Tissue & cell最新文献_第7页

NFYA transcriptionally activates GPX4 inhibiting ferroptosis in colorectal cancer NFYA转录激活GPX4抑制结直肠癌铁下垂

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2026-01-13 DOI: 10.1016/j.tice.2026.103325

Qingzhu Yang , Shuo Sun , Shuwei Dang , Zeyan Li , Lixue Feng , Qiaoyi Yang , Yanyan Sun , Xin Huang , Weiwei Zhang , Zhicheng Zhang , Guodong Li

Background

Nuclear transcription factor Y subunit α (NFYA) has been reported to play functional roles in a range of malignancies, while its precise mechanistic function in the context of colorectal cancerer (CRC) progression has yet to be established.

Methods

TIMER2, UALCAN, and Kaplan-Meier Plotter databases were leveraged to evaluate the expression of NFYA and to gauge its prognostic relevance in CRC. Determine NFYA and glutathione peroxidase 4 (GPX4) expression in cell lines (NCM460, DLD1 and HCT116) and clinical samples using Quantitative Real-time PCR (qPCR) and western immunoblotting assay. Assessment of cell viability, proliferation, and migration involved MTT, EdU staining assay, colony formation, and flow cytometry. Malondialdehyde (MDA) content and lipid reactive oxygen species (ROS) levels were assessed using specialized kits. Mitochondrial ultrastructural changes were observed using transmission electron microscopy (TEM). The transcriptional regulation of GPX4 by NFYA was investigated through Luciferase reporter assays and Chromatin Immunoprecipitation Assay (ChIP) experiments.

Results

Higher levels of NFYA were expressed in CRC cells and clinical samples, and the upregulation of this target was associated with a worse prognostic outcome for patients with CRC. In vitro,the inhibition of NFYA expression impaired CRC cell proliferative and migratory activity. NFYA was found to function in part by binding to the GPX4 promoter and activating transcription, leading to an increase in GPX4 levels and consequent reductions in lipid peroxide levels and ferroptosis. NFYA binds to the promoter region of GPX4, regulating the transcription of GPX4. In the recovery experiment, inhibition of NFYA-induced ferroptosis in cells was reversed by GPX4. Correspondingly, the ferroptosis caused by GPX4 suppression can be reversed by NFYA.

Conclusion

NFYA is thus a promising target for therapies aimed at treating CRC. NFYA is a key regulator of ferroptosis resistance in CRC while also providing direct mechanistic insights into the oncogenic function that this protein plays in these tumor cells. NFYA/GPX4 may be one of the underlying reasons for malignant growth of CRC cells.

核转录因子Y亚单位α (NFYA)已被报道在一系列恶性肿瘤中发挥功能作用，而其在结直肠癌（CRC）进展中的确切机制功能尚未确定。方法利用stimer2、alcan和Kaplan-Meier Plotter数据库评估NFYA的表达，并评估其与CRC预后的相关性。采用定量实时荧光定量PCR （qPCR）和western免疫印迹法检测NFYA和谷胱甘肽过氧化物酶4 （GPX4）在NCM460、DLD1和HCT116细胞系及临床样品中的表达。细胞活力、增殖和迁移的评估包括MTT、EdU染色法、菌落形成和流式细胞术。使用专用试剂盒评估丙二醛（MDA）含量和脂质活性氧（ROS）水平。透射电镜观察线粒体超微结构变化。通过荧光素酶报告基因检测和染色质免疫沉淀实验（ChIP）研究NFYA对GPX4的转录调控作用。结果更高水平的NFYA在CRC细胞和临床样本中表达，该靶点的上调与CRC患者更差的预后结果相关。在体外，抑制NFYA表达会损害结直肠癌细胞的增殖和迁移活性。研究发现NFYA的部分功能是通过与GPX4启动子结合并激活转录，导致GPX4水平增加，随后脂质过氧化水平降低和铁下垂。NFYA结合GPX4的启动子区域，调节GPX4的转录。在恢复实验中，GPX4逆转了nfya诱导的细胞铁下垂的抑制作用。相应的，NFYA可以逆转GPX4抑制引起的铁下垂。结论nfya是治疗结直肠癌的一个有希望的靶点。NFYA是CRC中铁下沉耐药性的关键调节因子，同时也为该蛋白在这些肿瘤细胞中的致癌功能提供了直接的机制见解。NFYA/GPX4可能是CRC细胞恶性生长的潜在原因之一。

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引用次数: 0

The dual regulation of mitophagy in myocardial injury: From molecular mechanisms to targeted therapies 心肌损伤中线粒体自噬的双重调控：从分子机制到靶向治疗

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2026-01-08 DOI: 10.1016/j.tice.2026.103318

Haiyan Yang , Lei Zhang , Haixia Qian

Cardiovascular diseases (CVDs) are the leading cause of death worldwide, far exceeding other diseases such as cancer. Myocardial injury is a key link in various CVDs; reducing myocardial injury is an effective means of preventing and treating CVDs. Mitochondrial dysfunction is the pathological basis of various CVDs. Mitophagy, as a process that selectively eliminates damaged or dysfunctional mitochondria, is of enormous significance in maintaining the normal function and structure of mitochondria in cardiomyocytes and alleviating myocardial injury. Therefore, this review systematically analyzes the role of mitophagy in myocardial injury, explores targeted intervention strategies, and hopes to provide a theoretical basis and effective therapeutic targets for clinical practice.

心血管疾病（cvd）是全世界导致死亡的主要原因，远远超过癌症等其他疾病。心肌损伤是各种心血管疾病的关键环节；减少心肌损伤是预防和治疗心血管疾病的有效手段。线粒体功能障碍是各种心血管疾病的病理基础。线粒体自噬作为一种选择性清除受损或功能失调线粒体的过程，对维持心肌细胞线粒体的正常功能和结构，减轻心肌损伤具有重要意义。因此，本文系统分析线粒体自噬在心肌损伤中的作用，探索有针对性的干预策略，希望能为临床实践提供理论依据和有效的治疗靶点。

引用次数: 0

U0126 induces osteoclast differentiation via the p38-NFATc-1 signaling pathway U0126通过p38-NFATc-1信号通路诱导破骨细胞分化。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-12-05 DOI: 10.1016/j.tice.2025.103263

Jiran Wang , Jinan Liu , Xueting Jia , Guangyong Chen , Shuzhen Chen , Xiaofeng Huang

Osteoclast differentiation plays an important role in bone metabolic diseases, such as osteoporosis, osteosclerosis and so on. In the study, we found that the ERK inhibitor, U0126, significantly increased the number of multinucleated osteoclasts after inducing differentiation of mouse mononuclear macrophage RAW264.7 cells. The Shh-p38-NFATc-1 signaling pathway has been reported to induce osteoclast differentiation in our previous work, and here U0126 also could increase pp38 and NFATc-1 expression as well as NFATc-1 entrance into the nucleus. Animal experiment demonstrated that U0126 accelerated tooth eruption in newborn mice and promoted alveolar bone resorption by inducing osteoclastogenesis. Furthermore, U0126 can rescue delayed tooth eruption caused by LDE225 (a Shh inhibitor) suppression of the p38 signaling pathway. Cytological experiments also revealed that U0126 could rescue the osteoclastic inhibitory effect of LDE225, but not Doramapimod (a p38 inhibitor). Therefore, we conclude that U0126 promotes osteoclast differentiation via the p38-NFATc-1 signaling pathway and relieves the inhibitory effect of LDE225 on osteoclastogenesis. Our study may provide a scientific foundation for dental treatment strategies to enhance osteoclast function in addressing tooth eruption issues, such as impacted teeth, delayed eruption of permanent teeth, and cranioclavicular dysplasia syndrome (CCD). It will also serve as a method for future research into novel approaches to treating disorders linked to bone metabolism.

破骨细胞分化在骨质疏松、骨硬化等骨代谢性疾病中起着重要作用。在本研究中，我们发现ERK抑制剂U0126诱导小鼠单核巨噬细胞RAW264.7细胞分化后，明显增加了多核破骨细胞的数量。在我们之前的工作中已经报道了sh -p38-NFATc-1信号通路诱导破骨细胞分化，而U0126也可以增加pp38和NFATc-1的表达以及NFATc-1进入细胞核。动物实验表明，U0126通过诱导破骨细胞生成，加速新生小鼠牙萌出，促进牙槽骨吸收。此外，U0126可以挽救由LDE225（一种Shh抑制剂）抑制p38信号通路引起的延迟出牙。细胞学实验也显示，U0126能恢复LDE225的破骨抑制作用，而对p38抑制剂Doramapimod不起作用。因此，我们认为U0126通过p38-NFATc-1信号通路促进破骨细胞分化，减轻LDE225对破骨细胞发生的抑制作用。本研究可为提高破骨细胞功能，解决埋伏牙、恒牙延迟萌牙、锁骨发育不良综合征（CCD）等牙齿萌牙问题提供科学依据。它还将为未来研究治疗与骨代谢有关的疾病的新方法提供一种方法。

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引用次数: 0

The dual role of autophagy in breast cancer stemness and treatment resistance 自噬在乳腺癌发病和治疗耐药中的双重作用

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-12-16 DOI: 10.1016/j.tice.2025.103279

Anu Jayanthi Panicker , Kirti S. Prabhu , Ummu Habeeba , Zahwa Mariyam , Affan Asim , Sarada Prasad Dakua , Shahab Uddin

Autophagy is a fundamental, highly conserved cellular process with a complex dual role in breast cancer progression and therapy resistance. Initially, autophagy functions as a tumor suppressor by maintaining genomic stability through clearance of damaged organelles and reducing oxidative stress, preventing tumor initiation. In established tumors, autophagy supports cancer cell survival under metabolic stress, sustains cancer stem cell stemness, and facilitates adaptation to hypoxia and nutrient deprivation in the tumor microenvironment. This pro-survival role enhances tumor growth, metastasis, and resistance to chemotherapy, radiotherapy, and targeted therapies. Autophagy extensively interacts with key signaling pathways governing cancer stem cell renewal and immune evasion, underscoring its multifaceted impact on tumor biology. Given its pivotal role, autophagy modulation via established inhibitors such as chloroquine alone and in combination with several other novel agents are under clinical investigation to investigate if its action that could be used to overcome therapy resistance and improve patient outcomes in breast cancer.

自噬是一个基本的、高度保守的细胞过程，在乳腺癌的进展和治疗抵抗中具有复杂的双重作用。最初，自噬作为肿瘤抑制因子，通过清除受损细胞器和减少氧化应激来维持基因组的稳定性，防止肿瘤的发生。在已建立的肿瘤中，自噬支持肿瘤细胞在代谢应激下存活，维持肿瘤干细胞的干性，并促进肿瘤微环境中对缺氧和营养剥夺的适应。这种促进生存的作用增强了肿瘤的生长、转移和对化疗、放疗和靶向治疗的耐药性。自噬广泛地与控制癌症干细胞更新和免疫逃避的关键信号通路相互作用，强调其对肿瘤生物学的多方面影响。鉴于其关键作用，通过已有的抑制剂如氯喹单独或与其他几种新型药物联合进行自噬调节正在进行临床研究，以研究其作用是否可用于克服治疗耐药并改善乳腺癌患者的预后。

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引用次数: 0

Fibrin hydrogel incorporated with microspheres containing vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) accelerated the healing of diabetic wounds in rats 纤维蛋白水凝胶掺入含有血管内皮生长因子（VEGF）和碱性成纤维细胞生长因子（bFGF）的微球可促进大鼠糖尿病伤口的愈合

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-12-29 DOI: 10.1016/j.tice.2025.103301

Abdullah Albelasi , Suad A. Alghamdi , Mohammed Alissa

Diabetic wounds are characterized by delayed healing due to impaired angiogenesis, chronic inflammation, and defective extracellular matrix formation. This study evaluated the therapeutic potential of a fibrin hydrogel incorporating microspheres loaded with vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) (FHM) in promoting wound repair in a streptozotocin-induced diabetic rat model. Rats were randomly assigned to control, fibrin hydrogel alone (FH), or FHM groups, and wounds were assessed on days 7 and 14. Mechanical properties, stereological parameters, collagen deposition, and cytokine expression were analyzed. FHM treatment significantly improved tensile strength and stress-bearing capacity of the wound tissue compared to FH and control groups (P < 0.05). Stereological analysis revealed increased fibroblast proliferation and neovascularization, with a concomitant reduction in inflammatory cell infiltration in FHM-treated wounds at both time points (P < 0.05). Masson's trichrome staining demonstrated enhanced collagen deposition and maturation in the FHM group, indicating improved extracellular matrix remodeling. Molecular analysis showed elevated transforming growth factor beta (TGF-β) and VEGF expression, alongside decreased pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β), suggesting a dual effect of promoting regeneration while attenuating inflammation. This multimodal approach holds promise as a potential therapeutic strategy for chronic diabetic wounds, offering both functional and structural benefits. Further long-term studies and clinical translation are warranted to evaluate safety and efficacy in human patients.

糖尿病伤口的特点是由于血管生成受损、慢性炎症和细胞外基质形成缺陷而延迟愈合。本研究评估了含有血管内皮生长因子（VEGF）和碱性成纤维细胞生长因子（bFGF）微球的纤维蛋白水凝胶在链脲佐菌素诱导的糖尿病大鼠模型中促进伤口修复的治疗潜力。将大鼠随机分为对照组、纤维蛋白水凝胶组和纤维蛋白水凝胶组，分别于第7天和第14天进行伤口评估。分析其力学性能、体视参数、胶原沉积和细胞因子表达。与FH组和对照组相比，FHM处理显著提高了创面组织的抗拉强度和应力承载能力（P <； 0.05）。体视学分析显示，在两个时间点，fhm治疗的伤口中，成纤维细胞增殖和新生血管形成增加，同时炎症细胞浸润减少（P <； 0.05）。马松三色染色显示FHM组胶原沉积和成熟增强，表明细胞外基质重塑改善。分子分析显示，转化生长因子β (TGF-β)和VEGF表达升高，促炎细胞因子肿瘤坏死因子α (TNF-α)和白细胞介素-1β (IL-1β)表达降低，提示具有促进再生和减轻炎症的双重作用。这种多模式方法有望成为慢性糖尿病伤口的潜在治疗策略，提供功能和结构上的好处。需要进一步的长期研究和临床转化来评估人类患者的安全性和有效性。

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引用次数: 0

Engineering bone regeneration: Strontium fluorophosphate, incorporation into collagen and gelatin-based hydrogels promotes osteogenesis in human adipose-derived mesenchymal stem cells 工程骨再生：将氟磷酸锶掺入胶原蛋白和明胶水凝胶中，可促进人脂肪来源的间充质干细胞成骨

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-12-22 DOI: 10.1016/j.tice.2025.103292

Sahel Noori , Faezeh Norouz , Raheleh Halabian , Hossein Aghamollaei , Elahe Eftekhari , Ali Salimi

Background

The incorporation of nanoparticles into hydrogels enhances their properties for biomedical applications. Strontium can enhance osteogenesis through osteoblast formation by substituting calcium in osteoblast-mediated processes.

Materials and methods

Collagen-gelatin hydrogels (COL-GEL) were synthesized with and without strontium fluorophosphate (SrFP) to study their effect on osteogenic differentiation of adipose-derived mesenchymal stem cells (AD-MSCs). Scaffolds were characterized using XRD and FTIR. Biocompatibility of SrFP and scaffolds was assessed using the MTT assay and acridine orange. Their osteogenic differentiation potential was evaluated by ALP activity, calcium content, alizarin red, von Kossa staining, real-time RT-PCR and immunocytochemistry.

Results

SrFP at 50 μg/ml significantly promoted proliferation by 1.5-fold over 3 days. The COL-GEL-0.1 %SrFP scaffold showed higher cell proliferation compared to COL-GEL-0.5 %SrFP. The COL-GEL-SrFP exhibited high ALP activity (1.5-fold enhancement) and calcium content (2.1-fold enhancement), consistent with the results of alizarin red (p ≤ 0.05) and von Kossa (p ≤ 0.01). Gene and protein analyses revealed the elevated levels of ALP, Col-I (1.6-fold), osteocalcin (1.7-fold) and RUNX2 (2.3-fold) gene expression, as well as a significant upregulation of osteocalcin and osteopontin protein levels (more than 3-fold) in the COL-GEL-SrFP after 14 day-differentiation.

Conclusion

Compared to the COL-GEL hydrogel, the COL-GEL-SrFP improved cell-scaffold interactions and demonstrated more effective osteogenic differentiation. These findings suggest that COL-GEL-SrFP represents a promising and biocompatible scaffold for increasing the osteogenic differentiation of AD-MSCs and subsequent mineralization. This study highlights the potential of collagen and gelatin-based hydrogels incorporated with SrFP nanoparticles as a novel alternative to current therapeutic approaches in bone regenerative medicine.

纳米颗粒掺入水凝胶增强了其生物医学应用的性能。锶可以通过在成骨细胞介导的过程中取代钙来促进成骨细胞的形成。材料与方法合成含氟磷酸锶（SrFP）和不含氟磷酸锶（SrFP）的胶原明胶水凝胶（COL-GEL），研究其对脂肪源性间充质干细胞（AD-MSCs）成骨分化的影响。采用XRD和FTIR对支架进行了表征。采用MTT法和吖啶橙评价SrFP与支架的生物相容性。通过ALP活性、钙含量、茜素红、von Kossa染色、实时RT-PCR和免疫细胞化学评价其成骨分化潜力。结果50 μg/ml的ssrfp在3 d内显著促进细胞增殖1.5倍。与COL-GEL-0.5 %SrFP相比，COL-GEL-0.1 %SrFP支架的细胞增殖能力更高。COL-GEL-SrFP表现出较高的ALP活性（提高1.5倍）和钙含量（提高2.1倍），与茜素红（p ≤ 0.05）和von Kossa （p ≤ 0.01）的结果一致。基因和蛋白分析显示，分化14天后，COL-GEL-SrFP中ALP、col - 1（1.6倍）、骨钙素（1.7倍）和RUNX2（2.3倍）基因表达水平升高，骨钙素和骨桥蛋白水平显著上调（3倍以上）。结论与COL-GEL水凝胶相比，COL-GEL- srfp改善了细胞-支架的相互作用，并表现出更有效的成骨分化。这些发现表明，COL-GEL-SrFP是一种很有前途的生物相容性支架，可以促进AD-MSCs的成骨分化和随后的矿化。这项研究强调了胶原蛋白和明胶基水凝胶与SrFP纳米颗粒结合的潜力，作为当前骨再生医学治疗方法的一种新的替代方案。

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引用次数: 0

Immunohistochemical distribution of extracellular signal-regulated kinase 1 and 2 (ERK1/2) in the rat carotid body 细胞外信号调节激酶1和2 （ERK1/2）在大鼠颈动脉体中的免疫组织化学分布

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-11-23 DOI: 10.1016/j.tice.2025.103247

Hiroki Saito, Takuya Yokoyama , Nobuaki Nakamuta, Yoshio Yamamoto

The sensitivity of the carotid body to hypoxic stimuli is enhanced by chronic intermittent hypoxia. Since extracellular signal-regulated kinase 1/2 (ERK1/2) may be involved in hypoxic responses and in sensory nerve facilitation induced by intermittent hypoxic stimuli, we examined the distribution of ERK1/2 in male Wistar rat carotid body. The results of RT-PCR and immunoblotting indicated that ERK1 and ERK2 were both expressed in the carotid body at the mRNA and protein levels. Immunoblotting also detected intense bands for phosphorylated ERK1 in the carotid body. Immunoreactivity for ERK1/2 was ubiquitously distributed in chemoreceptor cell clusters. Immunoreactivity for phosphorylated ERK1/2 (pERK1/2) was intense in some vesicular nucleotide transporter-immunoreactive chemoreceptor cells and in most P2X₂ purinoceptor-immunoreactive sensory nerve endings. In addition, pERK1/2 localization to the nuclei of chemoreceptor cells and sustentacular cells was observed. Immunoreactivity for pERK1/2 was intense in the vesicular glutamate transporter 2-immunoreactive areas of sensory nerve endings. These results suggest that ERK1/2 regulate hypoxic responses and sensitivity through the phosphorylation of their substrates in chemoreceptor cells and sensory nerve endings. ERK1/2 may be involved in transmission and sensory nerve facilitation in chemoreceptor cells and sensory nerve endings.

慢性间歇性缺氧可增强颈动脉体对缺氧刺激的敏感性。由于细胞外信号调节激酶1/2 （ERK1/2）可能参与缺氧反应和间歇性缺氧刺激诱导的感觉神经易化，我们检测了ERK1/2在雄性Wistar大鼠颈动脉体中的分布。RT-PCR和免疫印迹分析结果显示，ERK1和ERK2在颈动脉小体中mRNA和蛋白水平均有表达。免疫印迹也检测到颈动脉体磷酸化ERK1的强烈条带。ERK1/2的免疫反应性普遍分布在化学受体细胞簇中。磷酸化ERK1/2 （pERK1/2）在一些囊状核苷酸转运体免疫反应性化学受体细胞和大多数P2X2嘌呤受体免疫反应性感觉神经末梢中具有强烈的免疫反应性。此外，还观察到pERK1/2在化学受体细胞和支撑细胞细胞核中的定位。pERK1/2在感觉神经末梢的水疱性谷氨酸转运蛋白2免疫反应区具有强烈的免疫反应性。这些结果表明，ERK1/2通过磷酸化其在化学受体细胞和感觉神经末梢中的底物来调节缺氧反应和敏感性。ERK1/2可能参与化学受体细胞和感觉神经末梢的传递和感觉神经易化。

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引用次数: 0

The unique biogenesis pathway of extracellular vesicles in Hirudo nipponia salivary gland cells 日本水蛭唾液腺细胞胞外囊泡的独特生物发生途径。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-12-24 DOI: 10.1016/j.tice.2025.103296

Ya-Li Zhu, Meng-Xiang Jia, Ru-Yu Qu, Qian Li, Xia Qiu, Wen-Chen Zhao, Yuan-Yuan Luo

Extracellular vesicles (EVs) serve as crucial vehicles for the intercellular transfer of bioactive molecules. While the mechanisms of EV biogenesis are well characterized in mammals, they remain comparatively understudied in invertebrates. This knowledge gap is particularly notable for the medicinal leech, Hirudo nipponia. In this study, the ultrastructural features of Hirudo nipponia salivary glands in resting and secretory states were analyzed using scanning and transmission electron microscopy to investigate the biogenesis and release of EVs. For the first time, it is demonstrated that salivary gland cells possess dual pathways for EV biogenesis: a classical pathway and a unique pathway derived from secretory granules. These findings provide critical morphological evidence for the conservation of EV biogenesis in invertebrates and highlight a key secretory adaptation for specialized physiological functions.

细胞外囊泡（EVs）是生物活性分子在细胞间转移的重要载体。虽然EV的生物发生机制在哺乳动物中有很好的特征，但在无脊椎动物中的研究相对较少。这种知识差距对于药用水蛭日本水蛭来说尤其明显。本研究利用扫描电镜和透射电镜对日本水蛭静息和分泌状态下唾液腺的超微结构特征进行了分析，探讨了EVs的生物发生和释放。首次证明唾液腺细胞具有EV生物发生的双重途径：经典途径和来源于分泌颗粒的独特途径。这些发现为无脊椎动物EV生物发生的保护提供了重要的形态学证据，并强调了特殊生理功能的关键分泌适应。

引用次数: 0

Nifuroxazide attenuates bisphenol A–induced male reproductive toxicity by modulating oxidative stress, inflammation, and Nrf2/HO-1 and necroptosis pathways Nifuroxazide通过调节氧化应激、炎症、Nrf2/HO-1和坏死性坏死途径减轻双酚a诱导的男性生殖毒性。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-11-18 DOI: 10.1016/j.tice.2025.103235

Mohammed A. Alzoghaibi , Emad H.M. Hassanein , Mohammed F. Alotaibi , Abdullah M. Alzoghaibi , Hanan S. Althagafy , Hamada S. Qebesy , Amr M.T. Allam , Ayman M. Mahmoud

Bisphenol A (BPA) is a widely used industrial chemical with endocrine-disrupting properties. BPA is linked to male reproductive dysfunction through oxidative stress and cell death pathways. The intestinal antimicrobial nifuroxazide (NFZ) has recently been reported to possess antioxidant and anti-inflammatory activities. This study investigated whether NFZ protects against BPA-induced testicular dysfunction in rats, with a focus on redox imbalance, inflammatory signaling, and necroptosis. Adult male Wistar rats were divided into four groups: control, NFZ, BPA, and BPA + NFZ. Animals received daily oral NFZ, BPA, or both for 28 days, and samples were collected. BPA exposure induced pronounced testicular injury characterized by degenerative changes in seminiferous tubules, thickened basement membrane, collagen accumulation, and impaired sperm parameters. Hormonal analysis showed significant reductions in FSH, LH, and testosterone, along with downregulation of steroidogenic genes (StAR, 3β-HSD, 17β-HSD, and CYP17A1). BPA also increased lipid peroxidation, decreased antioxidant defenses, and upregulated NF-κB p65 and proinflammatory cytokines. Furthermore, BPA promoted necroptosis by elevating testicular RIP1, RIP3, MLKL, and caspase-8, while disrupting the Keap1/Nrf2/HO-1 pathway. NFZ markedly counteracted these effects, restoring testicular histoarchitecture, improving sperm quality, normalizing hormone levels, suppressing oxidative and inflammatory responses, attenuating necroptotic signaling, and activating Nrf2/HO-1-mediated cytoprotection. In conclusion, NFZ provides significant protection against BPA-induced testicular toxicity by targeting oxidative stress, inflammatory signaling, and necroptosis, in part through activation of the Keap1/Nrf2/HO-1 axis. These findings suggest NFZ as a promising candidate for preserving male reproductive health in the context of environmental toxicant exposure.

双酚A （BPA）是一种广泛使用的具有内分泌干扰特性的工业化学品。BPA通过氧化应激和细胞死亡途径与男性生殖功能障碍有关。肠道抗菌剂硝呋肼（NFZ）最近被报道具有抗氧化和抗炎活性。本研究探讨了NFZ是否对bpa诱导的大鼠睾丸功能障碍有保护作用，重点关注氧化还原失衡、炎症信号传导和坏死性坏死。成年雄性Wistar大鼠分为对照组、NFZ组、BPA组和BPA + NFZ组。动物每天口服NFZ、BPA或两者同时口服28天，并收集样本。双酚a暴露导致睾丸明显损伤，表现为精小管变性改变、基底膜增厚、胶原蛋白积累和精子参数受损。激素分析显示FSH、LH和睾酮显著降低，类固醇基因（StAR、3β-HSD、17β-HSD和CYP17A1）下调。BPA还会增加脂质过氧化，降低抗氧化防御，上调NF-κB p65和促炎细胞因子。此外，BPA通过提高睾丸RIP1、RIP3、MLKL和caspase-8来促进坏死坏死，同时破坏Keap1/Nrf2/HO-1通路。NFZ显著抵消了这些影响，恢复睾丸组织结构，改善精子质量，使激素水平正常化，抑制氧化和炎症反应，减弱坏死信号，激活Nrf2/ ho -1介导的细胞保护。综上所述，NFZ通过激活Keap1/Nrf2/HO-1轴，通过靶向氧化应激、炎症信号和坏死性坏死，对bpa诱导的睾丸毒性具有显著的保护作用。这些发现表明，在环境毒物暴露的背景下，NFZ是一种有希望的保护男性生殖健康的候选者。

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引用次数: 0

Innovative approaches for microfluidics techniques in tissue engineering and revolutionizing sports medicine: Enhancing athletic performance and recovery using finite element and statistical analysis 微流体技术在组织工程和革命性运动医学中的创新方法：利用有限元和统计分析提高运动表现和恢复。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-11-27 DOI: 10.1016/j.tice.2025.103251

Yu Ruida , Rong Siyu , Qi Yufei , A. Shahbaz , Sh. Baghaei

Microfluidics is the science and technology of systems that process tiny amounts of fluid using channels with dimensions ranging from 10 to 100 micrometers. This field addresses the behavior, precise control, and maintenance of fluids geometrically constrained to small scales, typically below the millimeter range. Microfluidic systems collaborate with various disciplines to design diverse applications. Microfluidics is inherently interdisciplinary, encompassing fields such as medicine, physics, biology, materials science, mechanical engineering, and electronics. Key drivers of microfluidics include molecular analysis, biosafety, molecular biology, and microelectronics. Microchannels can be fabricated on various substrates, including glass, polymers, plastics, ceramics, and metals. Fluid behavior at the micro-scale differs from the macro-scale due to low thermal mass and high surface-to-volume ratios, leading to rapid heat transfer and precise temperature control. Significant advancements in microfluidics were limited until recent decades, when researchers conducted extensive studies to develop new microfluidic components. This work employs Finite Element Analysis (FEA) to model fluid dynamics in key microfluidic systems. Complementarily, a statistical analysis of design parameters quantifies a critical performance trade-off, providing a data-driven framework for optimizing devices towards either high-throughput efficiency or high-precision measurement for targeted applications in sports medicine. The Lab-on-a-Chip (LOC) paradigm represents an integrative framework of cohesive unit operations engineered to provide precise, expedient, and efficient control within biological and chemical domains. Microfluidic technology holds immense potential to revolutionize healthcare, from diagnostics and therapeutics to regenerative and sport medicine. As a result, microfluidic technologies are set to revolutionize sports medicine, fostering a new era of tailored health management and sport performance optimization.

微流体学是一门科学和系统技术，它使用尺寸范围从10到100微米的通道处理微量流体。该领域解决了流体的行为、精确控制和维护问题，这些流体的几何尺寸通常小于毫米。微流控系统与不同学科合作设计不同的应用。微流体学本质上是跨学科的，涵盖了医学、物理学、生物学、材料科学、机械工程和电子学等领域。微流控的主要驱动力包括分子分析、生物安全、分子生物学和微电子学。微通道可以在各种基板上制造，包括玻璃、聚合物、塑料、陶瓷和金属。微观尺度下的流体行为不同于宏观尺度，这是由于低热质量和高表面体积比，从而导致快速的传热和精确的温度控制。直到最近几十年，当研究人员进行了广泛的研究以开发新的微流控元件时，微流控的重大进展才受到限制。本工作采用有限元分析（FEA）来模拟关键微流体系统的流体动力学。此外，设计参数的统计分析量化了关键性能权衡，为优化设备提供了数据驱动的框架，以实现高通量效率或高精度测量，用于运动医学的目标应用。芯片实验室（LOC）范例代表了一个内聚单元操作的综合框架，旨在在生物和化学领域提供精确，方便和有效的控制。从诊断和治疗到再生和运动医学，微流控技术具有巨大的潜力，可以彻底改变医疗保健。因此，微流控技术将彻底改变运动医学，开创量身定制的健康管理和运动表现优化的新时代。

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