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Selaginella Tamariscina extract reduces UVA-induced skin photodamage via regulating apoptosis and autophagy by AKT phosphorylation 卷柏提取物通过AKT磷酸化调控细胞凋亡和自噬,减轻uva诱导的皮肤光损伤
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-16 DOI: 10.1016/j.jphotobiol.2025.113343
Nan Zhao, Xiandong Zhou, Zhiwei Li, Ling Liang, Jinjing Bao, Xueyi Chen, Peng Shu, Jiangming Zhong
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。
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引用次数: 0
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 Gd(III)和Fe(III)离子交联透明质酸微凝胶复合材料包埋杂原子掺杂碳量子点,实现光动力治疗,提高生物成像能力
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-16 DOI: 10.1016/j.jphotobiol.2025.113342
Selin Sagbas Suner , Mehtap Sahiner , Evrim Umut , Nurettin Sahiner
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).
在这项研究中,我们报道了多功能CQ-dot@HA-Gd/Fe(III)微凝胶的开发,该微凝胶可以很容易地同时用于荧光/磁共振双模成像和光动力治疗作为诊断剂。采用微波一步法在3 min内制备了氮(N-)和硫(S-)掺杂碳量子点(CQ-dot)作为荧光光致抗致病性纳米材料。TEM图像显示,N/ s掺杂的cq点呈球形,波长为<; 50 nm,荧光强度高,最大λex为350 nm,发射波长为420 nm。将N/ s掺杂的cq点嵌入到离子交联透明质酸(HA)微凝胶中,采用三价金属离子Gd(III)或Fe(III)离子。制备的CQ-dot@HA-Gd/Fe(III)微凝胶<; 5mm尺寸范围可注射,可能用于静脉给药,并具有高荧光特性。测定CQ-dot@HA-Gd和CQ-dot@HA-Fe(III)微凝胶的等电点(IEP) pH为1.45。CQ-dot@HA-Gd/Fe(III)微凝胶具有优异的血液相容性,浓度高达500 mg/mL时不会引起明显的溶血和凝血。此外,CQ-dot@HA-Gd/Fe(III)微凝胶在100 mg/mL浓度时对L929成纤维细胞具有毒性,在DAPI滤光片下无任何荧光染料提供了明亮的细胞成像。同时,CQ-dot@HA-Gd/Fe(III)微凝胶悬浮液具有良好的MRI增强能力。在UV-A光处理30分钟后,CQ-dot@HA-Gd/Fe(III)微凝胶对SK-MEL 30黑色素瘤细胞的光诱导抗癌活性观察到,即使浓度为50 mg/mL。此外,通过光敏CQ-dot@HA-Gd/Fe(III)微凝胶对病原菌细胞进行30min UV-A光处理,触发金黄色葡萄球菌(ATCC 6538)的破坏,获得了高活性氧(ROS)生成。
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引用次数: 0
Hydroxysafflower yellow a protects against UVA- and UVB-induced skin aging by suppressing cell apoptosis and SASP via targeting JNK and p38 MAPK pathway 羟基红花黄a通过靶向JNK和p38 MAPK通路抑制细胞凋亡和SASP,从而防止UVA-和uvb诱导的皮肤衰老
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-13 DOI: 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.
红花(Carthamus tinctorius L.)是一种传统的中草药,长期以来被用来促进血液循环。其主要活性成分羟基红花黄A (HSYA)具有抗氧化和抗光老化的特性。然而,HSYA对皮肤光老化的保护作用机制仍不清楚。本研究旨在阐明HSYA如何缓解由UVA和uvb引发的角质形成细胞和成纤维细胞凋亡和衰老相关分泌表型(SASP)诱导的皮肤衰老。将BALB/c裸鼠、HaCaT角质形成细胞和HSF成纤维细胞分别暴露于UVA和UVB联合或单独照射下,建立损伤模型。随后进行了网络药理学分析,以探索HSYA抗光老化作用的分子机制。通过体外和体内实验验证了预测的靶点和信号通路。HSYA通过调节Bcl-2和Bax的表达,减少PARP和caspase 3的切割,从而减少uvb损伤的角质形成细胞和uva损伤的成纤维细胞的凋亡。它还抑制了两种细胞类型中的ROS积累。此外,HSYA通过下调TNF-α、IL-6、IL-8和基质金属蛋白酶(MMPs)的表达来抑制SASP。显著增强小鼠皮肤成纤维细胞I型前胶原表达,促进胶原纤维沉积,提示可逆转紫外线诱导的皮肤成纤维细胞衰老。机制上,HSYA通过抑制p38和JNK通路的激活发挥其保护作用。值得注意的是,HSYA对p38和JNK磷酸化的抑制作用与特异性MAPK抑制剂相当。这些发现表明,HSYA通过协调调节氧化应激、炎症、细胞凋亡和胶原重塑,部分通过靶向JNK/p38 MAPK通路,对紫外线诱导的皮肤损伤发挥保护作用。因此,HSYA在未来的抗光老化和皮肤再生产品的开发中成为一个有前途的活性成分。
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引用次数: 0
Curcumin-mediated photodynamic action disturbs TOM70-depedent MIC60 import to damage mitonchondria against breast cancer 姜黄素介导的光动力作用干扰tom70依赖的MIC60进口,以损害线粒体对抗乳腺癌。
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-11 DOI: 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 ,&nbsp;Min Yan ,&nbsp;Liang Zheng ,&nbsp;Chang-Long Gou ,&nbsp;Qi Huang ,&nbsp;Liu-Gen Li ,&nbsp;Xin-Ran Yu ,&nbsp;Jing-Yu Lu ,&nbsp;Cui Hu ,&nbsp;Si-Han Zhang ,&nbsp;Cunqing Kong ,&nbsp;Fan Leng ,&nbsp;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}
引用次数: 0
Refined photobiomodulation therapy ameliorates inflammatory bowel disease via modulation of immune pathways and gut microbiota 精细光生物调节疗法通过调节免疫途径和肠道微生物群改善炎症性肠病。
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-11 DOI: 10.1016/j.jphotobiol.2025.113330
Lee So Maeng , Jung Hwan Yoon , Bom Yee Chung , Kyung Jin Seo , Hae Kyung Lee , Moon Gyu Chung , Won Sang Park , Hiun Suk Chae

Background

Inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn's disease, are chronic conditions influenced by genetic and environmental factors. Current treatments are costly and not universally effective. This study aimed to evaluate the therapeutic potential of refined photobiomodulation (PBM) therapy by addressing limitations in light delivery and its impact on gut microbiota using a dextran sodium sulfate (DSS)-induced colitis mouse model.

Methods

PBM therapy was administered using an 830 nm infrared LED with optimized light delivery protocols, including abdominal hair removal and a four-directional irradiation approach. DSS-induced colitis was established in mice, and therapeutic efficacy was assessed through histological analysis, transcriptomic profiling, immune marker expression, and gut microbiota diversity using 16S rRNA sequencing.

Results

PBM therapy significantly ameliorated DSS-induced colitis by reducing inflammatory cell infiltration, crypt damage, and ulceration (p < 0.05). Colon length was restored, and disease activity index scores were reduced (p < 0.001). Transcriptomic profiling revealed modulation of inflammatory pathways, including downregulation of NF-κB signaling and apoptosis-related genes. PBM decreased neutrophil activity (MPO levels) and immune cell marker expression while promoting gut microbiota richness (Chao1 index, p < 0.05). PBM-treated mice exhibited altered microbial composition with increased abundance of protective taxa such as Bacteroides.

Conclusions

Refined PBM therapy effectively alleviates DSS-induced colitis by modulating immune responses and gut microbiota composition. These findings highlight PBM as a promising non-invasive strategy for IBD management, warranting further translational studies.
背景:炎症性肠病(IBD),如溃疡性结肠炎和克罗恩病,是受遗传和环境因素影响的慢性疾病。目前的治疗方法既昂贵又不是普遍有效。本研究旨在利用右旋糖酐硫酸钠(DSS)诱导的结肠炎小鼠模型,通过解决光传递的局限性及其对肠道微生物群的影响,评估精细光生物调节(PBM)疗法的治疗潜力。方法:采用830 nm红外LED进行PBM治疗,优化光传递方案,包括腹部脱毛和四方向照射方法。在小鼠中建立dss诱导的结肠炎,并通过组织学分析、转录组学分析、免疫标志物表达和使用16S rRNA测序的肠道微生物群多样性来评估治疗效果。结果:PBM治疗通过减少炎症细胞浸润、隐窝损伤和溃疡显著改善dss诱导的结肠炎(p结论:精制PBM治疗通过调节免疫反应和肠道微生物群组成有效缓解dss诱导的结肠炎。这些发现强调PBM是一种很有前途的IBD非侵入性治疗策略,值得进一步的转化研究。
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引用次数: 0
Priming cancer cells via photobiomodulation at NIR wavelength to enhance photodynamic action: Insights into mechanistic alterations and cellular migration 通过近红外波长的光生物调节来激活癌细胞以增强光动力作用:机制改变和细胞迁移的见解
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-11 DOI: 10.1016/j.jphotobiol.2025.113336
Büşra Sirek , Nermin Topaloğlu
Photodynamic therapy (PDT) is a successful therapy for cancer treatment, especially for the superficial and easily reachable types, such as prostate cancer. During photodynamic activation, the light-sensitive chemical, which generally does not have a toxic effect on cells, can induce oxidative stress by producing reactive oxygen species (ROS). Nevertheless, the outcome of the therapy may be diminished by certain drawbacks. For this, PDT can be coupled with other therapies. Different light therapies can also serve as effective anticancer strategies. The combination of photobiomodulation (PBM) with PDT has become increasingly popular in cancer management. In the present study, PBM, which lacks anticancer activity, was combined with Chlorin e6 (Ce6)-mediated PDT. Underlying causes of additional deaths were elucidated by various mechanistic analyses, including ROS, nitric oxide (NO), mitochondrial membrane potential (ΔΨm), etc. PBM priming at an energy density of 5 J/cm2 resulted in up to 64 % additional cell death, as demonstrated by colorimetric and dual-staining analyses, and nearly a 100 % decrease in cell migration compared to PDT alone. Besides, PBM priming induced an additional 0.5-fold reduction in NO levels, a 19.4 % increase in ROS levels, and a 1.2 % reduction in ΔΨm compared to only PDT applications. Thus, combining PDT with PBM priming can provide a more effective therapeutic approach and significantly diminish the invasiveness of cancer cells.
光动力疗法(PDT)是一种成功的癌症治疗方法,特别是对于表面和容易到达的类型,如前列腺癌。在光动力激活过程中,通常对细胞没有毒性作用的光敏化学物质可以通过产生活性氧(ROS)诱导氧化应激。然而,这种疗法的效果可能会因某些缺陷而降低。为此,PDT可以与其他疗法结合使用。不同的光疗法也可以作为有效的抗癌策略。光生物调节(PBM)与PDT的结合在癌症治疗中越来越受欢迎。在本研究中,缺乏抗癌活性的PBM与氯e6 (Ce6)介导的PDT联合使用。通过各种机制分析,包括活性氧、一氧化氮(NO)、线粒体膜电位(ΔΨm)等,阐明了额外死亡的潜在原因。比色法和双染色分析表明,以5 J/cm2的能量密度启动PBM可导致高达64%的额外细胞死亡,并且与单独使用PDT相比,细胞迁移减少了近100%。此外,与仅应用PDT相比,PBM启动诱导NO水平降低0.5倍,ROS水平增加19.4%,ΔΨm降低1.2%。因此,PDT联合PBM启动可以提供更有效的治疗方法,并显著降低癌细胞的侵袭性。
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引用次数: 0
Intermittent blue light-dark cycles: A new strategy for enhancing triterpenoid production in medicinal Sanghuangporus vaninii 间歇性蓝-暗循环:提高药用桑黄茯苓三萜产量的新策略。
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-11 DOI: 10.1016/j.jphotobiol.2025.113338
Yanjun Ma , Rong Li , Jiahui Li , Zilu Song , Fawen She , Xiaoyan Ma , Xuetai Zhu
Triterpenoids from medicinal fungi have significant biological activities and industrial potential, but their low yield limits large-scale production. Sanghuangporus vaninii, a widely cultivated medicinal fungus, is a promising source of triterpenoids, yet the regulatory role of light-dark cycles in its triterpenoid biosynthesis remains unclear. In this study, we demonstrated that intermittent intense blue light-dark cycles (IB/D; ∼110 μmol/m2·s, 10 h/14 h) dramatically enhance triterpenoid production in S. vaninii MF5. IB/D treatment increased triterpenoid yield by 154 % compared to dark controls, also outperforming constant light or white light-dark regimens. Mechanistically, IB/D was associated with: (i) hyperbranching morphology (42 % reduced internode length); (ii) membrane remodeling via upregulated fatty acid desaturases and transporters, enhancing permeability 2.88-fold; and (iii) transcriptional activation of the mevalonate pathway, which was accompanied by a dramatic induction of endogenous 3-hydroxy-3-methylglutaryl-CoA synthase (HMGS) expression 4497-fold. Subsequent cloning and characterization of the SvHMGS gene-through sequence homology with known HMGS genes from Sanghuangporus species, identification of conserved HMGS domains, and prediction of its association with the mevalonic acid (MVA) pathway-suggested its potential conserved function in triterpenoid biosynthesis. This photoperiodic strategy represents a paradigm shift from constant light suppression to rhythmic induction, offering a scalable, low-cost approach to boost triterpenoid production in this medicinal fungus.
药用真菌中的三萜具有显著的生物活性和工业潜力,但其产量低,限制了其大规模生产。桑黄孢是一种广泛种植的药用真菌,是一种很有前途的三萜来源,但光暗循环在其三萜生物合成中的调节作用尚不清楚。在这项研究中,我们证明了间歇性强蓝光-暗循环(IB/D; ~ 110 μmol/m2·s, 10 h/14 h)显著提高了s . vaninii MF5的三萜产量。与黑暗对照相比,IB/D处理增加了154%的三萜产量,也优于恒定光照或白光-黑暗方案。在机制上,IB/D与:(i)超分枝形态(节间长度减少42%);(ii)通过脂肪酸去饱和酶和转运蛋白上调的膜重塑,使通透性提高2.88倍;(iii)甲羟戊酸途径的转录激活,这伴随着内源性3-羟基-3-甲基戊二酰辅酶a合成酶(HMGS)表达的显著诱导4497倍。随后,通过与桑黄孢子属已知HMGS基因的序列同源性、鉴定保守的HMGS结构域以及预测其与甲羟戊酸(MVA)途径的关联,对SvHMGS基因进行了克隆和鉴定,表明其在三萜生物合成中可能具有保守功能。这种光周期策略代表了从恒定的光抑制到有节奏的诱导的范式转变,提供了一种可扩展的、低成本的方法来促进这种药用真菌的三萜生产。
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引用次数: 0
Molecular mechanism underlying the modulated toxicity of differently charged and sized nanoplastics by bovine serum albumin 牛血清白蛋白调节不同电荷和大小纳米塑料毒性的分子机制。
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-11 DOI: 10.1016/j.jphotobiol.2025.113337
Xingren Pan , Xiaozhang Yu , Pengfei Qin , Wanni Yu
The extensively presence of nanoplastics raises concerns about their harm to ecosystems and human health. They are easy to absorb serum albumin to form corona during the transport process. However, the regulation of serum albumin to the toxicity of nanoplastics with differing charges and sizes remains unknown. We examined the molecular mechanism of polystyrene nanoplastics (PS-NPs) to bovine serum albumin (BSA) and how corona modulates the mouse primary hepatocyte damage. In cells exposed to 100 mg/L of large PS-NH2-NPs and PS-COOH-NPs, a significant reduction in cell viability of 27 % and 22 % was noted, respectively, under BSA-free conditions. In contrast, the reductions were limited to 17 % and 13 % in the presence of BSA. Additionally, BSA pretreatment also lowered the reactive oxygen species (ROS) levels compared to the use of two modified PS-NPs (200 nm) alone. However, the addition of BSA did not significantly alter the cell viability or the levels of ROS in small PS-NPs (80 nm). Molecular investigations demonstrated that PS-NPs mainly bound to the hydrophobic cavity of BSA through moderate hydrophobic forces with the binding affinity approximately 105 M−1. The formation of corona not only induced conformational changes in BSA but also modified its esterase activity. The molecular and cellular experiments both revealed the size and surface charge-specific toxicity pattern of nanoplastics. Big PS-NPs (200 nm) bound more tightly to the protein compared to small nanoplastics (80 nm), and PS-NH2-NPs presented a greater risk to BSA than PS-COOH-NPs. This study elucidates how BSA corona formation modulates nanoplastic toxicity in a size- and charge-dependent manner.
纳米塑料的广泛存在引起了人们对其对生态系统和人类健康的危害的关注。它们在运输过程中容易吸收血清白蛋白形成电晕。然而,血清白蛋白对不同电荷和大小的纳米塑料毒性的调节尚不清楚。我们研究了聚苯乙烯纳米塑料(PS-NPs)对牛血清白蛋白(BSA)的分子机制以及电晕如何调节小鼠原发性肝细胞损伤。在无bsa的条件下,暴露于100 mg/L大的PS-NH2-NPs和PS-COOH-NPs的细胞活力分别显著降低27%和22%。相比之下,在BSA存在的情况下,减少的幅度被限制在17%和13%。此外,与单独使用两种改性PS-NPs (200 nm)相比,BSA预处理还降低了活性氧(ROS)水平。然而,BSA的加入并没有显著改变小PS-NPs (80 nm)的细胞活力和ROS水平。分子研究表明,PS-NPs主要通过中等疏水力与BSA的疏水腔结合,结合亲合力约为105 M-1。冠状结构的形成不仅引起牛血清白蛋白构象的改变,而且改变了其酯酶活性。分子和细胞实验都揭示了纳米塑料的尺寸和表面电荷特异性毒性模式。大的PS-NPs (200 nm)比小的纳米塑料(80 nm)与蛋白质的结合更紧密,PS-NH2-NPs比PS-COOH-NPs对BSA的风险更大。本研究阐明了BSA电晕形成如何以尺寸和电荷依赖的方式调节纳米塑性毒性。
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引用次数: 0
Effects of wavelength, fluence, irradiance, and irradiation mode of visible light on melanogenesis in B16F10 melanoma cells 可见光波长、通量、辐照度和照射方式对B16F10黑色素瘤细胞黑色素生成的影响
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-06 DOI: 10.1016/j.jphotobiol.2025.113335
Tianxiu Lu, Diya Shen, Yu Tian, Zihao Zheng, Fusheng Li, Qiuyi Han, Shanduan Zhang
High-fluence visible light (VL) has been reported to induce cutaneous pigmentation similarly to ultraviolet radiation. However, VL is a polychromatic light composed of different wavelengths. More experimental studies are required to elucidate the effects of VL parameters on melanin synthesis. In this study, using murine B16F10 melanoma cells as an in vitro model, we systematically investigated how wavelength, fluence, irradiance and irradiation mode jointly determine the melanogenic response to VL. We revealed that 448 nm blue light stimulated melanogenesis, whereas 560–733 nm light globally suppressed it, with 595 nm yellow light exhibiting the strongest inhibition. Furthermore, a biphasic response was observed: both 560 nm and 595 nm yellow light inhibited melanogenesis at 3–12 J/cm2 but markedly enhanced it at 48 J/cm2. 595 nm light suppressed melanin synthesis at 5–20 mW/cm2, yet switched to stimulation at ≥ 40 mW/cm2. Additionally, our results suggested that the 595 nm pulsed PBM (3000 Hz, 40 %–80 % duty cycle) outperformed continuous PBM, whereas the 20 % duty cycle (with a peak irradiance of 25 mW/cm2) abolished the inhibitory effect, indicating that high irradiance activates pro-melanogenic defense pathways. Experimental data indicated that these differences arise primarily from the distinct effects of light parameters on tyrosinase activity and the mRNA levels of microphthalmia-associated transcription factor (MITF), TYR, TRP1, and TRP2. In conclusion, the regulatory effect of VL on melanogenesis is dependent on the selection of these parameters. These data provide an experimental basis for optimizing LED phototherapy parameters and support subsequent in-depth mechanistic studies in human cutaneous melanocytes. In the future, optimized VL parameters may balance the efficacy and safety of phototherapy in skin disorders caused by pigmentation dysregulation, such as vitiligo and melasma.
据报道,高通量可见光(VL)与紫外线辐射类似,可诱导皮肤色素沉着。然而,VL是由不同波长组成的多色光。VL参数对黑色素合成的影响还需要更多的实验研究来阐明。本研究以小鼠B16F10黑色素瘤细胞为体外模型,系统研究了波长、辐照度、辐照度和辐照方式如何共同影响VL对黑色素生成的影响。我们发现,448 nm的蓝光刺激黑色素生成,而560-733 nm的光在整体上抑制黑色素生成,其中595 nm的黄光抑制作用最强。此外,观察到双相反应:560 nm和595 nm黄光在3-12 J/cm2时抑制黑素生成,但在48 J/cm2时显著增强黑素生成。595 nm光在5-20 mW/cm2时抑制黑色素合成,但在≥40 mW/cm2时转为刺激。此外,我们的研究结果表明,595 nm脉冲PBM (3000 Hz, 40% - 80%占空比)优于连续PBM,而20%占空比(峰值辐照度为25 mW/cm2)消除了抑制作用,表明高辐照度激活了促黑色素生成防御途径。实验数据表明,这些差异主要是由于光照参数对酪氨酸酶活性和小眼相关转录因子(MITF)、TYR、TRP1和TRP2 mRNA水平的不同影响。综上所述,VL对黑色素形成的调控作用取决于这些参数的选择。这些数据为优化LED光疗参数提供了实验基础,并支持后续在人类皮肤黑色素细胞中的深入机制研究。在未来,优化的VL参数可能会平衡光疗在白癜风和黄褐斑等色素沉着失调引起的皮肤疾病中的疗效和安全性。
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引用次数: 0
Femtosecond laser and bee venom as promising anti-arthritic treatments: Modulation of JAK/STAT and PI3K/AKT/mTOR signaling pathways in vivo 飞秒激光和蜂毒作为有前景的抗关节炎治疗:体内JAK/STAT和PI3K/AKT/mTOR信号通路的调节
IF 3.7 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-12-05 DOI: 10.1016/j.jphotobiol.2025.113334
Jihad M. El-Sayed , Sally M. Khadrawy , Hanaa M. Mohamed , Magdy Sayed Aly , Abdelwahab Khalil , Dina Sabry , Tarek Mohamed
Rheumatoid arthritis (RA) is a chronic condition characterized by joint degradation and systemic manifestations, which increase the risk of mortality and disability. This study compared the effects of bee venom (BV; subcutaneously administered at 1 mg/kg) and femtosecond laser irradiation (FSL; 830 nm wavelength, 200 mW power, 120 s exposure time, 0.8 cm2 beam area with a 0.5 cm radius, 0.25 W/cm2 power density, and 30 J/cm2 energy dose), either individually or in combination, on arthritic rats. Forty-two adult male Wistar rats were allocated into seven groups. Groups 1–3 served as the negative control, BV, and FSL groups, respectively, while group 4 functioned as the arthritic model group that received 100 μL/rat of complete Freund's adjuvant (CFA) in the right hind paw. Groups 5–7 included arthritic rats treated with BV, FSL, or their combination, respectively. Histological examination of RA development, showing synovitis, cellular infiltration, and cartilage degeneration. Treatment with BV injections and FSL irradiation significantly reduced right hind paw edema, improved histological abnormalities, and reduced serum levels of C-reactive protein (CRP) and rheumatoid factor (RF), alongside decreased tissue expressions of TNF-α, NF-KB, and IL-6 in the affected ankle joints. Moreover, both treatments mitigated oxidative stress, reduced DNA damage, and regulated PI3K/AKT/mTOR and JAK/STAT signaling pathways. Collectively, FSL, either alone or in combination with BV, demonstrated a superior capacity for cartilage regeneration and tissue repair. This highlights BV and FSL as a promising RA therapy, addressing underlying mechanisms beyond symptom relief.
类风湿性关节炎(RA)是一种以关节退化和全身表现为特征的慢性疾病,它增加了死亡和残疾的风险。本研究比较了蜂毒(BV;皮下注射剂量为1mg /kg)和飞秒激光照射(FSL; 830nm波长,200mw功率,120s照射时间,0.8 cm2光束面积,0.5 cm半径,0.25 W/cm2功率密度,30 J/cm2能量剂量)单独或联合对关节炎大鼠的影响。将42只成年雄性Wistar大鼠分为7组。1 ~ 3组分别作为阴性对照组、BV组和FSL组,4组作为关节炎模型组,右后爪给予100 μL/大鼠完全弗氏佐剂(CFA)。5-7组分别用BV、FSL或两者联合治疗关节炎大鼠。类风湿关节炎的组织学检查显示滑膜炎、细胞浸润和软骨变性。BV注射和FSL照射治疗可显著减轻右后足水肿,改善组织学异常,降低血清c反应蛋白(CRP)和类风湿因子(RF)水平,同时降低受影响踝关节组织中TNF-α、NF-KB和IL-6的表达。此外,这两种处理都减轻了氧化应激,减少了DNA损伤,并调节了PI3K/AKT/mTOR和JAK/STAT信号通路。总的来说,无论是单独使用FSL还是与BV联合使用FSL,都显示出更强的软骨再生和组织修复能力。这突出了BV和FSL作为一种有希望的RA治疗方法,解决了症状缓解之外的潜在机制。
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引用次数: 0
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Journal of photochemistry and photobiology. B, Biology
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