搜索结果：Journal of photochemistry and photobiology. B, Biology

Photobiomodulation (PBM) involves the application of low-intensity visible or near-infrared light (600-1100 nm) to tissues. PBM demonstrates considerable potential in chronic wound healing, neurodegenerative disease intervention, and adjunctive cancer therapy. The core mechanism of PBM relies on photon absorption at specific wavelengths by mitochondrial cytochrome c oxidase. By activating the mitochondrial electron transport chain, enhancing ATP synthesis, and regulating reactive oxygen species signaling, PBM mediates multiple downstream signaling pathways, including PI3K/Akt, MAPK, and NF-κB, thereby exhibiting significant wavelength- and dose-dependent bidirectional regulatory characteristics. Currently, domestic and international research primarily focuses on single signaling pathways or therapeutic effects for specific diseases, while lacking a systematic review of their multidimensional regulatory mechanisms and multisystem biological effects. This hinders the standardization of treatment parameters and optimization of clinical protocols. Accordingly, this review systematically summarizes the molecular mechanisms and research progress of PBM across five major areas: tissue repair and regeneration, anti-inflammatory and immunomodulatory effects, regulation of glucose and lipid metabolism, tumor intervention, and neuroprotection and analgesia. We identify current research bottlenecks and recognize the uncertainty in therapeutic efficacy caused by parameter variations, along with outlining pathways for its precise and personalized clinical translation. PBM offers unique advantages, including safety, minimal tissue damage, and low cost. These features make it a promising, novel adjunctive therapeutic modality and provide a systematic theoretical basis for developing non-invasive adjunctive phototherapy regimens for various refractory diseases.

Cutaneous leishmaniasis (CL) is a neglected tropical disease with limited therapeutic options due to toxicity, resistance, and high costs. Photodynamic therapy offers a promising alternative; however, the systematic evaluation of furanocoumarin-rich plant extracts in Leishmania models remains limited. Despite the well-established photodynamic properties of individual furanocoumarins, no systematic evaluation of Trichocline plicata extracts has been performed in protozoan parasites. This study aimed to provide an integrated evaluation of the chemical composition, intrinsic photophysical properties, and biological photodynamic efficacy of furanocoumarin-rich extracts from Trichocline plicata against Leishmania amazonensis. Extracts from aerial and subterranean parts were chemically characterized by UHPLC-DAD and GC-MS, and their photodynamic potential was assessed through singlet oxygen and superoxide anion radical generation under UVA irradiation. Antiparasitic activity was tested in vitro, and morphological alterations were examined by optical and scanning electron microscopy, while cytotoxicity was evaluated in Vero cells. The dichloromethane extract from subterranean parts (DCM-SP.Ext.) showed the highest production of singlet oxygen and superoxide anion radical. Photodynamic treatment reduced parasite viability by up to 97%, comparable to amphotericin B, and microscopy revealed severe morphological damage in irradiated parasites. Mechanistic analyses using ROS quenchers and anoxic conditions demonstrated that both oxygen-dependent (Type I/II) and oxygen-independent (Type III) pathways contribute to parasite inactivation, supporting a multimodal photodynamic mechanism. DCM-SP.Ext. exhibited low toxicity in Vero cells, suggesting high selectivity toward the parasite. These findings establish T. plicata extracts, particularly DCM-SP.Ext., as efficient and selective natural photosensitizers capable of inducing multiple photodynamic mechanisms, supporting their potential as cost-effective plant-based agents for the photodynamic treatment of cutaneous leishmaniasis. This work highlights the potential of native plants as renewable sources of bioactive compounds for photodynamic applications in infectious diseases.

Ultraviolet radiation (UVR), particularly UVA and UVB, is a major environmental source of photo-oxidative stress in skin. Absorption of UV photons by endogenous chromophores triggers excessive generation of reactive oxygen species (ROS), resulting in oxidative stress (OS), lipid peroxidation, mitochondrial dysfunction, DNA damage, and inflammation. These events contribute to photoaging, pigmentary alterations, impaired wound repair, and photocarcinogenesis. Adaptive responses are orchestrated by stress-responsive transcriptional networks, notably BTB and CNC homology 1 (Bach1) and BTB and CNC homology 2 (Bach2), members of the Broad-Complex, Tramtrack, and Bric-à-brac (BTB) and Cap 'n' Collar (CNC) family. Bach proteins function as redox-sensitive repressors that compete with Nuclear factor erythroid 2-related factor 2 (Nrf2) for antioxidant response elements (AREs) binding in association with small Maf proteins. Under basal conditions, Bach1 suppresses transcription of cytoprotective genes, including heme oxygenase-1 (HO-1), thereby maintaining a restrained antioxidant activity. UV-induced oxidative or heme stress promotes Bach1 nuclear export anddegradation, enabling Nrf2-driven antioxidant gene expression. Persistent or dysregulated Bach1 activity following chronic UV exposure has been linked to enhanced ferroptotic susceptibility, iron-dependent lipid peroxidation, mitochondrial metabolic imbalance, and increased genomic instability, promoting photodamage and tumor-associated redox adaptation. In contrast, Bach2 appears to exert context-dependent effects on immune regulation, autophagy, and cellular senescence, indicating functional divergence. Emerging evidence further indicates that Bach-mediated transcription intersects with iron metabolism, mitochondrial biogenesis, inflammatory signaling, and metabolic reprogramming, positioning these factors as central modulators of UV-induced redox thresholds. The dynamic balance between Bach proteins and Nrf2 defines the magnitude and duration of antioxidant responses following acute or chronic irradiation. Targeting this regulatory axis with natural antioxidants (e.g., eriodictyol, cannabidiol, and 3-acetyl-11-keto-β-boswellic acid), small-molecule modulators, or photodynamic strategies offers potential to enhance photoprotection and mitigate UV-driven pathology. A deeper mechanistic understanding of Bach-dependent signaling in photo-oxidative stress will advance the development of precision interventions for light-induced skin disorders and photocarcinogenesis.

Bioluminescence, generated through the luciferase-catalyzed oxidation of luciferin, produces visible light and is widely used in biomedical imaging and related fields. Imidazopyridine (ImPy) constitutes the core luminescent scaffold of coelenterazine-type fluorophores, and its oxidation yields an anionic dioxetanone intermediate that typically undergoes cleavage. This process generally involves charge transfer between substituents and the formation of radical electrons, a phenomenon known as charge-transfer-induced luminescence (CTIL). The anionic dioxetanone can also be converted to its neutral form through protonation or intramolecular bonding. Although neutral dioxetanone can likewise undergo cleavage accompanied by charge transfer between substituents, the transferred charge is small. It has therefore often been overlooked, leading to the prevailing assumption that neutral-state cleavage does not belong to the CTIL category. The mechanistic distinction between these two cleavage modes remains unresolved. In this work, an ImPy model was constructed based on the structures of coelenterazine and furimazine, two representative marine luciferins. Using density functional theory (DFT), we computed the oxidation pathway leading to dioxetanone formation and examined its cleavage under various anionic and neutral states. Charge-transfer behavior and reaction barriers were evaluated, and wavefunction analyses were performed to visualize the evolution of radical-electron distribution and atomic interactions throughout the reaction. Our results show that although the amount of charge transferred between substituents in the neutral state is small, it remains essential, as these subtle charge shifts initiate dioxetanone cleavage. Neutral-state cleavage should therefore be classified as part of the CTIL mechanism, consistent with the anionic case. In both neutral and anionic states, the reaction is triggered by the transfer of negative charge to the central CCOO four-membered ring, and this transferred charge induces dissociation of the two oxygens, thereby initiating dioxetanone cleavage. In the anionic state, the pyrazinamine (PMN) moiety, which carries a substantial negative charge adjacent to CCOO, acts as the donor. The donated charge initially drives the separation of the two oxygen atoms within CCOO, subsequently propagates through the dioxetanone framework, induces cleavage of the C-C bond, and ultimately results in dioxetanone dissociation. In the neutral state, the only available donor is a single carbonyl oxygen atom, and the donated negative charge is sufficient only to separate the two oxygen atoms but insufficient to cleave the C-C bond of the CCOO ring. Additional energy is therefore required to amplify charge transfer and achieve full C-C bond rupture. By varying the initial negative charge load on the donor moiety, we further identified that a higher negative charge facilitates transfer to CCOO and thereby lowers the reaction barrier.

Light is both the primary energy source for photosynthesis and a key regulator for circadian rhythms, influencing the comprehensive quality and the production cycle of plants. Light quality is a critical parameter of light parameters, and the response patterns of photosynthesis and circadian rhythm to different light qualities remain to be explored. Here, white (broad-spectrum), red, blue and purple lights were each applied to celery for two days (light/dark: 12 h/12 h), and stomatal openness, photosynthetic parameters, photosynthetic pigments contents, and the expression levels of photoreceptor-related genes were measured. The results showed, narrow-spectrum treatments outperformed white light in both photosynthetic parameters and pigments accumulation red light most effectively promoted stomatal openness and net photosynthetic rate (Pn), reached the maximum levels after 4 h of illumination. Compared with white light, the average contents of photosynthetic pigments were improved 1.12, 1.25 and 1.37 times higher under the red, blue, and purple light, respectively. Furthermore, within the two days, narrow-spectrum treatments upregulated the maximal relative expression of most photoreceptor genes (especially AgPHYB and AgPHOT2). The expression of circadian rhythm genes previously established under white light were disrupted, leading to disordered expression, complex uncoupling or loss of rhythmicity. This research provided references for light quality response mechanism researches and facility-based light supplementation in celery cultivation.

Bacterial luciferase is a member of the large family of flavin monooxygenases, among which it performs the unique bioluminescent reaction. We studied the interaction of two bacterial luciferases (Vibrio harveyi - of "slow" type and Photobacterium leiognathi - of "fast" type) with aliphatic aldehydes using experimental kinetic techniques, molecular docking, molecular dynamics and phylogenetic analysis. The aim was to understand the structural basis for the different kinetic properties of the two types of luciferase with aldehyde substrate. We found that a distinctive feature of the active site of V. harveyi luciferase was the presence of a minor aldehyde-binding pocket. In P. leiognathi luciferase, all aldehydes bound to the hydrophobic site of the active center in approximately the same conformation, differing only in the binding affinity. In V. harveyi luciferase, aldehydes C8 and C12 did not interact with αTrp194, consistent with their slow reaction kinetics. The molecular dynamics and free energy calculations indicated that the hydrophobic interaction between the aldehyde and protein is the driving force for the complex stability. Phylogenetic analysis of bacterial luciferase sequences revealed that amino acids from the aldehyde binding site at positions 6-8, 191-195, and 228-229 are under positive evolutionary selection. These data indicate that evolutionary processes have shaped a universal platform for binding the natural aldehyde tetradecanal, enabling efficient catalysis in both "fast" and "slow" luciferases. However, when shorter aldehydes are used in bioluminescent assays, the specific features of their interactions within the active site must be taken into account, as they determine the kinetics of the enzyme.

The growing demand for alternative cancer treatments has intensified interest in photodynamic therapy (PDT), a minimally invasive approach that combines light irradiation with photosensitizing agents (PSs) to achieve localized cytotoxicity. Phenothiazine derivatives are well established as antimicrobial and anticancer PSs, positioning 1,9-dimethyl methylene blue (DMMB) as a promising candidate. However, the photodynamic performance of DMMB against oropharyngeal carcinoma, particularly as a function of photosensitizer concentration and light dose, remains poorly explored. Here, we investigate the molecular interactions and photodynamic effects of DMMB using membrane-mimetic systems based on lipid extracts from human oropharyngeal carcinoma cells (HEp-2), complemented by in vitro cellular assays. Langmuir monolayers revealed strong membrane affinity of DMMB, leading to pronounced monolayer expansion (up to ∼90% at 1.0 μmol/L) and changes in elastic properties. Upon photoactivation, DMMB induced concentration- and light dose-dependent reductions in monolayer surface area, consistent with light-triggered photodynamic effects at the membrane interface. At 0.1 μmol/L, a modest decrease of ∼3.5% was observed, whereas at 1.0 μmol/L the surface area reduction increased from 6.9% to 13.4% as the light dose rose from 1 to 18 J/cm2. FTIR spectroscopy of Langmuir-Schaefer films revealed limited spectral changes mainly associated with interfacial lipid regions, particularly carbonyl hydration and relative intensity variations, while phosphate and acyl-chain regions were largely preserved. Cellular assays were consistent with the interfacial findings. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and LDH (lactate dehydrogenase) assays demonstrated pronounced phototoxicity in HEp-2 cells with no detectable dark toxicity, yielding IC₅₀ values that decreased from 0.82 μmol/L at 1 J/cm2 to 0.35 μmol/L at 18 J/cm2. Increased LDH release and confocal fluorescence microscopy revealed plasma membrane disruption and intracellular damage consistent with light-induced membrane perturbation inferred from the monolayer studies, which may involve lipid oxidation-related processes. Overall, these results support an association between DMMB-membrane interactions and cellular phototoxicity, highlighting how photosensitizer concentration and light dose modulate DMMB photodynamic effects under the investigated experimental conditions. DMMB thus emerges as a promising candidate for further investigation in oropharyngeal carcinoma PDT models.

Phytofabrication of polymer-based nanocomposites has emerged as a promising approach for developing multifunctional biomaterials with enhanced therapeutic efficacy. In the present study, chitosan-coated magnesium oxide nanocomposites (CS-MgONCs) were successfully synthesized via a green biogenic route using Abutilon indicum leaf extract, integrating the advantages of biopolymers and metal oxides. The formation of CS-MgONCs was preliminarily confirmed by UV-Vis spectroscopy with a characteristic absorption peak at 280 nm. FTIR analysis revealed the involvement of key functional groups responsible for reduction and stabilization, while XRD patterns confirmed the crystalline nature of the nanocomposites. HR-TEM demonstrated a predominantly semi-spherical morphology with an average particle size of 58.93 nm. DLS and zeta potential analyses indicated good colloidal stability, with a surface charge of +8.76 mV, attributed to the chitosan coating. Functionally, CS-MgONCs exhibited significant dose-dependent antioxidant activity, achieving a maximum DPPH radical scavenging efficiency of 78.37 ± 1.34% at 200 μg/mL. The nanocomposites also demonstrated potent antibacterial activity against both Gram-positive and Gram-negative pathogens, with notable zones of inhibition against Staphylococcus aureus (20.71 ± 0.74 mm) and Escherichia coli (19.71 ± 0.74 mm). Furthermore, marked anti-inflammatory activity was observed through inhibition of cyclooxygenase (COX), with 77.58 ± 1.37% suppression of COX-2 activity, suggesting effective modulation of inflammatory pathways. Biocompatibility assessment in zebrafish embryo models indicated acceptable safety profiles, with a 70% survival rate at 200 μg/mL. Importantly, the nanocomposites exhibited pronounced anticancer activity against HT-29 colon cancer cells, reducing cell viability to 21.48 ± 0.98% in a concentration-dependent manner. In conclusion, the findings highlight that biogenically synthesized CS-MgONCs integrate structural stability with multifunctional biological performance, positioning them as promising candidates for future biomedical and therapeutic applications.

Laser-assisted in-office bleaching has been proposed to enhance whitening efficacy by accelerating hydrogen peroxide (H₂O₂) degradation and optimizing oxidative reactions. Nevertheless, Er:YAG laser influence on thermal behavior, peroxide kinetics, optical performance, and trans-amelodentinal diffusion remains insufficiently elucidated. Thus, this in-vitro study evaluated the combined effects of Er:YAG laser activation and different H₂O₂ gel concentrations on thermal, chemical, and optical responses during enamel bleaching. 186 bovine incisors were allocated into six groups according to H₂O₂ concentration (9%, 17.5%, and 35%) and Er:YAG irradiation (with or without activation). Phase I assessed temperature at the enamel surface and pulp chamber, and H₂O₂ degradation at distinct evaluation periods. Phase II evaluated chromatic alteration (ΔE00), whitening index (WID) in relation to established perceptibility and acceptability thresholds, and trans-amelodentinal diffusion of H₂O₂. Statistical analyses were performed using ANOVA followed by Tukey post hoc tests (α = 0.05). Higher H₂O₂ concentrations resulted in significantly greater ΔE00 and WID values; however, these effects were accompanied by increased temperature and peroxide diffusion. Notably, comparisons between the highest and lowest H₂O₂ gel concentrations, irrespective of laser irradiation, exceeded the established whitening perceptibility threshold. Er:YAG irradiation significantly accelerated H₂O₂ degradation and enhanced whitening outcomes compared with non-irradiated groups. Notably, laser activation reduced trans-amelodentinal peroxide diffusion across all evaluated H₂O₂ gel concentrations. Overall, reductions in temperature and H₂O₂ gel concentration were observed over time. Er:YAG-assisted bleaching modulates peroxide degradation kinetics, enhances whitening efficacy, and influences thermal and trans-amelodentinal peroxide diffusion.

Currently, developing effective treatments for epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) resistant non-small cell lung cancer (NSCLC) is one of the main research focuses in the field. Receptor tyrosine kinase-like orphan receptor 1 (ROR1) is a member of the receptor tyrosine kinase family, whose knockdown could effectively inhibit the growth of EGFR-TKIs resistant NSCLC. Targeted inhibitor therapy and photodynamic therapy (PDT) combination is a promising strategy for reducing drug resistance and side effects. 12d, a novel small molecule ROR1 inhibitor we synthesized previously, exhibited promising antitumor activity both in vitro and in vivo. However, its poor water solubility significantly compromised therapeutic efficacy and bioavailability. Here, to improve the solubility of 12d and to take advantage of the PDT benefits of the photosensitizer Ce6, we constructed a light-activatable liposomal co-delivery system (12d/Ce6-LP) for the treatment of EGFR-TKIs resistant NSCLC. In vitro assays demonstrated that 12d/Ce6-LP significantly enhanced cellular uptake, provoked G2/M cell cycle arrest, promoted apoptosis, and impeded the ROR1, protein kinase B (AKT), and extracellular signal-regulated kinase (ERK) signaling pathways through a synergistic treatment with targeted inhibitor therapy and PDT. Furthermore, 12d/Ce6-LP revealed potent tumor growth inhibition in EGFR-TKIs resistant NSCLC xenograft models, prolonged systemic circulation, and excellent biodistribution. In summary, 12d/Ce6-LP represented a novel nanotherapeutic strategy of the EGFR-TKIs resistant NSCLC through a synergistic mechanism of "targeted inhibitor therapy and photodynamic" offering a promising paradigm for the treatment of drug-resistant malignancies.

Periodontitis is a chronic biofilm-induced inflammatory disease that is increasingly linked to systemic conditions. Effective treatment requires removing pathogenic biofilms and modulating the host inflammatory response. Antibacterial photodynamic therapy (aPDT) shows promising potential in the field of antibacterial treatment. However, issues such as the hypoxic microenvironment within periodontal pockets and biofilm structures, as well as the poor stability of traditional photosensitizers, pose challenges to the efficacy of aPDT. Here, we developed a multifunctional nanoparticle MB-MnO₂@PLGA NPs (MMP NPs) by co-encapsulating methylene blue (MB) and PVA-pre-dispersed manganese dioxide (MnO₂) nanosheets into a PLGA nanocarrier using a double emulsion-solvent evaporation method. Characterization confirmed their core-shell morphology, good colloidal stability, and high MB loading. Upon 660 nm irradiation, the nanoparticles generated reactive oxygen species and catalyzed H₂O₂ to produce oxygen, relieving local hypoxia and enhancing the cell compatibility of free MB. The MMP NPs disrupted P. gingivalis and F. nucleatum biofilms and exhibited superior antibacterial activity compared to free MB. Additionally, the nanoplatform significantly downregulated IL-6 and TNF-α levels. Importantly, the nanoplatform promoted macrophage polarization toward an anti-inflammatory M2 phenotype, as indicated by increased Arg-1 and CD206 expression. This work supports a synergistic in vitro strategy that simultaneously targets infection, hypoxia, and inflammation. It holds positive significance for promoting the development of periodontal disease treatment.

Ultraviolet B (UVB) radiation contributes to skin aging and damage via increasing oxidative stress and mediating inflammatory process in skin. The identification of effective agents to protect UVB-mediated deterioration against skin is necessitated. This study aims to examine the protective effects and mechanisms of avenanthramide C (AVN C), a phenolic compound enriched in oat sprout extract (Avena sativa), against UVB-induced photoaging in human keratinocyte cells (HaCaT) and a 3D reconstructed human skin model (Neoderm-ED). AVN C reduced oxidative stress by promoting the nuclear translocation of nuclear factor erythroid-2-related factor 2 (Nrf2) and upregulating antioxidant enzyme expression. AVN C also suppressed the production of inflammatory mediators, including COX-2, IL-1β, and TNF-α, through the inhibition of nuclear factor-kappa B (NF-κB) and upstream MAPK signaling. Moreover, AVN C inhibited UVB-induced matrix metalloproteinase (MMP)-1 and MMP-3 expression, thus preventing extracellular matrix degradation and wrinkle formation. In Neoderm-ED, AVN C protected against UVB-induced structural damage and inflammation by suppressing prostaglandin E2 production. AVN C exerts an effective anti-photoaging potential by suppression of UVB-induced ROS generation and inflammatory progression. These findings suggest that AVN C may be a promising candidate for anti-photoaging treatment and skin protection.

Ultraviolet A (UVA) radiation induces skin photoaging. The yeast Clavispora lusitaniae P8, isolated from the Turpan Basin, was studied as a potential source of novel natural anti-photoaging agents. This study aimed to analyze the composition of its fermented filtrate (P8) and investigate its protective effects and mechanism against UVA-induced damage in human skin cells. The chemical profile of P8 was analyzed using Liquid Chromatography-Mass Spectrometry (LC-MS). Optimal UVA dose and a protective P8 concentration were determined by MTT assay. In HaCaT and HFF-1 cells, protective effects were evaluated by measuring markers including Lactate Dehydrogenase (LDH) release, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), cell migration, malondialdehyde (MDA), and antioxidant enzyme activities. P8 contained photoaging-related compounds (carboxylic acids and derivatives, organooxygen compounds, fatty acyls, and flavonoids) and significantly alleviated UVA-induced cellular damage by reducing oxidative stress markers, restoring mitochondrial function, promoting cell migration, increasing type I collagen levels, and suppressing matrix metalloproteinases expression. Transcriptomic and metabolomic analyses identified the Interleukin-17 (IL-17) signaling pathway as the key pathway. Western blotting confirmed that P8 inhibited UVA-induced activation of the IL-17 pathway, reducing expression of interleukin-17 receptor A (IL-17RA) and phosphorylated nuclear factor kappa B (p-NF-κB). Furthermore, using the IL-17 A neutralizing antibody Ixekizumab verified that the anti-photoaging effect is primarily mediated through the IL-17 A/NF-κB axis. This study is the first to link P8 with the inhibition of the IL-17/NF-κB axis, confirming its potential as a promising anti-photoaging candidate.

This prospective study investigated the effects of photobiomodulation therapy (PBMT) at 810&#xa0;nm on rescue in vitro maturation (rescue-IVM) of human immature oocytes following controlled ovarian stimulation (COS). A total of 260 immature oocytes (germinal vesicles (GV): 143; metaphase I (MI): 117) were collected from 114 women undergoing COS between December 2023 and July 2025, denuded, and randomized into control or PBMT groups; ten in vivo-matured MII oocytes served as references. PBMT was applied at 810&#xa0;nm, 1.0&#xa0;W, 60&#xa0;J/cm2 for 1&#xa0;min, and nuclear maturation and morphology were assessed up to 6&#xa0;h of IVM. ATP content, mitochondrial oxidative phosphorylation (OxPhos) activity, and lipid peroxidation (MDA) were measured using luminometric, oximetric, and spectrophotometric assays. PBMT accelerated maturation, with GV and MI oocytes progressed to the next maturation stage 112.5% and 92.3% faster, respectively, within 1&#xa0;h. ATP content increased markedly in PBMT-treated oocytes (P&#xa0;<&#xa0;0.0001), with early-resuming MI oocytes exceeding levels of in vivo MII oocytes. OxPhos activity increased by 240% (GV) and 194% (MI) immediately after irradiation without mitochondrial uncoupling, while MDA levels remained stable. Collectively, these results demonstrated that PBMT accelerated cell cycle progression to GV and MI oocytes by enhancing mitochondrial OxPhos and ATP production without inducing oxidative stress. Limitations include the need for larger cohorts, evaluation of safety through assessment of potential DNA damage, and validation in poor-prognosis or advanced maternal age patients. This pioneering proof-of-concept study highlights the potential of PBMT to temporally accelerate rescue-IVM of immature oocytes - and possibly cumulus-oocyte complexes - in poor-responder patients undergoing IVF or fertility preservation.

The tumor microenvironment (TME), characterised by immunosuppression, hypoxia, acidity, and high interstitial pressure, creates a unique microenvironment that facilitates tumorigenesis and treatment resistance. Photodynamic therapy (PDT) has emerged as a promising and effective modality for cancer treatment. Beyond the intrinsic parameters of PDT, increasing evidence indicates that the TME critically regulates therapeutic efficacy and contributes to the development of acquired resistance. Targeted modulation of the TME to enhance PDT outcomes and overcome resistance has therefore become an attractive therapeutic strategy. This review systematically summarizes the effects of key TME characteristics-including acidic conditions, immunosuppressive states, hypoxia, and elevated interstitial fluid pressure on PDT efficacy and the mechanisms underlying PDT-acquired resistance. Furthermore, current combination strategies aimed at remodeling the TME to improve PDT performance are comprehensively discussed, with particular emphasis on biomaterial-based therapeutic approaches. Finally, in view of the limitations of existing combination therapies, future research directions are highlighted, focusing on a deeper understanding of the dynamic evolution of the TME and the development of intelligent nanomaterial-based targeted delivery platforms to enable precise and personalized PDT.

This study used ultraviolet (UV)-C light-emitting diodes (LEDs) and titanium dioxide (TiO2) photocatalyst to design a high-efficiency bioaerosol disinfection reactor. It conducted experiments and simulations to investigate the effects of baffle angle (-10&#xb0;, 0&#xb0;, and 10&#xb0;) on the airflow field, irradiance distribution, and photocatalytic efficiency of the designed reactor. When baffle surfaces were not coated with photocatalyst, a baffle angle of 0&#xb0; effectively prolonged the microbial residence time, causing bacteria to receive the maximum UV fluence of 22.07&#xa0;mJ/cm2, which led to the highest log inactivation value of 1.91. However, when the baffle surfaces were coated with TiO2 photocatalyst, a baffle angle of -10&#xb0; resulted in the highest photocatalytic disinfection efficiency and log inactivation value. After the baffles were coated, the log inactivation value under a baffle angle of -10&#xb0; increased from 1.67 to 2.40, representing an increase of approximately 44%. This improvement was attributable to the baffle angle of -10&#xb0; substantially increasing the photocatalytic efficiency at the channel turns and the probability of bioaerosols coming into contact with the photocatalyst. Overall, the current findings can provide a reference for the design of bioaerosol disinfection reactors comprising UV-C LEDs and TiO2 photocatalyst.

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Ultraviolet (UV) radiation-induced DNA damage is a major driver of skin carcinogenesis and premature aging. Understanding the mechanisms of DNA damage repair is crucial for preventing these skin disorders. Proteomic profiling revealed a significant downregulation of RNA helicase DDX5 in the UVB-irradiated cells, which strongly correlated with nucleotide excision repair and mRNA metabolic processes. Although DDX5 has been implicated in cell cycle regulation and helicase-dependent facilitation of DNA repair, its specific function and underlying mechanisms in mitigating UV-triggered DNA damage remain unclear. Consistent with proteomic data, western blotting analysis confirmed that UVB radiation could cause the upregulation of DDX5 both in vitro and in vivo. To further confirm the effects of DDX5, DDX5 expression was modulated in UVB-irradiated HaCaT cells by siRNA transfection and lipofection, and in mice by AAV transduction. Functional assays demonstrated that DDX5 overexpression robustly reversed UVB-triggered apoptosis, DNA damage, &#x3b3;H2AX focus formation, and the production of cyclobutane pyrimidine dimers, whereas DDX5 knockdown exacerbated these effects. Co-immunoprecipitation revealed direct interactions between DDX5 and methyltransferase complex subunits, including RBM15 and METTL14. MeRIP-seq and MeRIP-qPCR further revealed that DDX5 overexpression elevated m6A modification on mRNAs encoding key DNA repair factors (LIG1, RFC2, and RAD51), which was accompanied by markedly increased mRNA and protein levels of these repair mediators. Consistently, inhibiting m6A methylation with cycloleucine or knocking down RBM15/METTL14 abolished the protective effects of DDX5 and reversed the DDX5-mediated upregulation of repair factor expression. Collectively, these findings illustrated that DDX5 interacts with RBM15/METTL14 to promote m6A modification of DNA repair factor mRNAs, thereby enhancing their expression and facilitating the repair of UV-induced DNA damage.