Abstract: In breast cancer radiotherapy, exposure of the heart and its substructures to radiation is one of the important risk factors for long-term cardiovascular diseases, which is particularly prominent in patients with left-sided breast cancer. The deep inspiration breath hold (DIBH) technique is an effective method to reduce cardiac radiation dose by having the patient take a deep breath and hold it, thereby moving the heart away from the target area. This article systematically reviews the principles, dosimetric advantages of the DIBH technique, and its application effects when combined with different radiotherapy techniques involving three-dimensional conformal radiation therapy (3DCRT), intensity modulated radiation therapy (IMRT), volumetric modulated arc therapy (VMAT) and proton therapy technology. Studies have shown that the DIBH technique can significantly reduce the mean heart dose (MHD) and the doses to substructures such as the left anterior descending artery (LAD) and left ventricle (LV). Among them, it is found that DIBH combined with 3DCRT or proton therapy technology has the best cardioprotective effect. While when combining IMRT and VMAT with DIBH, further consideration of target dose uniformity and cardiac dose is needed to select the optimal method. In addition, regarding the correlation between cardiac substructure doses and the risk of cardiovascular events, it is necessary to combine relevant factors such as anatomical characteristics, biomarkers, and dose parameters to construct an individualized risk prediction model. In the future, we should focus on technical optimization, patient selection, and multimodal image guidance. Through these measures, maximizing the use of the DIBH technique will enable us to minimize radiotherapy-related cardiac toxicity.
Key words: breast cancer; radiation therapy; deep inspiration breath hold; cardiac protection; dosimetry
（Acta Laser Biology Sinica, 2026, 35(1): 010-018）

Abstract: Lactate has long been regarded as a metabolic byproduct of glycolysis. Recent studies, however, have revealed its pivotal role in regulating the tumor immune microenvironment (TIME). Excess lactate accumulation disrupts metabolic balance, suppresses the activity of T cells and NK cells, and induces the polarization of immunosuppressive cells, thereby reshaping the immune landscape of TIME. Meanwhile, lactylation, as a novel post-translational protein modification, mediates the regulation of epigenetic events by metabolic signals, promoting the expression of immune-related genes, such as PD-L1, IL-10, and Arg1, and further enhancing immune evasion. This review focuses on the metabolic-epigenetic coordination of lactate and lactylation in TIME, elaborating on lactate production and shuttling, immune-cell metabolic interactions, and the clinical potential of targeting lactate homeostasis. A deeper understanding of the lactate-lactylation axis may provide novel molecular targets and research directions for future tumor immunotherapy.
Key words: lactate; lactylation; tumor metabolism; immune regulation; therapeutic resistance
（Acta Laser Biology Sinica, 2025, 34(6): 515-522）

Abstract: Radiation therapy is an important treatment for malignant tumors. Although it can effectively kill tumor cells, it also causes ionizing radiation (IR) damage to normal tissues, resulting in a variety of acute and chronic adverse reactions. Currently, there are significant limitations in the efficacy, targeting, and safety of clinically available radioprotective drugs, and there is an urgent need for the development of new, more efficient and safer protection strategies. Extracellular vesicles (EVs), as natural nanocarriers, are capable of delivering functional molecules and participating in various processes, such as DNA repair, alleviation of oxidative stress, modulation of apoptosis, and immune microenvironment, which have demonstrated a wide range of potentials for the alleviation of IR-associated tissue damage. Numerous studies have shown that mesenchymal stem cell-derived EVs (MSC-EVs), immune cell-derived EVs, and engineered EVs are effective in attenuating IR-induced tissue damage in various animal models. In this paper, we systematically reviewed the multiple mechanisms of EVs-mediated radioprotection, sorted out their main sources and biological properties, and focused on the optimization strategy of their engineering and the challenges of their clinical applications, with the aim of providing a theoretical basis and research references for the development and translation of EVs as a novel means of radioprotection.
Key words: extracellular vesicles; radioprotection; MSC-EVs; DNA repair; oxidative stress
（Acta Laser Biology Sinica, 2026, 35(1): 001-009）

Abstract: Optical coherence tomography (OCT) is a non-invasive imaging technique that uses visible and near-infrared light to provide detailed cross-sectional images of human tissue, widely used for the examination of fundus diseases. Currently, OCT is mainly divided into two types: time-domain and Fourier-domain, with the Fourier-domain further divided into spectral-domain and swept-source types. These types of OCT each have their own characteristics in terms of image acquisition methods, scanning speed, axial and lateral resolution, and imaging range. Swept-source OCT (SS-OCT) often uses scanning light sources with wavelengths of 1 050 nm or 1 300 nm, which have strong tissue penetration capabilities. Combined with faster scanning speeds and a wider scanning range, it can clearly display the deep structures of the retina and choroid, demonstrating unique advantages in the quantitative assessment of the fundus. Based on recent research advances, this paper will review the application of SS-OCT in ocular diseases, aiming to provide a reference for early diagnosis, elucidation of pathological mechanisms, and evaluation of therapeutic effects in ophthalmology.
Key words: swept-source optical coherence tomography; fundus diseases; choroidal vessel volume index; non-invasive imaging technology; fundus disease examination
（Acta Laser Biology Sinica, 2025, 34(6): 481-488）

Abstract: Nasopharyngeal carcinoma (NPC) is a highly prevalent malignant tumor in Southeast Asia and Southern China, with a strong association with Epstein-Barr virus (EBV) infection. Although early-stage NPC exhibits favorable local control with chemoradiotherapy, recurrence, metastasis, and drug resistance remain major clinical challenges. Immune cells play a critical role in tumor progression, among which macrophages — originating from bone marrow hematopoietic stem cells (differentiated via monocytes) — serve as core components of innate immunity, widely distributed in tissues to regulate inflammation and tissue repair. Tumor-associated macrophages (TAMs), a central constituent of the tumor microenvironment, are recruited and differentiated from monocytes by tumor-secreted cytokines, displaying high plasticity with two primary subtypes: pro-tumor M2 and anti-tumor M1. M2-type TAMs drive tumor progression by promoting proliferation, invasion, angiogenesis, and immunosuppression, e. g. , overexpressing programmed death-ligand 1 (PD-L1) and secreting interleukin-10 (IL-10). In contrast, M1-type TAMs exert direct anti-tumor effects through antibody-dependent cellular cytotoxicity (ADCC), reactive oxygen species/nitric oxide (ROS/NO)-induced apoptosis, and activation of adaptive immunity via enhanced antigen presentation and CD8+ T-cell infiltration. Clinical studies indicate that high infiltration of M2-type TAMs correlates with reduced patient survival, chemoradiotherapy resistance, and diminished immunotherapy response, highlighting their potential as prognostic biomarkers and therapeutic targets. Current therapeutic strategies targeting TAMs include: inhibiting M2 recruitment by blocking the CCL2-CCR2/CSF-1R signaling axis; enhancing M1 function via epigenetic regulation or CD40 bispecific antibodies; depleting pro-tumor TAMs using clodronate liposomes or photothermal/photodynamic therapy; and combining with chemoradiotherapy or immunotherapy. This article systematically reviews the origin, classification, functions, and clinical relevance of TAMs in NPC, summarizes advancements in targeted therapeutic strategies, and provides theoretical and practical insights for individualized NPC treatment.
Key words: nasopharyngeal carcinoma; tumor-associated macrophages; tumor microenvironment; macrophage polarization; targeted therapy
（Acta Laser Biology Sinica, 2025, 34(6): 504-514）

Abstract: To identify the pathogen and its taxonomic status causing a new leaf spot disease in the Yongzhou tobacco-growing area of Hunan Province, and to screen effective control agents through laboratory toxicity assays, in this study, tobacco leaves were collected from the tobacco-growing regions of Yongzhou. The pathogen was isolated via tissue culture, single-spore isolation, and purification. Pathogenicity was confirmed through in vitro inoculation. The pathogen was identified by PCR amplification and sequencing of the ITS region, followed by phylogenetic analysis, combined with morphological characterization of colonies and spores. The indoor toxicity of nine fungicides, including 43% Fluopyram·Trifloxystrobin (SC), against the pathogen was determined using the mycelial growth rate method. Laboratory toxicity tests indicated that 43% Fluopyram‌·Trifloxystrobin (SC), 70% Thiophanate-methyl (WP), and 42.4% Pyraclostrobin·Fluopyram (SC) exhibited the strongest inhibitory effects against Corynespora. cassiicola, with EC50 values of 3.028 5 mg/L, 5.148 0 mg/L, and 8.787 9 mg/L, respectively. Moderately effective fungicides included 70% Mancozeb (WP), 75% Trifloxystrobin·Tebuconazole (WG), 32.5% Benzovindiflupyr·Azoxystrobin (SC), and 38% Pyraclostrobin·Boscalid (WG), with EC50 values of 21.844 3 mg/L, 31.841 8 mg/L, 32.080 1 mg/L, and 41.867 6 mg/L, respectively. The least effective agents were 40% Mefentrifluconazole·Pyraclostrobin (SC) and 75% Chlorothalonil (WP), with EC50 values of 192.466 9 mg/L and 1 341.062 0 mg/L, respectively. This study revealed that the new leaf spot disease on tobacco in Yongzhou was caused by C. cassiicola. C. cassiicola was identified as the causal agent of Corynespora leaf spot disease in tobacco. Strobilurin and benzimidazole fungicides showed superior inhibitory efficacy. The findings provide a scientific basis for the effective local control of tobacco Corynespora leaf spot disease.
Key words: tobacco; Corynespora leaf spot disease; Corynespora cassiicola; indoor virulence assay; fungicide
（Acta Laser Biology Sinica, 2026, 35(1): 053-061）

Abstract: Hearing loss is a widespread global health issue that affects all regions and countries. It is classified into conductive hearing loss, sensorineural hearing loss, and mixed hearing loss. Oxidative stress and redox homeostasis imbalance are important factors causing cochlear damage, and NRF2 is a crucial antioxidant regulatory factor. In the human body, the Nfe2l2 gene is widely expressed in the central nervous system, auditory organs, and metabolism-related organs and tissues, playing a significant role in maintaining cellular redox homeostasis, responding to oxidative stress, and regulating metabolism, inflammation, autophagy, and immune responses. In noise exposure experiments, Nrf2-KO mice showed more severe hearing impairment compared to wild-type mice. In zebrafish, nrf2a is widely expressed in the early stages of embryonic development and acts as a core transcription factor to regulate the expression of a series of antioxidant genes, constituting an important defense mechanism against exogenous oxidative damage from chemicals and heavy metals. Besides its antioxidant function, this gene is crucial for the development and homeostasis maintenance of various organs in zebrafish, such as the liver and nervous system, and plays an important protective role in regulating inflammatory responses, metabolic processes, and inhibiting apoptosis. To study the specific mechanism of this gene in the development of inner ear and lateral line hair cells, a zebrafish nrf2a gene knockout line was constructed using CRISPR/Cas9 gene editing technology. First, online analysis tools were used to screen the knockout target sites of the nrf2a gene, and the guide DNA of this gene was amplified and synthesized by polymerase chain reaction. This was then used as a template for transcription, and the transcribed sgRNA was mixed with Cas9 protein at a ratio of 5: 1 and injected into 1-cell stage zebrafish embryos. Subsequently, the effectiveness of the gene knockout was verified. The results showed that there was a large fragment deletion in the nrf2a gene, and translation was prematurely terminated, indicating successful knockout of the gene. After screening, a homozygous mutant of the nrf2a gene was obtained, laying the foundation for studying the role of this gene in the development of inner ear and lateral line hair cells.
Key words: zebrafish; CRISPR/Cas9; nrf2a gene; hearing loss; inner ear development
（Acta Laser Biology Sinica, 2026, 35(1): 072-080）

Abstract: Sowing date is a critical factor affecting the growth and yield of millet, and its optimal management is essential for maximizing productivity. In this study, the effects of sowing date on the growth and yield of foxtail millet were investigated through field experiments combined with APSIM-Millet model simulations. Using historical meteorological data (1984—2023), we further explored strategies for optimizing sowing date management. The APSIM-Millet model accurately simulated the growth process of foxtail millet across different sowing dates and varieties. Historical simulation revealed that the optimal sowing date for millet in Shanxi Province was gradually delayed from north to south, with additional variations due to irrigation conditions. For the late-maturing variety Jingu 21, the best rain-fed sowing window ranged from March 30 to April 19 in northern Datong City, shifting southward to May 21 to June 10 in the southernmost Yuncheng City. Under irrigation conditions, the optimal sowing date was 20～30 days later than under rain-fed conditions. In contrast, the early-maturing millet variety Tonggu 30 exhibited a later optimum sowing date than Jingu 21, with a 70-day north-south span. Irrigation further aggravated regional differences. These findings highlight the close relationship between sowing date responsiveness and regional water/heat resource distribution. In cold northern regions, early sowing helps avoid later-season drought, while the warm and humid southern areas benefit from delaying sowing to optimize light and temperature utilization. Integrating field experiment results, the rain-fed early sowing mode was preferred in arid northern Shanxi, and gradient sowing being adjusted to irrigation availability in the warmer southern Shanxi, and climate-resource efficiency was realized through varietal adaptations, e.g. , limited southward extension the late maturing variety Jingu 21 and enhanced north-south sowing differentiation for the early maturing variety Tonggu 30. This study provides a theoretical foundation for optimizing regional sowing dates in Shanxi’s millet production systems.
Key words: millet; variety; sowing date; APSIM-Millet model; yield
（Acta Laser Biology Sinica, 2026, 35(1): 062-071）

Abstract: To investigate the early radiochemical processes of γ-ray-induced DNA single-strand breaks (SSB), this study employed the Monte Carlo simulation tool TOPAS and its extended module TOPAS-nBio to construct a water sphere-plasmid microscale simulation model. The model was used to simulate the irradiation of supercoiled pUC19 plasmids by 60Coγ-rays in an aqueous environment and the subsequent induction of SSB in plasmid DNA. The study quantitatively compared the SSB yield under systematically varied conditions of radiation dose, DNA concentration, and hydroxyl radical (·OH) scavenger concentration. The simulation results showed that the SSB yield increased with the elevation of radiation dose. A higher DNA concentration in the environment led to an approximately linear increase in the absolute SSB yield, while the damage efficiency per unit mass of DNA decreased with increasing concentration. An increase in the concentration of ·OH scavengers significantly reduced the SSB yield, indicating that the ·OH scavenging capacity exerts a marked inhibitory effect on SSB formation. The findings of this study provide certain theoretical support for the optimization of radiotherapy, the formulation of radiation protection strategies, and the health risk assessment of nuclear environments.
Key words: gamma ray; plasmid DNA; free radical; Monte Carlo simulation; DNA single strand break
（Acta Laser Biology Sinica, 2026, 35(1): 028-034）

Abstract: Although diet and gut microbial composition have been linked to chronic respiratory diseases, these associations remain difficult to interpret because of confounding and reverse causation. The gut-lung axis provides a plausible framework for this interaction, yet direct genetic evidence is limited. Using a two-step, two-sample Mendelian randomization (MR) framework, supplemented by multivariable MR (MVMR) to adjust for pleiotropic effects and Benjamini-Hochberg false discovery rate (FDR) correction for multiple testing, we assessed the causal contributions of dietary habits and gut microbial taxa to major chronic respiratory diseases. We identified 22 dietary factors with causal effects on disease risk and 225 microbial taxa that acted as independent risk or protective contributors. Mediation analyses further showed that the effects of 12 dietary habits were transmitted through 32 specific microbial taxa. Notably, genetically predicted pork intake increased the risk of chronic obstructive pulmonary disease (COPD) (OR=10.53, 95% CI [8.54, 13.00]), an effect partly mediated by elevated abundance of CAG-485 sp002404675. In contrast, bread consumption conferred protection against asthma (OR=0.68, 95% CI [0.64, 0.72]), whereas this benefit was offset by approximately 45% through a pathway involving reduced Veillonella abundance. Collectively, these findings provide genetic support for the gut-lung axis and demonstrate that the gut microbiome functions as a causal mediator linking diet to chronic respiratory disease risk. However, since this study was based on individuals of European ancestry, caution is warranted when generalizing these causal estimates to non-European populations, such as East Asian groups. This work suggests new opportunities for microbiota-targeted prevention and therapeutic strategies.
Key words: Mendelian randomization; gut microbiome; respiratory disease; dietary; European descent populations
CLC number: R56                 Document code: A        DOI: 10.3969/j. issn.1007-7146.2026.01.005

Abstract: Acupoint application combined with Modified Bazhen Decoction mediated the effect of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway on bone marrow hematopoietic function in mice with bone marrow inhibition. The BALB/c mice were randomly divided into control group, model group, acupoint application group, Modified Bazhen Decoction group, and combined drug group, with 10 mice in each group. Tail vein blood was collected to measure the levels of hemoglobin, white blood cells, and platelets in peripheral blood. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of serum erythropoietin (EPO), thrombopoietin (TPO) and granulo-monocyte colony-stimulating factor (GM-CSF). Bone marrow nucleated cell counts were performed in each group of rats. For the myeloid nucleated cells of each group, colony forming unit-granulocyte and macrophage (CFU-GM), colony forming unit-erythrocyte (CFU-E) and colony forming unit-megakaryocyte, erythrocyte and granulocyte (CFU-Meg) were detected. The kit was used to detect the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in serum. The expression of p-JAK1, JAK1, p-JAK2, JAK2, p-STAT3, STAT3 proteins in mouse nucleated bone marrow cells were detected by Western blot. The results showed that compared with the control group, the number of hemoglobin, leukocytes, platelets, EPO, TPO, GM-CSF, SOD, bone marrow nucleated cells and the number of cell colonies of hematopoietic progenitor cells CFU-GM, CFU-E and CFU-Meg in the model group decreased (P<0.05), and the MDA, p-JAK1/JAK1, p-JAK2/JAK2, p-STAT3/STAT3 increased (P<0.05). Compared with the model group, the number of hemoglobin, leukocytes, platelets, EPO, TPO, GM-CSF, SOD, bone marrow nucleated cells and the number of cell colonies of hematopoietic progenitor cells CFU-GM, CFU-E and CFU-Meg increased in the acupuncture point application group, Modified Bazhen Decoction group and combined drug group (P<0.05), and the MDA, p-JAK1/JAK1, p-JAK2/JAK2, p-STAT3/STAT3 decreased (P<0.05). Acupoint application and Modified Bazhen Decoction could synergize (P<0.05). It indicated that acupoint application combined with Modified Bazhen Decoction synergistically improves the bone marrow hematopoietic function of mice with bone marrow suppression by reducing oxidative stress, and its mechanism may be related to the inhibition of JAK/STAT signaling pathway.
Key words: acupoint application; Modified Bazhen Decoction; bone marrow inhibition; Janus kinase/signal transducer and activator of transcription signaling pathway; oxidative stress
（Acta Laser Biology Sinica, 2026, 35(1): 088-096）

Abstract: Skin aging is characterized by dermal atrophy, degeneration of elastic fibers, collagen depletion, and attenuated epidermal turnover. Photobiomodulation therapy (PBMT), particularly red light irradiation, has demonstrated promising anti-aging potential; however, its underlying molecular mechanisms remain incompletely elucidated. In this study, we established a natural aging mouse model (18～20 months) to investigate the rejuvenating effects and mechanisms of red light treatment with parameter of 630～635 nm, fluence 8 J/cm2, power density 6.67 mW/cm2, 20 min per session for 28 consecutive days. Our results demonstrated that red light significantly increased dermal thickness and enhanced type I collagen deposition in aged mice. Mechanistic investigations revealed that red light promoted collagen synthesis in fibroblasts via activation of the AKT signaling pathway; concurrently, AKT activation stimulated keratinocyte proliferation with elevated Ki67 expression, and differentiation with increased cytokeratin 10 expression, effects that were abrogated by the AKT inhibitor API-2. These findings collectively indicate that red light mediates coordinated dermal-epidermal remodeling through AKT signaling, providing a theoretical foundation for the application of photobiomodulation therapy in the prevention and treatment of skin aging.
Key words: photobiomodulation; red light; skin aging; AKT signaling pathway; collagen; keratinocyte
（Acta Laser Biology Sinica, 2026, 35(2): 179-184）

Abstract: To investigate the effects of propofol (Pro) on hypoxia/reoxygenation (H/R) injury in H9C2 cardiomyocytes via regulation of the silent information regulator 1(SIRT1)/p53 signaling pathway-mediated ferroptosis, an in vitro H9C2 cell H/R model was established. Cells were divided into the following groups: Control group, H/R group, H/R+Pro group, H/R+Pro+erastin group, H/R+Pro+si-NC group, and H/R+Pro+si-SIRT1 group. The cytotoxic effect of Pro on H9C2 cells was assessed using the cell counting kit-8 (CCK-8) assay. Intracellular reactive oxygen species (ROS) levels were measured using the 2', 7'-dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe. Mitochondrial ultrastructure was examined by transmission electron microscopy (TEM). Oxidative stress markers were quantified using corresponding assay kits. Expression levels of ferroptosis-related proteins were detected by Western blot. Results demonstrated that compared to the Control group, the H/R group exhibited significantly reduced cell viability, elevated levels of ROS and malondialdehyde (MDA), decreased levels of catalase (CAT) and superoxide dismutase (SOD), nuclear membrane rupture, increased mitochondrial membrane density, loss of mitochondrial cristae, swelling and rupture of mitochondria, increased Fe2+ content and lactate dehydrogenase (LDH) activity, elevated levels of acyl-CoA synthetase long-chain family member 4 (ACSL4) and p53, and reduced levels of glutathione peroxidase 4 (GPX4) and SIRT1 (P<0.05). Pro treatment significantly ameliorated H/R injury, increasing cell viability and elevating SOD, CAT, GPX4, and SIRT1 levels, while reducing Fe2+ content, ROS, MDA, ACSL4, and p53 levels, and restoring mitochondrial structure (P<0.05). Erastin partially reversed the protective effects of Pro (P<0.05). Conversely, si-SIRT1 completely abolished the effects of Pro, resulting in decreased GPX4 levels and increased Fe2+ content and ACSL4 levels (P<0.05). This study revealed that Propofol likely protects cardiomyocytes against H/R injury by activating the SIRT1/p53 pathway to inhibit ferroptosis. This finding provides crucial mechanistic insight into Propofol-mediated cardioprotection and suggests a potential novel strategy for the prevention and treatment of myocardial ischemia-reperfusion injury.
Key words: propofol; silent information regulator 1/p53 signaling pathway; ferroptosis; cardiomyocytes; hypoxia/reoxygenation injury
（Acta Laser Biology Sinica, 2025, 34(6): 561-568）

Abstract: Telomeres are specialized structures at the ends of chromosomes, composed of repetitive DNA sequences and associated proteins. Their primary role is to maintain chromosomal stability and integrity by preventing progressive loss of chromosome ends and unwanted chromosomal rearrangements. Changes in telomere length are closely linked to a variety of diseases, including cancer, aging, and cardiovascular disorders. Therefore, measuring telomere length holds significant biological importance. Driven by technological advances, a diverse array of methods for telomere-length assessment has emerged, forming a rich technical landscape. Each method carries distinct advantages and limitations, making it suitable for particular research goals and application contexts. This review summarizes current findings on all major telomere-measurement techniques and offers recommendations for future technological development, emphasizing the potential of integrating innovative approaches to enhance disease diagnosis and treatment strategies, providing researchers and clinicians with a guide for selecting optimal methods and facilitating the translation of telomere biology into precise diagnostics and personalized therapies.
Key words: telomere length; detection methods; cellular senescence; biomarker; accurate diagnosis
（Acta Laser Biology Sinica, 2025, 34(6): 496-503）

Abstract: As a complex neurodegenerative disorder, Alzheimer’s disease (AD) urgently requires multi-targeted and personalized treatment strategies. Transcranial photobiomodulation (tPBM), a non-invasive neuromodulation technique, utilizes near-infrared light to penetrate the cranium and to target multiple pathological processes, such as mitochondrial dysfunction, neurovascular unit impairment, and glymphatic system dysregulation. Possessing dual properties of metabolic regulation and neuromodulation, tPBM demonstrates significant potential for multi-target intervention, aligning with mainstream drug development strategies, e.g., amyloid β-protein (Aβ) clearance and inflammation modulation. This review provides an analysis of 42 included clinical studies, specifically focusing on sample characteristics, intervention parameters and clinical outcomes, and comprehensively synthesizes mechanistic evidence, clinical advancements, and dosing dosimetric methods of tPBM in AD intervention, emphasizing its applicability in home-based and wearable device trends, while proposing a translational framework that links transcranial optical dosimetry with biological effects. Future advancements may enable tPBM to evolve from population-wide effectiveness to individualized therapy through constructing personalized photon dose-response models integrated with real-time physiological feedback and brain-imaging navigation, thereby positioning tPBM as a pivotal non-pharmacological intervention for AD synergistic treatment and long-term management.
Key words: Alzheimer’s disease; transcranial photobiomodulation; dosimetry; multitarget therapy; neuromodulation
（Acta Laser Biology Sinica, 2026, 35(2): 149-161）

Abstract: To investigate the therapeutic efficacy and underlying mechanisms of cylindrin combined with metronidazole for traumatic oral ulcers, we randomly assigned 36 SD rats to different groups. After successful modeling, the rats received respective drug treatments for 7 days. General conditions of each group were observed and recorded. Pathological changes in oral mucosa were examined via hematoxylin-eosin staining, while plasma levels of IL-1 and IL-6 were detected using ELISA. The results showed that the rats in each group exhibited symptoms after successful modeling, such as hunching and curling, reduced behaviors and lethargy, as well as decreased appetite. After drug intervention, these symptoms improved, for one example, the weight of the high-dose group of combined medication is the closest to the blank control group. It was observed that the oral ulcer wounds in the high-dose group of combined medication showed the best effect by treatment. The result of hematoxylin-eosin staining revealed pathological changes in the epithelial structure of the modeling group, while the high-dose group of combined medication showed the best recovery after treatment. Compared to the cylindrin group and the metronidazole group, the results of ELISA indicated that the expression levels of IL-1 and IL-6 were significantly reduced in both the high and low-dose groups of combined medication (P<0.001). This study demonstrated that the mixed solution of cylindrin and metronidazole suppresses the expression of inflammatory factors IL-1 and IL-6, which contributes a more excellent therapeutic influence than single-agent on traumatic oral ulcers. It is expected to provide a better strategy for the clinical treatment of oral ulcers.
Key words: traumatic oral ulcer; cylindrin; metronidazole solution; combination therapy; inflammatory factor
（Acta Laser Biology Sinica, 2025, 34(6): 551-560）

Abstract: Photobiomodulation therapy (PBMT) has emerged as a promising non-pharmacological physical intervention for myopia control. However, the optimal irradiation parameters and the underlying mechanisms remain to be further clarified. In this study, a form-deprivation myopia (FDM) mouse model was established, and 650 nm PBMT protocols with different power densities were applied to systematically evaluate the inhibitory effect of PBMT on myopia-associated axial elongation. Changes in dopamine (DA) and nitric oxide (NO) levels in the retinal were quantified, and the efficacy and safety of long-term PBMT were further assessed. In addition, ex vivo cell experiments were performed to investigate downstream molecular responses to DA. The results showed that PBMT significantly suppressed abnormal axial elongation in FDM mice (P<0.05), with the most prominent effect observed at a power density of 0.25 mW/cm2. PBMT also markedly increased DA and NO secretion in the retinal (P<0.05) in a dose-dependent manner. Long-term PBMT stably inhibited axial elongation during myopia development without significantly affecting axial length in normal mice, suggesting a favorable safety profile. Furthermore, DA upregulated cellular FBJ osteosarcoma oncogene (c-Fos) expression and promoted tissue inhibitor of metalloproteinases (TIMP2) gene expression in retinal pigment epithelial cells, and these effects were attenuated by D1R inhibition, indicating that the DA-D1R-mediated c-Fos/TIMP2 pathway may contribute to PBMT-induced suppression of axial elongation. Collectively, these findings demonstrate that PBMT effectively alleviates myopia progression in FDM mice, potentially by activating retinal DA/NO signaling and modulating molecular networks associated with tissue remodeling, thereby providing experimental evidence for parameter optimization and mechanistic exploration of red-light-based myopia interventions.
Key words: photobiomodulation therapy; dopamine; myopia; sclera; retinal pigment epithelium
（Acta Laser Biology Sinica, 2026, 35(2): 185-192）

Abstract: To investigate the expression of circular RNA (circRNA) circKRT75 in tongue squamous cell carcinoma (TSCC) tissues and the effects of silencing its expression on the proliferation and invasion of TSCC cells. The cBioPortal database was used to analyze the expression of circKRT75 in TSCC tissues and the correlation between circKRT75 expression and survival in TSCC patients. Quantitative real-time polymerase chain reaction (qPCR) was used to detect circKRT75 expression in TSCC cell lines H357, Tca8113, TSCCA, HN13, and SCC-9. si-circKRT75 and control plasmids were transfected into H357 cells using lipofectamine, defining them as the si-circKRT75 and si-NC groups, respectively. The effects of low-expression circKRT75 on the proliferation and invasion of H357 cells were assessed by MTT and Transwell assays, respectively. Western blot analysis was used to examine the effects of low-expression circKRT75 on the expression of Cyclin E and Cyclin-dependent kinase 2 (CDK2), matrix metalloproteinase-2 (MMP-2) and Alpha-smooth muscle actin (α-SMA) in H357 cells. Dual-luciferase reporter assays were used to validate the targeting relationship between circKRT75 and miR-128-3p. The cBioPortal database was used to analyze the correlation between the expression of circKRT75 and miR-128-3p in TSCC tissues. qPCR was used to detect the effect of low-expression circKRT75 on miR-128-3p expression. circKRT75 expression was higher in TSCC tissues than in normal oral mucosa tissues (P<0.01). circKRT75 expression was negatively correlated with TSCC patient survival (P<0.01). Compared with normal human oral keratinocytes (HOK) cells, circKRT75 expression was higher in TSCC cell lines H357, Tca8113, TSCCA, HN13, and SCC-9 (all P<0.05). Compared with the si-NC group, low circKRT75 expression inhibited the proliferation (P<0.05) and invasion (P<0.01) of H357 cells. Low circKRT75 expression downregulated the expression of Cyclin E, CDK2, MMP-2, and α-SMA proteins in H357 cells (all P<0.01). circKRT75 had a targeting relationship with miR-128-3p (P<0.01). The expression of circKRT75 in TSCC tissues was negatively correlated with the expression of miR-128-3p (P<0.01). Compared with the si-NC group, low expression of circKRT75 upregulated miR-128-3p expression (P<0.01). circKRT75 is highly expressed in TSCC tissues and cell lines, and low expression of circKRT75 inhibits the proliferation and invasion of TSCC cells by regulating miR-128-3p expression. circKRT75 may become a molecular therapeutic target for TSCC.
Key words: circular RNA; tongue squamous cell carcinoma; microRNA; cell proliferation; cell migration
（Acta Laser Biology Sinica, 2026, 35(1): 081-087）

Abstract: The GCN2-eIF2α pathway regulates cell growth and serves as a key component of the integrated stress response (ISR). In malignant tumors, cancer cells reside in a microenvironment characterized by chronic hypoxia and nutrient deprivation. Under such conditions, the level of amino acid catabolism increases, which activates the GCN2-eIF2α pathway and inhibits protein synthesis to maintain the cellular homeostasis of cancer cells. In this study, a total of 9 pairs of tissue samples, including cancerous tissues and their matched adjacent normal tissues, were collected from patients diagnosed with non-small cell lung cancer (NSCLC). A combined analysis using histology, transcriptomics, qRT-PCR, and Western blotting was performed to investigate the molecular mechanism by which the GCN2-eIF2α pathway regulates cancer cell proliferation. Results of paraffin sections showed that in the tumor tissues of lung cancer patients, alveolar cells were densely packed, alveolar septa were narrow, and nuclear staining was heterogeneous, exhibiting typical malignant histopathological features. Transcriptomic studies revealed that the enriched pathways and differentially expressed genes among samples were identified based on gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment results from the transcriptome, which confirmed that the GCN2-eIF2α pathway plays an important role in lung carcinogenesis. Further screening was performed to select key genes for validation at the molecular and protein levels. qRT-PCR results demonstrated that these genes were expressed in both cancerous and normal tissue cells, with their expression levels mostly upregulated in cancerous tissue cells (P<0.05), which was consistent with the gene abundance analysis results in the transcriptome. At the protein level, the expression levels of general control nonderepressible 2 kinase (GCN2) and eukaryotic translation initiation 2α (eIF2α) in cancerous tissues were significantly higher than those in adjacent normal tissues, indicating that the GCN2-eIF2α pathway is implicated in lung carcinogenesis. This study can provide a reference for eIF2α and GCN2 to serve as new therapeutic targets for tumors, and also propose the possibility of inhibiting cancer cell progression by suppressing GCN2-mediated phosphorylation of eIF2α, thereby offering a solution to address the limitations of current anti-tumor therapies.
Key words: lung cancer; GCN2-eIF2α pathway; transcriptomics; cancer pathogenesis; targeted tumor therapy
（Acta Laser Biology Sinica, 2025, 34(6): 530-540）