Pub Date : 2025-12-29DOI: 10.1016/j.jphotobiol.2025.113351
Luis Henrique Oliveira de Moraes , Camila Pereira Sabadini , Nayara Formenton da Silva , Thiago Augusto do Nascimento , Tereza Cristina Buzinari , Natália Fernanda do Couto , Shane A. Phillips , Gerson Jhonatan Rodrigues
Photobiomodulation (PBM) is a promising non-pharmacological approach to improve vascular function via nitric oxide (NO)-mediated pathways. However, its effectiveness can be limited under conditions of endothelial dysfunction. This study investigated whether Panax ginseng and Angelica keiskei, two medicinal plants known for their antioxidant and vasorelaxant properties, can enhance PBM-induced vasodilation through mechanisms involving endothelial nitric oxide synthase (eNOS). Aortic rings from Wistar rats were treated with increasing doses of a standardized plant extract combination and exposed to 660 nm laser irradiation. Optimal doses (50–200 mg/kg) significantly potentiated PBM-induced vasodilation, an effect abolished by pharmacological inhibition of NO signaling and endothelium removal. In a chronic eNOS inhibition model (L-NAME), the plant combination did not restore PBM effects but partially recovered acetylcholine-induced vasorelaxation, suggesting endothelial compensation. In mesenteric arteries, the herbal treatment improved acetylcholine sensitivity but did not alter flow-induced or laser-induced vasodilation, especially under hypertensive conditions. These findings highlight a synergistic interaction between phytotherapy and PBM, mediated primarily by eNOS activation and redox modulation, with potential translational relevance for vascular disorders.
{"title":"Enhancement of laser-induced vasodilation by medicinal plants: The eNOS-dependent and antioxidant actions of Panax ginseng and Angelica keiskei","authors":"Luis Henrique Oliveira de Moraes , Camila Pereira Sabadini , Nayara Formenton da Silva , Thiago Augusto do Nascimento , Tereza Cristina Buzinari , Natália Fernanda do Couto , Shane A. Phillips , Gerson Jhonatan Rodrigues","doi":"10.1016/j.jphotobiol.2025.113351","DOIUrl":"10.1016/j.jphotobiol.2025.113351","url":null,"abstract":"<div><div>Photobiomodulation (PBM) is a promising non-pharmacological approach to improve vascular function via nitric oxide (NO)-mediated pathways. However, its effectiveness can be limited under conditions of endothelial dysfunction. This study investigated whether <em>Panax ginseng</em> and <em>Angelica keiskei</em>, two medicinal plants known for their antioxidant and vasorelaxant properties, can enhance PBM-induced vasodilation through mechanisms involving endothelial nitric oxide synthase (eNOS). Aortic rings from Wistar rats were treated with increasing doses of a standardized plant extract combination and exposed to 660 nm laser irradiation. Optimal doses (50–200 mg/kg) significantly potentiated PBM-induced vasodilation, an effect abolished by pharmacological inhibition of NO signaling and endothelium removal. In a chronic eNOS inhibition model (L-NAME), the plant combination did not restore PBM effects but partially recovered acetylcholine-induced vasorelaxation, suggesting endothelial compensation. In mesenteric arteries, the herbal treatment improved acetylcholine sensitivity but did not alter flow-induced or laser-induced vasodilation, especially under hypertensive conditions. These findings highlight a synergistic interaction between phytotherapy and PBM, mediated primarily by eNOS activation and redox modulation, with potential translational relevance for vascular disorders.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"275 ","pages":"Article 113351"},"PeriodicalIF":3.7,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145979923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1016/j.jphotobiol.2025.113349
Paulo E. da Costa , Maurício S. Baptista
Depending on geographic location and seasonality, human epidermal tissue is exposed to varying levels of solar radiation. Following light absorption by endogenous photosensitizers, solar photons generate reactive oxidants, inducing oxidative stress that is counteracted by nitric oxide, which inhibits lipid peroxidation and activates antioxidant signaling pathways. Nitric oxide is also quickly transformed in several more stable compounds, which can release nitric oxide at specific conditions, here called nitric oxide reserves. During sun exposure, photolysis of nitric oxide reserves releases bioactive nitric oxide, while inducible nitric oxide synthase is expressed later, synthesizing nitric oxide and replenishing nitric oxide stores. This dynamic process establishes a photoinduced steady state of nitric oxide release and storage. The balance between nitric oxide and reactive oxidants levels is regulated by solar radiation and fluctuates with seasonal and latitudinal variations. Sunlight exposure promotes bioactive nitric oxide production, helping to sustain a healthy nitric oxide/reactive oxidants equilibrium. However, this mechanism is disrupted in chronic inflammatory skin conditions. In this context, elevated expression of inducible nitric oxide synthase is commonly observed in patients with psoriasis, atopic dermatitis and vitiligo. These patients display nitric oxide dysregulation alongside impaired redox regulators, including Nrf2 and NADPH oxidase. Inducible nitric oxide synthase dysregulation, combined with upregulated NADPH oxidase, promotes peroxynitrite formation, further disrupting the nitric oxide-reactive oxidants balance. Pathological inducible nitric oxide synthase activation also leads to nitrite accumulation, impairing redox networks and cellular antioxidant systems. During winter months, reduced solar radiation decreases photolysis-derived nitric oxide and downregulates Nrf2, while inducible nitric oxide synthase and NADPH oxidase remain elevated, exacerbating these conditions. Similar effects occur at high latitudes. Photonic therapies aimed at restoring nitric oxide equilibrium have shown promise in treating such skin disorders.
{"title":"Photo-induced nitric oxide modulation in human skin: Impacts of geographic location and seasonality on health and disease","authors":"Paulo E. da Costa , Maurício S. Baptista","doi":"10.1016/j.jphotobiol.2025.113349","DOIUrl":"10.1016/j.jphotobiol.2025.113349","url":null,"abstract":"<div><div>Depending on geographic location and seasonality, human epidermal tissue is exposed to varying levels of solar radiation. Following light absorption by endogenous photosensitizers, solar photons generate reactive oxidants, inducing oxidative stress that is counteracted by nitric oxide, which inhibits lipid peroxidation and activates antioxidant signaling pathways. Nitric oxide is also quickly transformed in several more stable compounds, which can release nitric oxide at specific conditions, here called nitric oxide reserves. During sun exposure, photolysis of nitric oxide reserves releases bioactive nitric oxide, while inducible nitric oxide synthase is expressed later, synthesizing nitric oxide and replenishing nitric oxide stores. This dynamic process establishes a photoinduced steady state of nitric oxide release and storage. The balance between nitric oxide and reactive oxidants levels is regulated by solar radiation and fluctuates with seasonal and latitudinal variations. Sunlight exposure promotes bioactive nitric oxide production, helping to sustain a healthy nitric oxide/reactive oxidants equilibrium. However, this mechanism is disrupted in chronic inflammatory skin conditions. In this context, elevated expression of inducible nitric oxide synthase is commonly observed in patients with psoriasis, atopic dermatitis and vitiligo. These patients display nitric oxide dysregulation alongside impaired redox regulators, including Nrf2 and NADPH oxidase. Inducible nitric oxide synthase dysregulation, combined with upregulated NADPH oxidase, promotes peroxynitrite formation, further disrupting the nitric oxide-reactive oxidants balance. Pathological inducible nitric oxide synthase activation also leads to nitrite accumulation, impairing redox networks and cellular antioxidant systems. During winter months, reduced solar radiation decreases photolysis-derived nitric oxide and downregulates Nrf2, while inducible nitric oxide synthase and NADPH oxidase remain elevated, exacerbating these conditions. Similar effects occur at high latitudes. Photonic therapies aimed at restoring nitric oxide equilibrium have shown promise in treating such skin disorders.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"276 ","pages":"Article 113349"},"PeriodicalIF":3.7,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146049145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-23DOI: 10.1016/j.jphotobiol.2025.113350
Jiali Yang , Haokuan Qin , Xiaojing Miao , Longfei Huo , Qiqi Fu , Hui Jiang , Jianfeng Niu , Muqing Liu
Blue light (400–500 nm) photobiomodulation (PBM), particularly utilizing light-emitting diodes (LEDs), has garnered extensive attention for its therapeutic efficacy across various conditions, including oncology. Nevertheless, its impact on osteosarcoma cells remain inadequately characterized. This study sought to investigate the tumor-suppressive properties and underlying molecular mechanisms of LED blue light PBM in human osteosarcoma cell lines HOS and MG63. The results indicated that blue light PBM effectively suppressed cell proliferation and triggered G2/M phase cell cycle arrest. Moreover, blue light PBM activated apoptosis and ferroptosis, characterized by significant changes in ferroptosis-associated proteins (HO-1, PTGS2, GPX4). Concurrently, ROS accumulation triggered oxidative stress, as demonstrated by increased MDA and LPO levels, well-established markers of ferroptosis. These findings underscore the promising potential of LED blue light PBM as an innovative, non-pharmacological therapeutic strategy for osteosarcoma, warranting further investigation for future clinical applications.
{"title":"LED blue light photobiomodulation induces ferroptosis and apoptosis via ROS-mediated oxidative damage in osteosarcoma cells","authors":"Jiali Yang , Haokuan Qin , Xiaojing Miao , Longfei Huo , Qiqi Fu , Hui Jiang , Jianfeng Niu , Muqing Liu","doi":"10.1016/j.jphotobiol.2025.113350","DOIUrl":"10.1016/j.jphotobiol.2025.113350","url":null,"abstract":"<div><div>Blue light (400–500 nm) photobiomodulation (PBM), particularly utilizing light-emitting diodes (LEDs), has garnered extensive attention for its therapeutic efficacy across various conditions, including oncology. Nevertheless, its impact on osteosarcoma cells remain inadequately characterized. This study sought to investigate the tumor-suppressive properties and underlying molecular mechanisms of LED blue light PBM in human osteosarcoma cell lines HOS and MG63. The results indicated that blue light PBM effectively suppressed cell proliferation and triggered G2/M phase cell cycle arrest. Moreover, blue light PBM activated apoptosis and ferroptosis, characterized by significant changes in ferroptosis-associated proteins (HO-1, PTGS2, GPX4). Concurrently, ROS accumulation triggered oxidative stress, as demonstrated by increased MDA and LPO levels, well-established markers of ferroptosis. These findings underscore the promising potential of LED blue light PBM as an innovative, non-pharmacological therapeutic strategy for osteosarcoma, warranting further investigation for future clinical applications.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113350"},"PeriodicalIF":3.7,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145836859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-22DOI: 10.1016/j.jphotobiol.2025.113347
Ruining Liu , Shuang Ge , Jinyuan Sun , Yi Liu , Liping Sun , Yang Yu , Deqing Wang
Acute myeloid leukemia (AML) remains challenging due to drug resistance and relapse, and novel therapeutic approaches are urgently needed. Here, we demonstrated that ultraviolet-treated riboflavin (RF-UV) elicited strong antileukemia effects in AML cell lines and primary patient samples, while showing minimal toxicity in normal cells. Mechanistically, inhibition of mitochondrial respiratory Complex I by RF-UV elevated reactive oxygen species (ROS) levels and resulted in ROS-mediated apoptosis, endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Crucially, in vivo research showed RF-UV considerably slowed the development of AML and extended the survival time of mice. Our research unveiled the clinical application potential of RF-UV as a complex I inhibitor in leukemia treatment.
{"title":"Ultraviolet-treated riboflavin induces ROS-mediated apoptosis via inhibiting mitochondrial complex I in acute myeloid leukemia","authors":"Ruining Liu , Shuang Ge , Jinyuan Sun , Yi Liu , Liping Sun , Yang Yu , Deqing Wang","doi":"10.1016/j.jphotobiol.2025.113347","DOIUrl":"10.1016/j.jphotobiol.2025.113347","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) remains challenging due to drug resistance and relapse, and novel therapeutic approaches are urgently needed. Here, we demonstrated that ultraviolet-treated riboflavin (RF-UV) elicited strong antileukemia effects in AML cell lines and primary patient samples, while showing minimal toxicity in normal cells. Mechanistically, inhibition of mitochondrial respiratory Complex I by RF-UV elevated reactive oxygen species (ROS) levels and resulted in ROS-mediated apoptosis, endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Crucially, in vivo research showed RF-UV considerably slowed the development of AML and extended the survival time of mice. Our research unveiled the clinical application potential of RF-UV as a complex I inhibitor in leukemia treatment.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113347"},"PeriodicalIF":3.7,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-17DOI: 10.1016/j.jphotobiol.2025.113345
Mario Diaz , Sergio de Armas-Rillo , Fernando Lobo , Daniel Pereda de Pablo , Kevin Soler-Carracedo , Pablo Delgado , Mitzi Rodriguez , Ana Canerina-Amaro , Catalina Valdes-Baizabal , Raquel Marín , Dácil Hernández , Alicia Boto , Fernando Lahoz
Endoxifen is the most powerful metabolite of tamoxifen (TX), the main endocrine therapy administered worldwide for the treatment of estrogen-receptor (ER) positive metastatic breast cancer. Tamoxifen itself is a prodrug with weak affinity for ER, but it is converted into endoxifen, with up to 100-fold higher affinity for ER than TX. In this study, we introduce the first fluorescent endoxifen derivative (FLTX3), formed by covalent attachment of the small fluorophore NBD to the basic side chain of endoxifen. We have characterized the optical properties of FLTX3, demonstrating its ability as a laser dye. FLTX3 is an efficient target-directed fluorescent probe for the cellular labelling of ER in MCF7 breast cancer cell line as well as in uterine tissues. FLTX3 is also endowed with an intrinsic photodynamic effect when irradiated at the optimal excitation wavelength of FLTX3. Further, we show that FLTX3 has an optical gain behaviour that leads to random laser (RL) when the light emitted by the drug is scattered in the cell cultures. Indeed, analyses of coherent spectra by power function Fourier transform revealed a RL dominant cavity in the range of average cell sizes. As one of the main causes for tamoxifen treatment failure is resistance, we explored the potential discriminative value of FLTX3-induced RL between tamoxifen-resistant and tamoxifen-sensitive MCF7 cells. Using multivariate approaches, we unravelled significant differences in the RL signal between tamoxifen-sensitive and tamoxifen-resistant cells. These findings indicate that FLTX3-generated RL might provide a target-directed diagnostic tool for tamoxifen resistance in metastatic ER+ breast cancer.
{"title":"Optical and random laser properties of the novel multifunctional endoxifen derivative (FLTX3) and its potential for the diagnosis of breast cancer resistance","authors":"Mario Diaz , Sergio de Armas-Rillo , Fernando Lobo , Daniel Pereda de Pablo , Kevin Soler-Carracedo , Pablo Delgado , Mitzi Rodriguez , Ana Canerina-Amaro , Catalina Valdes-Baizabal , Raquel Marín , Dácil Hernández , Alicia Boto , Fernando Lahoz","doi":"10.1016/j.jphotobiol.2025.113345","DOIUrl":"10.1016/j.jphotobiol.2025.113345","url":null,"abstract":"<div><div>Endoxifen is the most powerful metabolite of tamoxifen (TX), the main endocrine therapy administered worldwide for the treatment of estrogen-receptor (ER) positive metastatic breast cancer. Tamoxifen itself is a prodrug with weak affinity for ER, but it is converted into endoxifen, with up to 100-fold higher affinity for ER than TX. In this study, we introduce the first fluorescent endoxifen derivative (FLTX3), formed by covalent attachment of the small fluorophore NBD to the basic side chain of endoxifen. We have characterized the optical properties of FLTX3, demonstrating its ability as a <u>laser dye</u>. FLTX3 is an efficient target-directed <u>fluorescent probe</u> for the cellular labelling of ER in MCF7 breast cancer cell line as well as in uterine tissues. FLTX3 is also endowed with an intrinsic <u>photodynamic</u> effect when irradiated at the optimal excitation wavelength of FLTX3. Further, we show that FLTX3 has an <u>optical gain behaviour</u> that leads to random laser (RL) when the light emitted by the drug is scattered in the cell cultures. Indeed, analyses of coherent spectra by power function Fourier transform revealed a RL dominant cavity in the range of average cell sizes. As one of the main causes for tamoxifen treatment failure is resistance, we explored the potential discriminative value of FLTX3-induced RL between tamoxifen-resistant and tamoxifen-sensitive MCF7 cells. Using multivariate approaches, we unravelled significant differences in the RL signal between tamoxifen-sensitive and tamoxifen-resistant cells. These findings indicate that FLTX3-generated RL might provide a <u>target-directed diagnostic tool</u> for tamoxifen resistance in metastatic ER+ breast cancer.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113345"},"PeriodicalIF":3.7,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vachellia gummifera (Willd.) Kyal. & Boatwr. (formerly known as Acacia gummifera) is a thorny, flowering plant endemic to Morocco. It was selected due to the limited research on its potential skin-protective properties, despite other species of the same genus being traditionally used to treat various skin ailments. In this study we annotated the phytochemical profile of its aqueous leaf extract using HPLC-MS/MS and evaluated its skin protective potential through in vitro assays, including antioxidant, anti-elastase, and anti-tyrosinase activities. Additionally, we assessed its protective potential against UVA-induced oxidative stress in immortalized human keratinocyte cell line (HaCaT), along with the underlying signaling pathways. LC-MS/MS analysis revealed 48 metabolites, mainly flavonoids and their glycosides. The extract exhibited in vitro antioxidant activities with IC50 values of 30.96 ± 2.10 and 232.33 ± 8.40 μg/mL for DPPH and ABTS, respectively, and a FRAP activity of 8.42 ± 0.52 mM FeSO₄/g extract. It also demonstrated moderate anti-tyrosinase properties with an IC50 value of 369.23 ± 12.01 μg/mL. In silico analyses of most of the identified compounds did not predict any skin sensitization. Accordingly, when tested on HaCaT cells up to 400 μg/mL, the extract showed no cytotoxic effects, suggesting its biocompatibility. Cells pre-treated with the extract effectively mitigated UVA-induced cellular damage, as it significantly inhibited reactive oxygen species production and glutathione depletion, measured by DCFDA and DTNB assays, respectively. Furthermore, the extract modulated the mitogen-activated protein kinase (MAPK) pathway by inhibiting UVA-induced phosphorylation of p38. Finally, a molecular docking analyses identified citric acid, hydroxycinnamic acid pentosyl hexoside and myricetin malonyl hexoside as the enzymes exhibiting the highest binding affinity towards tyrosinase. These findings suggest that V. gummifera possesses promising antioxidant and anti-aging properties, with potential applications in skin care and photoprotection.
海葵（野生）Kyal。& Boatwr。（以前被称为金合欢gummifera）是一种摩洛哥特有的多刺开花植物。选择它是因为对其潜在的皮肤保护特性的研究有限，尽管同一属的其他物种传统上用于治疗各种皮肤疾病。在这项研究中，我们使用HPLC-MS/MS对其水叶提取物的植物化学特征进行了注释，并通过体外实验评估了其皮肤保护潜力，包括抗氧化、抗弹性酶和抗酪氨酸酶活性。此外，我们评估了其对永生化人角化细胞（HaCaT）抗uva诱导的氧化应激的保护潜力，以及潜在的信号通路。LC-MS/MS分析共发现48种代谢物，主要为黄酮类化合物及其苷类化合物。提取物对DPPH和ABTS的IC50值分别为30.96±2.10和232.33±8.40 μg/mL， FRAP活性为8.42±0.52 mM FeSO₄/g提取物。具有中等抗酪氨酸酶活性，IC50值为369.23±12.01 μg/mL。对大多数已确定的化合物的计算机分析不能预测任何皮肤致敏性。因此，当浓度达到400 μg/mL时，提取物对HaCaT细胞无细胞毒作用，表明其具有生物相容性。通过DCFDA和DTNB测定，用提取物预处理的细胞有效地减轻了uva诱导的细胞损伤，因为它显著抑制了活性氧的产生和谷胱甘肽的消耗。此外，提取物通过抑制uva诱导的p38磷酸化来调节丝裂原活化蛋白激酶（MAPK）途径。最后，通过分子对接分析，确定了柠檬酸、羟基肉桂酸戊酰基己糖和杨梅素丙二酰己糖是与酪氨酸酶结合亲和力最高的酶。这些研究结果表明，胶霉具有良好的抗氧化和抗衰老特性，在皮肤护理和光防护方面具有潜在的应用前景。
{"title":"Vachellia gummifera (Willd.) Kyal. & Boatwr. mitigates UVA-induced oxidative stress in HaCaT keratinocytes","authors":"Hassan Annaz , Paola Imbimbo , Mohamed A.O. Abdelfattah , Ismail Mahdi , Nidal Fahsi , Badreddine Drissi , Nawal Merghoub , Daria Maria Monti , Mansour Sobeh","doi":"10.1016/j.jphotobiol.2025.113341","DOIUrl":"10.1016/j.jphotobiol.2025.113341","url":null,"abstract":"<div><div><em>Vachellia gummifera</em> (Willd.) Kyal. & Boatwr. (formerly known as <em>Acacia gummifera</em>) is a thorny, flowering plant endemic to Morocco. It was selected due to the limited research on its potential skin-protective properties, despite other species of the same genus being traditionally used to treat various skin ailments. In this study we annotated the phytochemical profile of its aqueous leaf extract using HPLC-MS/MS and evaluated its skin protective potential through <em>in vitro</em> assays, including antioxidant, anti-elastase, and anti-tyrosinase activities. Additionally, we assessed its protective potential against UVA-induced oxidative stress in immortalized human keratinocyte cell line (HaCaT), along with the underlying signaling pathways. LC-MS/MS analysis revealed 48 metabolites, mainly flavonoids and their glycosides. The extract exhibited <em>in vitro</em> antioxidant activities with IC<sub>50</sub> values of 30.96 ± 2.10 and 232.33 ± 8.40 μg/mL for DPPH and ABTS, respectively, and a FRAP activity of 8.42 ± 0.52 mM FeSO₄/g extract. It also demonstrated moderate anti-tyrosinase properties with an IC<sub>50</sub> value of 369.23 ± 12.01 μg/mL. <em>In silico</em> analyses of most of the identified compounds did not predict any skin sensitization. Accordingly, when tested on HaCaT cells up to 400 μg/mL, the extract showed no cytotoxic effects, suggesting its biocompatibility. Cells pre-treated with the extract effectively mitigated UVA-induced cellular damage, as it significantly inhibited reactive oxygen species production and glutathione depletion, measured by DCFDA and DTNB assays, respectively. Furthermore, the extract modulated the mitogen-activated protein kinase (MAPK) pathway by inhibiting UVA-induced phosphorylation of p38. Finally, a molecular docking analyses identified citric acid, hydroxycinnamic acid pentosyl hexoside and myricetin malonyl hexoside as the enzymes exhibiting the highest binding affinity towards tyrosinase. These findings suggest that <em>V. gummifera</em> possesses promising antioxidant and anti-aging properties, with potential applications in skin care and photoprotection.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113341"},"PeriodicalIF":3.7,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145834191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ultraviolet (UV) radiation, particularly in the UVA spectrum (320–400 nm), induces significant damage to both dermal and epidermal layers of skin, generating reactive oxygen species (ROS) and triggering apoptotic pathways that compromise skin health. Selaginella tamariscina (P. Beauv.), a traditional medicinal plant widely used throughout Asia, contains numerous flavonoid compounds with recognized therapeutic value in Chinese medicine. Through comprehensive molecular analyses including Western blotting, RT-qPCR, and flow cytometry, we demonstrated that the Selaginella tamariscina (P. Beauv.) extract (STE) significantly reduces UVA-induced apoptosis while simultaneously activating protective autophagic responses. Mechanistically, STE modulates AKT phosphorylation to regulate two critical downstream pathways: (1) the JNK-mediated apoptotic cascade and (2) the AKT/mTOR autophagic axis. In vivo experiments revealed that topical STE application provided substantial protection against UVA-induced photodamage in murine dorsal skin models. Liquid chromatography analysis identified amentoflavone as the principal bioactive component responsible for these protective properties. These findings collectively establish STE as a promising therapeutic agent against UVA photodamage, functioning through its dual capacity to attenuate apoptosis while promoting cytoprotective autophagy.
紫外线（UV）辐射，特别是UVA光谱（320-400 nm），会对皮肤真皮层和表皮层造成严重损伤，产生活性氧（ROS）并引发损害皮肤健康的细胞凋亡途径。卷柏（Selaginella tamariscina， P. Beauv.）是一种在亚洲广泛使用的传统药用植物，其含有大量的类黄酮化合物，具有公认的中药治疗价值。通过Western blotting、RT-qPCR和流式细胞术等综合分子分析，我们发现卷柏（Selaginella tamariscina， P. Beauv.）提取物（STE）可显著降低uva诱导的细胞凋亡，同时激活保护性自噬反应。从机制上讲，STE通过调节AKT磷酸化来调节两个关键的下游通路：(1)jnk介导的凋亡级联；(2)AKT/mTOR自噬轴。体内实验表明，局部STE应用对小鼠背部皮肤模型uva诱导的光损伤具有实质性的保护作用。液相色谱分析确定了阿门托黄酮是负责这些保护特性的主要生物活性成分。这些发现共同证明STE是一种很有前景的抗UVA光损伤治疗剂，通过其双重能力来减轻细胞凋亡，同时促进细胞保护性自噬。
{"title":"Selaginella Tamariscina extract reduces UVA-induced skin photodamage via regulating apoptosis and autophagy by AKT phosphorylation","authors":"Nan Zhao, Xiandong Zhou, Zhiwei Li, Ling Liang, Jinjing Bao, Xueyi Chen, Peng Shu, Jiangming Zhong","doi":"10.1016/j.jphotobiol.2025.113343","DOIUrl":"10.1016/j.jphotobiol.2025.113343","url":null,"abstract":"<div><div>Ultraviolet (UV) radiation, particularly in the UVA spectrum (320–400 nm), induces significant damage to both dermal and epidermal layers of skin, generating reactive oxygen species (ROS) and triggering apoptotic pathways that compromise skin health. <em>Selaginella tamariscina</em> (P. Beauv.), a traditional medicinal plant widely used throughout Asia, contains numerous flavonoid compounds with recognized therapeutic value in Chinese medicine. Through comprehensive molecular analyses including Western blotting, RT-qPCR, and flow cytometry, we demonstrated that the <em>Selaginella tamariscina</em> (P. Beauv.) extract (STE) significantly reduces UVA-induced apoptosis while simultaneously activating protective autophagic responses. Mechanistically, STE modulates AKT phosphorylation to regulate two critical downstream pathways: (1) the JNK-mediated apoptotic cascade and (2) the AKT/mTOR autophagic axis. In vivo experiments revealed that topical STE application provided substantial protection against UVA-induced photodamage in murine dorsal skin models. Liquid chromatography analysis identified amentoflavone as the principal bioactive component responsible for these protective properties. These findings collectively establish STE as a promising therapeutic agent against UVA photodamage, functioning through its dual capacity to attenuate apoptosis while promoting cytoprotective autophagy.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113343"},"PeriodicalIF":3.7,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In this study, we report the development of multifunctional CQ-dot@HA-Gd/Fe(III) microgels that can be readily simultaneously used in fluorescence/MR dual-mode imaging and photodynamic therapy as theragnostic agents. Nitrogen (N-) and sulfur (S-) heteroatom-doped carbon quantum dots (CQ-dot) were prepared in one step microwave treatment within 3 min as a fluorescence and photoinduced antipathogenic nanomaterial. The N/S-doped CQ-dots were spherical shaped and < 50 nm via TEM images and showed high fluorescence intensity with 420 nm emission wavelength at maximum λex:350 nm. The N/S-doped CQ-dots were embedded into ionically crosslinked hyaluronic acid (HA) microgels, employing trivalent metal ions Gd(III) or Fe(III) ions. The prepared CQ-dot@HA-Gd/Fe(III) microgels <5 mm size range are injectable for possible intravenous administration and possess high fluorescent properties. The isoelectric point (IEP) of CQ-dot@HA-Gd and CQ-dot@HA-Fe(III) microgels was determined as pH 1.45. The CQ-dot@HA-Gd/Fe(III) microgels exhibit excellent hemocompatibility without causing noticeable hemolysis and blood clotting at concentrations up to 500 mg/mL. Furthermore, the toxicity of CQ-dot@HA-Gd/Fe(III) microgels on L929 fibroblast cells was found as 100 mg/mL concentration and provide brilliant cell imaging under DAPI filter without any fluorescence dye. Also, the CQ-dot@HA-Gd/Fe(III) microgel suspension afforded great MRI contrast enhancement ability. Photoinduced anticancer activity was observed for CQ-dot@HA-Gd/Fe(III) microgels even at 50 mg/mL against SK-MEL 30 melanoma cells under UV-A light treatment for 30 min. In addition, high reactive oxygen species (ROS) generation was obtained for the pathogenic bacteria cells by light-sensitive CQ-dot@HA-Gd/Fe(III) microgels upon 30 min UV-A light treatment that triggered the destruction of the Staphylococcus aureus (ATCC 6538).
{"title":"Gd(III) and Fe(III) ion crosslinked hyaluronic acid microgels composites embedding hetero atom doped carbon quantum dots render photodynamic therapy with improved bioimaging capability","authors":"Selin Sagbas Suner , Mehtap Sahiner , Evrim Umut , Nurettin Sahiner","doi":"10.1016/j.jphotobiol.2025.113342","DOIUrl":"10.1016/j.jphotobiol.2025.113342","url":null,"abstract":"<div><div>In this study, we report the development of multifunctional CQ-dot@HA-Gd/Fe(III) microgels that can be readily simultaneously used in fluorescence/MR dual-mode imaging and photodynamic therapy as theragnostic agents. Nitrogen (N-) and sulfur (S-) heteroatom-doped carbon quantum dots (CQ-dot) were prepared in one step microwave treatment within 3 min as a fluorescence and photoinduced antipathogenic nanomaterial. The N/S-doped CQ-dots were spherical shaped and < 50 nm via TEM images and showed high fluorescence intensity with 420 nm emission wavelength at maximum λ<sub>ex</sub>:350 nm. The N/S-doped CQ-dots were embedded into ionically crosslinked hyaluronic acid (HA) microgels, employing trivalent metal ions Gd(III) or Fe(III) ions. The prepared CQ-dot@HA-Gd/Fe(III) microgels <5 mm size range are injectable for possible intravenous administration and possess high fluorescent properties. The isoelectric point (IEP) of CQ-dot@HA-Gd and CQ-dot@HA-Fe(III) microgels was determined as pH 1.45. The CQ-dot@HA-Gd/Fe(III) microgels exhibit excellent hemocompatibility without causing noticeable hemolysis and blood clotting at concentrations up to 500 mg/mL. Furthermore, the toxicity of CQ-dot@HA-Gd/Fe(III) microgels on L929 fibroblast cells was found as 100 mg/mL concentration and provide brilliant cell imaging under DAPI filter without any fluorescence dye. Also, the CQ-dot@HA-Gd/Fe(III) microgel suspension afforded great MRI contrast enhancement ability. Photoinduced anticancer activity was observed for CQ-dot@HA-Gd/Fe(III) microgels even at 50 mg/mL against SK-MEL 30 melanoma cells under UV-A light treatment for 30 min. In addition, high reactive oxygen species (ROS) generation was obtained for the pathogenic bacteria cells by light-sensitive CQ-dot@HA-Gd/Fe(III) microgels upon 30 min UV-A light treatment that triggered the destruction of the <em>Staphylococcus aureus</em> (ATCC 6538).</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113342"},"PeriodicalIF":3.7,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-13DOI: 10.1016/j.jphotobiol.2025.113340
Biao Guo , Meiyun Wu , Liying Tong , Jiahui Yu , Ruoyun Liu , Meng Deng , Yijing Ma , Hao Li , Zile Yang , Xiyun Ye , Yongyan Dang
Safflower (Carthamus tinctorius L.) is a traditional Chinese medicinal herb that has long been used to promote blood circulation. Its major active component, hydroxysafflor yellow A (HSYA), exhibits potent antioxidant and anti-photoaging properties. However, the mechanisms underlying HSYA's protective effects against skin photoaging remain largely unclear. This study aimed to elucidate how HSYA mitigates skin aging induced by UVA- and UVB-triggered apoptosis and the senescence-associated secretory phenotype (SASP) in keratinocytes and fibroblasts. Damage models were established by exposing BALB/c nude mice, HaCaT keratinocytes, and HSF fibroblasts to either combined or individual UVA and UVB irradiation. Network pharmacology analysis was subsequently performed to explore the molecular mechanisms underlying the anti-photoaging effects of HSYA. The predicted targets and signaling pathways were validated through both in vitro and in vivo experiments. HSYA reduced apoptosis in UVB-damaged keratinocytes and UVA-damaged fibroblasts by regulating the expression of Bcl-2 and Bax and reducing cleavage of PARP and caspase 3. It also suppressed ROS accumulation in both cell types. Furthermore, HSYA inhibited SASP by downregulating the expression of TNF-α, IL-6, IL-8, and matrix metalloproteinases (MMPs). It significantly enhanced type I procollagen expression of skin fibroblasts and promoted collagen fiber deposition in mouse skin, suggesting a reversal of UV-induced senescence of skin fibroblasts. Mechanistically, HSYA exerted its protective effects by inhibiting the activation of the p38 and JNK pathways. Notably, the inhibitory effects of HSYA on p38 and JNK phosphorylation were comparable to those of specific MAPK inhibitors. These findings identify that HSYA exerts the protective effects against UV-induced skin damage through coordinated regulation of oxidative stress, inflammation, apoptosis, and collagen remodeling, in part by targeting the JNK/p38 MAPK pathway. Thus, HSYA emerges as a promising active ingredient for the development of anti-photoaging and skin-rejuvenation products in the future.
{"title":"Hydroxysafflower yellow a protects against UVA- and UVB-induced skin aging by suppressing cell apoptosis and SASP via targeting JNK and p38 MAPK pathway","authors":"Biao Guo , Meiyun Wu , Liying Tong , Jiahui Yu , Ruoyun Liu , Meng Deng , Yijing Ma , Hao Li , Zile Yang , Xiyun Ye , Yongyan Dang","doi":"10.1016/j.jphotobiol.2025.113340","DOIUrl":"10.1016/j.jphotobiol.2025.113340","url":null,"abstract":"<div><div>Safflower (<em>Carthamus tinctorius L.</em>) is a traditional Chinese medicinal herb that has long been used to promote blood circulation. Its major active component, hydroxysafflor yellow A (HSYA), exhibits potent antioxidant and anti-photoaging properties. However, the mechanisms underlying HSYA's protective effects against skin photoaging remain largely unclear. This study aimed to elucidate how HSYA mitigates skin aging induced by UVA- and UVB-triggered apoptosis and the senescence-associated secretory phenotype (SASP) in keratinocytes and fibroblasts. Damage models were established by exposing BALB/c nude mice, HaCaT keratinocytes, and HSF fibroblasts to either combined or individual UVA and UVB irradiation. Network pharmacology analysis was subsequently performed to explore the molecular mechanisms underlying the anti-photoaging effects of HSYA. The predicted targets and signaling pathways were validated through both <em>in vitro</em> and <em>in vivo</em> experiments. HSYA reduced apoptosis in UVB-damaged keratinocytes and UVA-damaged fibroblasts by regulating the expression of Bcl-2 and Bax and reducing cleavage of PARP and caspase 3. It also suppressed ROS accumulation in both cell types. Furthermore, HSYA inhibited SASP by downregulating the expression of <em>TNF-α, IL-6, IL-8</em>, and matrix metalloproteinases (MMPs). It significantly enhanced type I procollagen expression of skin fibroblasts and promoted collagen fiber deposition in mouse skin, suggesting a reversal of UV-induced senescence of skin fibroblasts. Mechanistically, HSYA exerted its protective effects by inhibiting the activation of the p38 and JNK pathways. Notably, the inhibitory effects of HSYA on p38 and JNK phosphorylation were comparable to those of specific MAPK inhibitors. These findings identify that HSYA exerts the protective effects against UV-induced skin damage through coordinated regulation of oxidative stress, inflammation, apoptosis, and collagen remodeling, in part by targeting the JNK/p38 MAPK pathway. Thus, HSYA emerges as a promising active ingredient for the development of anti-photoaging and skin-rejuvenation products in the future.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113340"},"PeriodicalIF":3.7,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145797083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-11DOI: 10.1016/j.jphotobiol.2025.113339
Xiang-Yi Zhao , Min Yan , Liang Zheng , Chang-Long Gou , Qi Huang , Liu-Gen Li , Xin-Ran Yu , Jing-Yu Lu , Cui Hu , Si-Han Zhang , Cunqing Kong , Fan Leng , Tong-Fei Li
The regulation of mitochondrial membrane proteins is of crucial significance for breast cancer therapy. TOM70, which located in mitochondria outer membrane, could import MIC family molecules to preserve mitochondrial homeostasis. However, there are few agents targeting TOM70. Therein, the effects of curcumin and it's mediated photodynamic therapy (PDT) on the TOM70 and mitochondrial function for breast cancer treatment were investigated. The 4 T1 and MDA-MB-231 cells were utilized as the breast cancer cells. The 4 T1 cell-bearing mice were constructed as the breast cancer animal model. The anti-cancer efficacy was validated using the CCK-8, Annexin-V/PI staining, colony formation. The associated molecules were detected by Western blots (WB), RT-qPCR, and Immunohistochemistry (IHC). The target was verified by molecular docking, CETSA, and DARTS. The mitochondrial proteins and DNA were extracted for the MIC60 and mtDNA damage detection. Curcumin treatment showed poor efficacy in the breast cancer model, as characterized by cell viability, apoptosis, proliferation of breast cancer cells, and the growth of tumor grafts in mice. However, curcumin-mediated PDT inhibited breast cancer in vitro and in vivo. Further exploration identified curcumin bond to TOM70, which is highly expressed in breast cancer, thereby activating it. But curcumin-induced PDT inactivated TOM70 through generated reactive oxygen species (ROS), which in turn interfered with the binding of MIC60 and its translocation into mitochondria. Curcumin-triggered PDT led to severe mitochondrial damage compared with the curcumin treatment, which could be blocked by the N-Acetylcysteine (NAC). Additional TOM70 rescue dampened curcumin PDT-mediated mitochondrial damage and anti-breast cancer efficacy. To summarize, the present research identifies curcumin-induced PDT inactivated TOM70, thereby attenuating MIC60 import, leading to mitochondrial damage against breast cancer. We propose a novel approach to tumor treatment through the regulation of mitochondrial membrane proteins using the phytomedicine-driven PDT.
线粒体膜蛋白的调控对乳腺癌的治疗具有重要意义。TOM70位于线粒体外膜，可导入MIC家族分子维持线粒体稳态。然而，很少有靶向TOM70的药物。本文研究了姜黄素及其介导的光动力疗法（PDT）对乳腺癌TOM70和线粒体功能的影响。4个T1细胞和MDA-MB-231细胞作为乳腺癌细胞。构建4只T1细胞小鼠作为乳腺癌动物模型。通过CCK-8、Annexin-V/PI染色、菌落形成验证其抗癌效果。Western blots （WB）、RT-qPCR和免疫组化（IHC）检测相关分子。通过分子对接、CETSA、dart等方法对该靶点进行了验证。提取线粒体蛋白和DNA进行MIC60和mtDNA损伤检测。姜黄素治疗在乳腺癌模型中效果不佳，表现为细胞活力、凋亡、乳腺癌细胞增殖和小鼠肿瘤移植物生长。然而，姜黄素介导的PDT在体外和体内均能抑制乳腺癌。进一步探索发现姜黄素与TOM70结合，TOM70在乳腺癌中高度表达，从而激活TOM70。但姜黄素诱导的PDT通过产生活性氧（ROS）使TOM70失活，进而干扰MIC60的结合及其转运到线粒体。与姜黄素治疗相比，姜黄素引发的PDT导致严重的线粒体损伤，这可以被n-乙酰半胱氨酸（NAC）阻断。额外的TOM70救援抑制姜黄素pdt介导的线粒体损伤和抗乳腺癌疗效。综上所述，本研究发现姜黄素诱导的PDT灭活TOM70，从而减弱MIC60的输入，导致乳腺癌的线粒体损伤。我们提出了一种通过使用植物药驱动的PDT调节线粒体膜蛋白来治疗肿瘤的新方法。
{"title":"Curcumin-mediated photodynamic action disturbs TOM70-depedent MIC60 import to damage mitonchondria against breast cancer","authors":"Xiang-Yi Zhao , Min Yan , Liang Zheng , Chang-Long Gou , Qi Huang , Liu-Gen Li , Xin-Ran Yu , Jing-Yu Lu , Cui Hu , Si-Han Zhang , Cunqing Kong , Fan Leng , Tong-Fei Li","doi":"10.1016/j.jphotobiol.2025.113339","DOIUrl":"10.1016/j.jphotobiol.2025.113339","url":null,"abstract":"<div><div>The regulation of mitochondrial membrane proteins is of crucial significance for breast cancer therapy. TOM70, which located in mitochondria outer membrane, could import MIC family molecules to preserve mitochondrial homeostasis. However, there are few agents targeting TOM70. Therein, the effects of curcumin and it's mediated photodynamic therapy (PDT) on the TOM70 and mitochondrial function for breast cancer treatment were investigated. The 4 T1 and MDA-MB-231 cells were utilized as the breast cancer cells. The 4 T1 cell-bearing mice were constructed as the breast cancer animal model. The anti-cancer efficacy was validated using the CCK-8, Annexin-V/PI staining, colony formation. The associated molecules were detected by Western blots (WB), RT-qPCR, and Immunohistochemistry (IHC). The target was verified by molecular docking, CETSA, and DARTS. The mitochondrial proteins and DNA were extracted for the MIC60 and mtDNA damage detection. Curcumin treatment showed poor efficacy in the breast cancer model, as characterized by cell viability, apoptosis, proliferation of breast cancer cells, and the growth of tumor grafts in mice. However, curcumin-mediated PDT inhibited breast cancer in vitro and in vivo. Further exploration identified curcumin bond to TOM70, which is highly expressed in breast cancer, thereby activating it. But curcumin-induced PDT inactivated TOM70 through generated reactive oxygen species (ROS), which in turn interfered with the binding of MIC60 and its translocation into mitochondria. Curcumin-triggered PDT led to severe mitochondrial damage compared with the curcumin treatment, which could be blocked by the N-Acetylcysteine (NAC). Additional TOM70 rescue dampened curcumin PDT-mediated mitochondrial damage and anti-breast cancer efficacy. To summarize, the present research identifies curcumin-induced PDT inactivated TOM70, thereby attenuating MIC60 import, leading to mitochondrial damage against breast cancer. We propose a novel approach to tumor treatment through the regulation of mitochondrial membrane proteins using the phytomedicine-driven PDT.</div></div>","PeriodicalId":16772,"journal":{"name":"Journal of photochemistry and photobiology. B, Biology","volume":"274 ","pages":"Article 113339"},"PeriodicalIF":3.7,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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