which enable photo-regulated ROS generation and scavenging using near infrared (NIR) laser. Upon NIR laser irradiation, BSA-IrOx NCs exhibit enhanced photodynamic therapy, destroying biofilms and killing bacteria. When the NIR laser is off, the nanoclusters' antioxidant enzyme-like activities prevent inflammation and repair damaged tissue through ROS clearance. Transcriptomic and metabolomic analyses revealed that BSA-IrOx NCs inhibit bacterial nitric oxide synthase, blocking bacterial growth and biofilm formation. Furthermore, the nanoclusters repair impaired skin by strengthening cell junctions and reducing mitochondrial damage in a fibroblast model. In vivo studies using rat infected wound models confirmed the efficacy of BSA-IrOx NCs. This study presents a promising strategy for treating biofilm-induced infected wounds by regulating the ROS microenvironment, addressing the challenges associated with current ROS-based antibacterial approaches.

A phased small interfering RNA-derived pathway mediates lead stress tolerance in maize.

Phased small interfering RNAs (phasiRNAs) are a distinct class of endogenous small interfering RNAs, which regulate plant growth, development and environmental stress response. To determine the effect of phasiRNAs on maize (Zea mays L.) tolerance to lead (Pb) stress, the roots of 305 maize lines under Pb treatment were subjected to generation of individual databases of small RNAs. We identified 55 high-confidence phasiRNAs derived from 13 PHAS genes (genes producing phasiRNAs) in this maize panel, of which 41 derived from nine PHAS loci were negatively correlated with Pb content in the roots. The potential targets of the 41 phasiRNAs were enriched in ion transport and import. Only the expression of PHAS_1 (ZmTAS3j, Trans-Acting Short Interference RNA3) was regulated by its cis-expression quantitative trait locus and thus affected the Pb content in the roots. Using the Nicotiana benthamiana (N. benthamiana) transient expression system, 5'-rapid amplification of cDNA ends, and Arabidopsis heterologously expressed, we verified that ZmTAS3j was cleaved by zma-miR390 and thus generated tasiRNA targeting ARF genes (tasiARFs), and that the 5' and 3' zma-miR390 target sites of ZmTAS3j were both necessary for efficient biosynthesis and functional integrity of tasiARFs. We validated the involvement of the zma-miR390-ZmTAS3j-tasiARF-ZmARF3-ZmHMA3 pathway in Pb accumulation in maize seedlings using genetic, molecular, and cytological methods. Moreover, the increased Pb tolerance in ZmTAS3j-overexpressed lines was likely attributed to the zma-miR390-ZmTAS3j-tasiARF-ZmARF3-SAURs pathway, which elevated indole acetic acid levels and thus reactive oxygen species scavenging capacity in maize roots. Our study reveals the importance of the TAS3-derived tasiRNA pathway in plant adaptation to Pb stress.