Arginine monomethylation by PRMT7 controls MAVS-mediated antiviral innate immunity.

Accurate control of innate immune responses is required to eliminate invading pathogens and simultaneously avoid autoinflammation and autoimmune diseases. Here, we demonstrate that arginine monomethylation precisely regulates the mitochondrial antiviral-signaling protein (MAVS)-mediated antiviral response. Protein arginine methyltransferase 7 (PRMT7) forms aggregates to catalyze MAVS monomethylation at arginine residue 52 (R52), attenuating its binding to TRIM31 and RIG-I, which leads to the suppression of MAVS aggregation and subsequent activation. Upon virus infection, aggregated PRMT7 is disabled in a timely manner due to automethylation at arginine residue 32 (R32), and SMURF1 is recruited to PRMT7 by MAVS to induce proteasomal degradation of PRMT7, resulting in the relief of PRMT7 suppression of MAVS activation. Therefore, we not only reveal that arginine monomethylation by PRMT7 negatively regulates MAVS-mediated antiviral signaling in vitro and in vivo but also uncover a mechanism by which PRMT7 is tightly controlled to ensure the timely activation of antiviral defense.

Asymmetric arginine dimethylation of cytosolic RNA and DNA sensors by PRMT3 attenuates antiviral innate immunity.

The cytosolic RNA and DNA sensors initiate type I interferon signaling when binding to RNA or DNA. To effectively protect the host against virus infection and concomitantly avoid excessive interferonopathy at resting states, these sensors must be tightly regulated. However, the key molecular mechanisms regulating these sensors' activation remain elusive. Here, we identify PRMT3, a type I protein arginine methyltransferase, as a negative regulator of cytosolic RNA and DNA sensors. PRMT3 interacts with RIG-I, MDA5, and cGAS and catalyzes asymmetric dimethylation of R730 on RIG-I, R822 on MDA5, and R111 on cGAS. These modifications reduce RNA-binding ability of RIG-I and MDA5 as well as DNA-binding ability and oligomerization of cGAS, leading to the inhibition of downstream type I interferon production. Furthermore, mice with loss of one copy of Prmt3 or in vivo treatment of the PRMT3 inhibitor, SGC707, are more resistant to RNA and DNA virus infection. Our findings reveal an essential role of PRMT3 in the regulation of antiviral innate immunity and give insights into the molecular regulation of cytosolic RNA and DNA sensors' activation.

Kill Two Birds with One Stone: Dual-Metal MOF-Nanozyme-Decorated Hydrogels with ROS-Scavenging, Oxygen-Generating, and Antibacterial Abilities for Accelerating Infected Diabetic Wound Healing.

Diabetic wounds tend to develop into nonhealing wounds associated with the complex inflammatory microenvironment of uncontrollable bacterial infection, reactive oxygen species (ROS) accumulation, and chronic hypoxia. Damaged blood vessels hinder metabolic circulation, aggravating hypoxia, and ROS accumulation and further exacerbating the diabetic wound microenvironment. However, existing treatments with a single functionality have difficulty healing complicated diabetic wounds. Therefore, developing an integrative strategy to improve the hostility of the diabetic wound microenvironment is urgently needed. Herein, multifunctional genipin (GP)-crosslinked chitosan (CS)-based hydrogels decorated with the biomimetic metal-organic framework (MOF)-nanozymes and the natural antibacterial agent chlorogenic acid (CGA), which is named MOF/CGA@GP-CS (MCGC), are prepared. With catalase (CAT)-like activity, these dual-metal MOF-nanozymes are promising bioreactors for simultaneously alleviating ROS accumulation and hypoxia by converting elevated endogenous H2O2 into dissolved oxygen in diabetic wounds. In addition, the other component of natural polyphenolic CGA acts as a mild antibacterial agent, efficiently inhibiting wound infection and avoiding antibiotic resistance. Impressively, the MCGC hydrogels accelerate infected diabetic wound healing by eliminating oxidative stress, increasing oxygenation, and reversing bacterial infection in vivo. In this work, an effective strategy based on multifunctional hydrogel wound dressings is successfully developed and applied in diabetic wound management.

Deep-learning enhanced high-quality imaging in metalens-integrated camera.

Because of their ultra-light, ultra-thin, and flexible design, metalenses exhibit significant potential in the development of highly integrated cameras. However, the performances of metalens-integrated camera are constrained by their fixed architectures. Here we proposed a high-quality imaging method based on deep learning to overcome this constraint. We employed a multi-scale convolutional neural network (MSCNN) to train an extensive pair of high-quality and low-quality images obtained from a convolutional imaging model. Through our method, the imaging resolution, contrast, and distortion have all been improved, resulting in a noticeable overall image quality with SSIM over 0.9 and an improvement in PSNR over 3 dB. Our approach enables cameras to combine the advantages of high integration with enhanced imaging performances, revealing tremendous potential for a future groundbreaking imaging technology.

S-S Bond Strategy at Sulfide Heterointerface: Reversing Charge Transfer and Constructing Hydrogen Spillover for Boosted Hydrogen Evolution.

Developing efficient electrocatalyst in sulfides for hydrogen evolution reaction (HER) still poses challenges due to the lack of understanding the role of sulfide heterointerface. Here, we report a sulfide heterostructure RuSx/NbS2, which is composed of 3R-type NbS2 loaded by amorphous RuSx nanoparticles with S-S bonds formed at the interface. As HER electrocatalyst, the RuSx/NbS2 shows remarkable low overpotential of 38 mV to drive a current density of 10 mA cm-2 in acid, and also low Tafel slope of 51.05 mV dec-1. The intrinsic activity of RuSx/NbS2 is much higher than that of Ru/NbS2 reference as well as the commercial Pt/C. Both experiments and theoretical calculations unveil a reversed charge transfer at the interface from NbS2 to RuSx that driven by the formation of S-S bonds, resulting in electron-rich Ru configuration for strong hydrogen adsorption. Meanwhile, electronic redistribution induced by the sulfide heterostructure facilitates hydrogen spillover (HSo) effect in this system, leading to accelerated hydrogen desorption at the basal plane of NbS2. This study provides an effective S-S bond strategy in sulfide heterostructure to synergistically modulate the charge transfer and adsorption thermodynamics, which is very valuable for the development of efficient electrocatalysts in practical applications.

Zebrafish Hif3α modulates erythropoiesis via regulation of gata1 to facilitate hypoxia tolerance.

The hypoxia-inducible factors 1α and 2α (HIF1α and HIF2α) are master regulators of the cellular response to O2. In addition to HIF1α and HIF2α, HIF3α is another identified member of the HIFα family. Even though the question of whether some HIF3α isoforms have transcriptional activity or repressive activity is still under debate, it is evident that the full length of HIF3α acts as a transcription factor. However, its function in hypoxia signaling is largely unknown. Here, we show that loss of hif3a in zebrafish reduced hypoxia tolerance. Further assays indicated that erythrocyte number was decreased because red blood cell maturation was impeded by hif3a disruption. We found that gata1 expression was downregulated in hif3a null zebrafish, as were several hematopoietic marker genes, including alas2, band3, hbae1, hbae3 and hbbe1 Hif3α recognized the hypoxia response element located in the promoter of gata1 and directly bound to the promoter to transactivate gata1 expression. Our results suggested that hif3a facilities hypoxia tolerance by modulating erythropoiesis via gata1 regulation.

PDM-SHD NFDM transmission with envelope-detection feedback polarization tracking and optical injection locking.

Nonlinear frequency division multiplexing (NFDM) systems, especially the eigenvalue communications have the potential to overcome the nonlinear Shannon capacity limit. However, the baud rate of eigenvalue communications is typically restricted to a few GBaud, making it challenging to mitigate laser frequency impairments such as the phase noise and frequency offset (FO) using digital signal processing (DSP) algorithms in intradyne detections (IDs). Therefore, we introduce the polarization division multiplexing-self-homodyne detection (PDM-SHD) into the NFDM link, which could overcome the impact of phase noise and FO by transmitting a pilot carrier originating from the transmitter laser to the receiver through the orthogonal polarization state of signal. To separate the signal from the carrier at the receiver, a carrier to signal power ratio (CSPR) unrestricted adaptive polarization controlling strategy is proposed and implemented by exploiting the optical intensity fluctuation of the light in a particular polarization rather than its direct optical power as the feedback. Optical injection locking (OIL) is used subsequently to amplify optical power of pilot carrier and mitigate the impact of signal-signal beat interference (SSBI). Additionally, the effects of cross-polarization modulation (XPolM) and modulation instability (MI) in long haul transmission are explored and inhibited. The results show that the tolerable FO range is about 3.5 GHz, which is 17 times larger than the ID one. When 16-amplitude phase shift keying (APSK) or 64-APSK constellations are used, identical Q-factor performance can be obtained by using distributed feedback (DFB, ∼10 MHz) laser, external cavity laser (ECL, ∼100kHz), or fiber laser (FL, ∼100 Hz), respectively, which demonstrates that our proposed PDM-SHD eigenvalue communication structure is insensitive to the laser linewidth. Under the impact of cycle slip, the Q-factor difference of 16-APSK signal between the ECL-ID system and ECL-SHD system can be up to 8.73 dB after 1500 km transmission.

Zebrafish otud6b Negatively Regulates Antiviral Responses by Suppressing K63-Linked Ubiquitination of irf3 and irf7.

Ovarian tumor domain-containing 6B (OTUD6B) belongs to the OTU deubiquitylating enzyme family. In this study, we report that zebrafish otud6b is induced upon viral infection, and overexpression of otud6b suppresses cellular antiviral response. Disruption of otud6b in zebrafish increases the survival rate upon spring viremia of carp virus and grass carp reovirus exposure. Further assays indicate that otud6b interacts with irf3 and irf7 and diminishes traf6-mediated K63-linked polyubiquitination of irf3 and irf7. In addition, the OTU domain is required for otud6b to repress IFN-1 activation and K63-linked polyubiquitination of irf3 and irf7. Moreover, otud6b also attenuates tbk1 to bind to irf3 and irf7, resulting in the impairment of irf3 and irf7 phosphorylation. This study provides, to our knowledge, novel insights into otud6b function and sheds new lights on the regulation of irf3 and irf7 by deubiquitination in IFN-1 signaling.

Zebrafish prmt2 Attenuates Antiviral Innate Immunity by Targeting traf6.

TNFR-associated factor 6 (TRAF6) not only recruits TBK1/IKKε to MAVS upon virus infection but also catalyzes K63-linked polyubiquitination on substrate or itself, which is critical for NEMO-dependent and -independent TBK1/IKKε activation, leading to the production of type I IFNs. The regulation at the TRAF6 level could affect the activation of antiviral innate immunity. In this study, we demonstrate that zebrafish prmt2, a type I arginine methyltransferase, attenuates traf6-mediated antiviral response. Prmt2 binds to the C terminus of traf6 to catalyze arginine asymmetric dimethylation of traf6 at arginine 100, preventing its K63-linked autoubiquitination, which results in the suppression of traf6 activation. In addition, it seems that the N terminus of prmt2 competes with mavs for traf6 binding and prevents the recruitment of tbk1/ikkε to mavs. By zebrafish model, we show that loss of prmt2 promotes the survival ratio of zebrafish larvae after challenge with spring viremia of carp virus. Therefore, we reveal, to our knowledge, a novel function of prmt2 in the negative regulation of antiviral innate immunity by targeting traf6.

Zebrafish sirt7 Negatively Regulates Antiviral Responses by Attenuating Phosphorylation of irf3 and irf7 Independent of Its Enzymatic Activity.

Sirt7 is one member of the sirtuin family proteins with NAD (NAD+)-dependent histone deacetylase activity. In this study, we report that zebrafish sirt7 is induced upon viral infection, and overexpression of sirt7 suppresses cellular antiviral responses. Disruption of sirt7 in zebrafish increases the survival rate upon spring viremia of carp virus infection. Further assays indicate that sirt7 interacts with irf3 and irf7 and attenuates phosphorylation of irf3 and irf7 by preventing tbk1 binding to irf3 and irf7. In addition, the enzymatic activity of sirt7 is not required for sirt7 to repress IFN-1 activation. To our knowledge, this study provides novel insights into sirt7 function and sheds new light on the regulation of irf3 and irf7 by attenuating phosphorylation.

Formononetin Inhibits Mast Cell Degranulation to Ameliorate Compound 48/80-Induced Pseudoallergic Reactions.

Formononetin (FNT) is a plant-derived isoflavone natural product with anti-inflammatory, antioxidant, and anti-allergic properties. We showed previously that FNT inhibits immunoglobulin E (IgE)-dependent mast cell (MC) activation, but the effect of FNT on IgE-independent MC activation is yet unknown. Our aim was to investigate the effects and possible mechanisms of action of FNT on IgE-independent MC activation and pseudoallergic inflammation. We studied the effects of FNT on MC degranulation in vitro with a cell culture model using compound C48/80 to stimulate either mouse bone marrow-derived mast cells (BMMCs) or RBL-2H3 cells. We subsequently measured ß-hexosaminase and histamine release, the expression of inflammatory factors, cell morphological changes, and changes in NF-κB signaling. We also studied the effects of FNT in several in vivo murine models of allergic reaction: C48/80-mediated passive cutaneous anaphylaxis (PCA), active systemic anaphylaxis (ASA), and 2,4-dinitrobenzene (DNCB)-induced atopic dermatitis (AD). The results showed that FNT inhibited IgE-independent degranulation of MCs, evaluated by a decrease in the release of ß-hexosaminase and histamine and a decreased expression of inflammatory factors. Additionally, FNT reduced cytomorphological elongation and F-actin reorganization and attenuated NF-κB p65 phosphorylation and NF-κB-dependent promoter activity. Moreover, the administration of FNT alleviated pseudoallergic responses in vivo in mouse models of C48/80-stimulated PCA and ASA, and DNCB-induced AD. In conclusion, we suggest that FNT may be a novel anti-allergic drug with great potential to alleviate pseudoallergic responses via the inhibition of IgE-independent MC degranulation and NF-κB signaling.

Zebrafish phd3 Negatively Regulates Antiviral Responses via Suppression of Irf7 Transactivity Independent of Its Prolyl Hydroxylase Activity.

Prolyl hydroxylase domain (PHD)-containing enzyme 3 belongs to the Caenorhabditis elegans gene egl-9 family of prolyl hydroxylases, which has initially been revealed to hydroxylate hypoxia-inducible factor α (HIF-α) and mediate HIF-α degradation. In addition to modulating its target function by hydroxylation, PHD3 has been also shown to influence its binding partners' function independent of its prolyl hydroxylase activity. In this study, we report that overexpression of zebrafish phd3 suppresses cellular antiviral response. Moreover, disruption of phd3 in zebrafish increases the survival rate upon spring viremia of carp virus exposure. Further assays indicate that phd3 interacts with irf7 through the C-terminal IRF association domain of irf7 and diminishes K63-linked ubiquitination of irf7. However, the enzymatic activity of phd3 is not required for phd3 to inhibit irf7 transactivity. This study provides novel insights into phd3 function and sheds new light on the regulation of irf7 in retinoic acid-inducible gene I-like receptor signaling.

Color tuning in a compact core-shell nanocrystal based on intense and high-purity green and red photon upconversion.

To date, color-tunable photon upconversion (UC) in a single nanocrystal (NC) still suffers from cumbersome structures. Herein, we prepared a compact two-layer NC with bright and high-purity red and green UC emission upon 980 and 1530 nm excitation, respectively. The effects of trace Tm3+ doping and inert-shell coating on the UC color and intensity were discussed. In addition, the color tuning via various dual-excitation configurations and the color stability with temperature and excitation intensity were demonstrated. The proposed UC NC, featuring compact structure and high-quality color tuning, can lower the synthesis time cost and difficulty of its kind and can find wide applications in multi-channel imaging, display devices, anti-counterfeiting, and so on.

Zebrafish prmt3 negatively regulates antiviral responses.

Arginine methylation catalyzed by protein arginine methyltransferases (PRMT) is a common post-translational modification in histone and nonhistone proteins, which regulates many cellular functions. Protein arginine methyltransferase 3 (prmt3), a type I arginine methyltransferase, has been shown to carry out the formation of stable monomethylarginine as an intermediate before the establishment of asymmetric dimethylarginine. To date, however, the role of PRMT3 in antiviral innate immunity has not been elucidated. This study showed that zebrafish prmt3 was upregulated by virus infection and that the overexpression of prmt3 suppressed cellular antiviral response. The PRMT3 inhibitor, SGC707, enhanced antiviral capability. Consistently, prmt3-null zebrafish were more resistant to Spring Viremia of Carp Virus (SVCV) and Grass Carp Reovirus (GCRV) infection. Further assays showed that the overexpression of prmt3 diminished the phosphorylation of irf3 and prmt3 interacted with rig-i. In addition, both zinc-finger domain and catalytic domain of prmt3 were required for the suppressive function of prmt3 on IFN activation. Our findings suggested that zebrafish prmt3 negatively regulated the antiviral responses, implicating the vital role of prmt3-or even arginine methylation-in antiviral innate immunity.

CALB Immobilized onto Magnetic Nanoparticles for Efficient Kinetic Resolution of Racemic Secondary Alcohols: Long-Term Stability and Reusability.

In this study, an immobilization strategy for magnetic cross-linking enzyme aggregates of lipase B from Candida antarctica (CALB) was developed and investigated. Magnetic particles were prepared by conventional co-precipitation. The magnetic nanoparticles were modified with 3-aminopropyltriethoxysilane (APTES) to obtain surface amino-functionalized magnetic nanoparticles (APTES⁻Fe3O4) as immobilization materials. Glutaraldehyde was used as a crosslinker to covalently bind CALB to APTES⁻Fe3O4. The optimal conditions of immobilization of lipase and resolution of racemic 1-phenylethanol were investigated. Under optimal conditions, esters could be obtained with conversion of 50%, enantiomeric excess of product (eep) > 99%, enantiomeric excess of substrate (ees) > 99%, and enantiomeric ratio (E) > 1000. The magnetic CALB CLEAs were successfully used for enzymatic kinetic resolution of fifteen secondary alcohols. Compared with Novozym 435, the magnetic CALB CLEAs exhibited a better enantioselectivity for most substrates. The conversion was still greater than 49% after the magnetic CALB CLEAs had been reused 10 times in a 48 h reaction cycle; both ees and eep were close to 99%. Furthermore, there was little decrease in catalytic activity and enantioselectivity after being stored at -20 °C for 90 days.

Tumor Microenvironment Heterogeneity, Potential Therapeutic Avenues, and Emerging Therapies.

OBJECTIVE: This review describes the comprehensive portrait of tumor microenvironment (TME). Additionally, we provided a panoramic perspective on the transformation and functions of the diverse constituents in TME, and the underlying mechanisms of drug resistance, beginning with the immune cells and metabolic dynamics within TME. Lastly, we summarized the most auspicious potential therapeutic strategies. RESULTS: TME is a unique realm crafted by malignant cells to withstand the onslaught of endogenous and exogenous therapies. Recent research has revealed many small-molecule immunotherapies exhibiting auspicious outcomes in preclinical investigations. Furthermore, some pro-immune mechanisms have emerged as a potential avenue. With the advent of nanosystems and precision targeting, targeted therapy has now transcended the "comfort zone" erected by cancer cells within TME. CONCLUSION: The ceaseless metamorphosis of TME fosters the intransigent resilience and proliferation of tumors. However, existing therapies have yet to surmount the formidable obstacles posed by TME. Therefore, scientists should investigate potential avenues for therapeutic intervention and design innovative pharmacological and clinical technologies.

DNA Methylation-Based Diagnosis and Treatment of Breast Cancer.

DNA methylation is a key epigenetic modifier involved in tumor formation, invasion, and metastasis. The development of breast cancer is a complex process, and many studies have now confirmed the involvement of DNA methylation in breast cancer. Moreover, the number of genes identified as aberrantly methylated in breast cancer is rapidly increasing, and the accumulation of epigenetic alterations becomes a chronic factor in the development of breast cancer. The combined effects of external environmental factors and the internal tumor microenvironment promote epigenetic alterations that drive tumorigenesis. This article focuses on the relevance of DNA methylation to breast cancer, describing the role of detecting DNA methylation in the early diagnosis, prediction, progression, metastasis, treatment, and prognosis of breast cancer, as well as recent advances. The reversibility of DNA methylation is utilized to target specific methylation aberrant promoters as well as related enzymes, from early prevention to late targeted therapy, to understand the journey of DNA methylation in breast cancer with a more comprehensive perspective. Meanwhile, methylation inhibitors in combination with other therapies have a wide range of prospects, providing hope to drug-resistant breast cancer patients.

Effective neoadjuvant immunotherapy and chemotherapy in stage IIIA adenosquamous carcinoma of the lung with a complete response and surgical success: A case report.

There has been rapid advancement in the development of neoadjuvant therapy for non-small cell lung cancer (NSCLC), which holds great promise as an effective treatment strategy. Some clinical trials have confirmed that immunotherapy in combination with chemotherapy can be a recommended first-line regimen for neoadjuvant treatment of NSCLC. The present study describes the case of a male patient aged 65 years who was diagnosed with stage IIIA (cT2N2M0) adenosquamous carcinoma of the lung. After the administration of two cycles of neoadjuvant immunotherapy (sintilimab) in combination with chemotherapy, stable disease was observed in the primary tumor, whereas partial remission was detected in the mediastinal lymph nodes based on imaging assessment. The patient underwent an immediate upper lobectomy of the left lung. Pathological analysis revealed a complete response in the primary lesion, with only minimal presence of tumor cells observed in the lymph nodes surrounding the mediastinum and bronchi. This indicated that the present neoadjuvant therapy could be used in the treatment of stage III adenosquamous lung carcinoma; however, to conclusively determine its efficacy, further studies targeting this specific cancer type are essential.

Association of preoperative coronavirus disease 2019 with mortality, respiratory morbidity and extrapulmonary complications after elective, noncardiac surgery: An observational cohort study.

STUDY OBJECTIVE: To assess the impact of preoperative infection with the contemporary strain of severe acute respiratory coronavirus 2 (SARS-CoV-2) on postoperative mortality, respiratory morbidity and extrapulmonary complications after elective, noncardiac surgery. DESIGN: An ambidirectional observational cohort study. SETTING: A tertiary and teaching hospital in Shanghai, China. PATIENTS: All adult patients (≥ 18 years of age) who underwent elective, noncardiac surgery under general anesthesia at Huashan Hospital of Fudan University from January until March 2023 were screened for eligibility. A total of 2907 patients were included. EXPOSURE: Preoperative coronavirus disease 2019 (COVID-19) positivity. MEASUREMENTS: The primary outcome was 30-day postoperative mortality. The secondary outcomes included postoperative pulmonary complications (PPCs), myocardial injury after noncardiac surgery (MINS), acute kidney injury (AKI), postoperative delirium (POD) and postoperative sleep quality. Multivariable logistic regression was used to assess the risk of postoperative mortality and morbidity imposed by preoperative COVID-19. MAIN RESULTS: The risk of 30-day postoperative mortality was not associated with preoperative COVID-19 [adjusted odds ratio (aOR), 95% confidence interval (CI): 0.40, 0.13-1.28, P = 0.123] or operation timing relative to diagnosis. Preoperative COVID-19 did not increase the risk of PPCs (aOR, 95% CI: 0.99, 0.71-1.38, P = 0.944), MINS (aOR, 95% CI: 0.54, 0.22-1.30; P = 0.168), or AKI (aOR, 95% CI: 0.34, 0.10-1.09; P = 0.070) or affect postoperative sleep quality. Patients who underwent surgery within 7 weeks after COVID-19 had increased odds of developing delirium (aOR, 95% CI: 2.26, 1.05-4.86, P = 0.036). CONCLUSIONS: Preoperative COVID-19 or timing of surgery relative to diagnosis did not confer any added risk of 30-day postoperative mortality, PPCs, MINS or AKI. However, recent COVID-19 increased the risk of POD. Perioperative brain health should be considered during preoperative risk assessment for COVID-19 survivors.

Effect of NaOH Pretreatment on Permeability and Surface Properties of Three Wood Species.

To improve the permeability of wood, three chemical reagents were used to pretreat Chinese fir, white oak, and poplar. Through a factorial experiment with the mass change rate of the wood as the indicator, NaOH was preliminarily selected as the pretreatment agent. Further orthogonal experiments were conducted to explore the effects of NaOH concentration, temperature, and treatment time on the mass change rate, dye uptake rate, transverse dye penetration rate, and color difference of the wood. A fuzzy, comprehensive analysis was used to optimize the pretreatment process. The results showed that after NaOH pretreatment, the highest mass change rates of Chinese fir, white oak, and poplar were 11.30, 10.66, and 8.53%, respectively. Compared with untreated wood, the dye uptake rate of three wood species increased by 1.05, 1.43, and 1.13 times, respectively; the radial dye penetration rate increased by 5.05, 4.14, and 3.38 times, respectively; and the tangential dye penetration rate increased by 3.91, 3.45, and 3.84 times, respectively. These findings indicate an enhancement in permeability for all three wood species following NaOH pretreatment. The brightness of the three wood species decreased after NaOH pretreatment, while the yellow and red colors increased in Chinese fir and poplar and decreased in white oak. Scanning electron microscopy showed that pits in the wood opened after pretreatment, while extractives decreased. Infrared spectroscopy analysis indicated varying degrees of extraction effects from NaOH pretreatment across the three wood species, along with increased active hydroxyl groups within the wood structure. X-ray diffraction analysis revealed that NaOH dissolved noncrystalline substances in wood, leading to improved crystallinity. These experimental findings provide essential data for future endeavors in wood pretreatment and subsequent staining processes.