Tissue & cell最新文献_第9页

HAX1 overexpression induces osteogenic differentiation of periodontal ligament stem cells via the MEK/ERK signaling cascade HAX1过表达通过MEK/ERK信号级联诱导牙周韧带干细胞成骨分化

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2026-01-06 DOI: 10.1016/j.tice.2026.103311

Peiqi Hao , Xin-yu Zhang , Mengting Wang, Fan Bao, Hui Guo

Background

Periodontitis is characterized by periodontal tissue destruction and subsequent tooth loss, significantly impacting quality of life. The potential of HAX1, a gene implicated in periodontitis pathogenesis, to modulate the differentiation of periodontal ligament stem cells (PDLSCs) and its therapeutic potential remains unexplored.

Methods

PDLSCs were randomly divided into seven experimental groups, undergoing either HAX1 overexpression or knockdown treatments, followed by lipogenic or osteogenic induction. Lipogenic differentiation was assessed via Oil Red O staining, while osteogenic differentiation was evaluated by ALP staining. Mineralization capacity was determined by Alizarin red staining, and proliferative activity was measured with CCK-8 assays. RT-qPCR and Western blot analyses were employed to quantify mRNA and protein expression of genes associated with the RAF/MEK/ERK signaling pathway and to validate the efficacy of HAX1 manipulation.

Results

Validation of mRNA and protein expression confirmed successful establishment and screening of HAX1-overexpressing and -knockdown cell lines. Subsequent investigations revealed that HAX1 overexpression enhanced osteogenic differentiation and mineralization of PDLSCs while suppressing proliferation and lipogenic differentiation. Conversely, HAX1 knockdown yielded opposing effects. Analysis of the RAF/MEK/ERK signaling pathway demonstrated that HAX1 overexpression significantly promoted MEK/ERK phosphorylation and pathway activation, without affecting the RAF family.

Conclusion

HAX1 overexpression activates the ERK/MEK-mediated MAPK signaling pathway, which promotes osteogenic differentiation and inhibits lipid differentiation in PDLSCs, with positive therapeutic implications in periodontitis.

牙周炎的特点是牙周组织破坏和随后的牙齿脱落，严重影响生活质量。HAX1是一种与牙周炎发病机制有关的基因，其调节牙周韧带干细胞（PDLSCs）分化的潜力及其治疗潜力仍未被探索。方法将spdlscs随机分为7个实验组，分别进行HAX1过表达或敲低处理，然后诱导成脂或成骨。油红O染色评估成脂分化，ALP染色评估成骨分化。采用茜素红染色法测定矿化能力，CCK-8法测定增殖活性。采用RT-qPCR和Western blot分析定量RAF/MEK/ERK信号通路相关基因的mRNA和蛋白表达，验证HAX1操作的有效性。结果mRNA和蛋白表达验证证实了hax1过表达和低表达细胞系的成功建立和筛选。随后的研究表明，HAX1过表达增强了PDLSCs的成骨分化和矿化，同时抑制了增殖和脂质分化。相反，HAX1基因敲低会产生相反的效果。对RAF/MEK/ERK信号通路的分析表明，HAX1过表达可显著促进MEK/ERK磷酸化和通路激活，而不影响RAF家族。结论hax1过表达激活ERK/ mek介导的MAPK信号通路，促进PDLSCs成骨分化，抑制脂质分化，对牙周炎具有积极的治疗意义。

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引用次数: 0

Gut-derived Helicobacter rodentium aggravates Tfh/Tfr imbalance and neuroinflammation via PI3K/AKT activation in anti-NMDAR encephalitis mice 在抗nmdar脑炎小鼠中，肠道源性螺杆菌通过激活PI3K/AKT加重Tfh/Tfr失衡和神经炎症

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-11-25 DOI: 10.1016/j.tice.2025.103242

Yanfei Yang, Lili Yang, Yabin Li, Yanfen Wang

Background

The gut microbiota is essential for the bidirectional communication between the gut and the brain. However, its specific role and underlying mechanisms in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis remain largely unclear.

Methods

An anti-NMDAR encephalitis model was induced by GluN1 peptide immunization, and brain histopathology was assessed by hematoxylin-eosin staining. Behavioral performance was assessed through the Y-maze and open field tests. Flow cytometry was employed to quantify T follicular helper (Tfh) and T follicular regulatory (Tfr) cell populations. Enzyme-linked immunosorbent assay and western blot were used to assess inflammatory cytokines and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway-related protein levels, respectively. 16S rRNA sequencing and Helicobacter rodentium gavage (1.5 mL, 1 ×10 ¹¹ CFU/mL) were used to assess microbiota composition and bacterial function.

Results

16S rRNA sequencing revealed a trend toward reduced gut microbial diversity in anti-NMDAR encephalitis mice. Helicobacter rodentium colonization further exacerbated behavioral deficits and inflammatory cell infiltration in the cerebral cortex. This was accompanied by a marked increase in tumor necrosis factor alpha (TNF-α) and interleukin (IL)-21 levels and a reduction in IL-10 concentrations in both cerebrospinal fluid and serum. Moreover, the Tfh/Tfr cell ratio was further elevated following Helicobacter rodentium exposure. Targeted suppression of the PI3K/AKT pathway with LY294002 significantly restored Tfh/Tfr balance and alleviated neurobehavioral impairments and cortical inflammation.

Conclusion

Helicobacter rodentium exacerbates anti-NMDAR encephalitis by inducing PI3K/AKT-mediated Tfh/Tfr imbalance, highlighting a potential therapeutic target in autoimmune encephalitis.

肠道微生物群对于肠道和大脑之间的双向交流至关重要。然而，其在抗n -甲基- d -天冬氨酸受体（NMDAR）脑炎中的具体作用和潜在机制仍不清楚。方法采用GluN1肽免疫诱导抗nmdar脑炎模型，苏木精-伊红染色观察脑组织病理学变化。通过y形迷宫和野外测试评估行为表现。流式细胞术定量T滤泡辅助（Tfh）和T滤泡调节（Tfr）细胞群。采用酶联免疫吸附法和western blot分别检测炎症因子和磷酸肌苷3-激酶/蛋白激酶B （PI3K/AKT）通路相关蛋白水平。采用16S rRNA测序和螺杆菌灌胃（1.5 mL, 1 ×10 ¹¹CFU/mL）评估菌群组成和细菌功能。结果16s rRNA测序显示抗nmdar脑炎小鼠肠道微生物多样性降低的趋势。啮齿螺杆菌的定植进一步加剧了行为缺陷和大脑皮层的炎症细胞浸润。脑脊液和血清中肿瘤坏死因子α (TNF-α)和白细胞介素(IL)-21水平显著升高，IL-10浓度降低。此外，幽门螺杆菌暴露后，Tfh/Tfr细胞比值进一步升高。LY294002靶向抑制PI3K/AKT通路可显著恢复Tfh/Tfr平衡，减轻神经行为障碍和皮质炎症。结论啮齿螺杆菌通过诱导PI3K/ akt介导的Tfh/Tfr失衡加重抗nmdar脑炎，提示自身免疫性脑炎的潜在治疗靶点。

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引用次数: 0

TPM2 as a novel inflammatory regulator in severe obstetric disorders: Integrative bioinformatics and functional validation TPM2作为一种新的炎症调节剂在严重产科疾病：综合生物信息学和功能验证

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-11-10 DOI: 10.1016/j.tice.2025.103222

Zonggao Liao, Fei Zhao, Yao Li, Xiaofang Chen, Juan Le

Background and objective

Severe obstetric disorders, such as preeclampsia and severe maternal infections, are major contributors to maternal and perinatal morbidity. Inflammation plays a central role in their pathogenesis, yet the underlying molecular regulators remain poorly defined. We sought to uncover key genes and signaling pathways involved in inflammatory responses of severe obstetric disorders through integrated bioinformatics and functional validation.

Methods

The identification of differentially expressed genes (DEGs) was performed through the integration of transcriptomic datasets (GSE131411 as well as GSE233557), which subsequently underwent a series of analyses such as protein-protein interaction (PPI) network development, enrichment analysis,and single-sample gene set enrichment analysis(ssGSEA). Key genes were validated using qRT-PCR and Western blot in placental tissues and LPS-treated HTR-8/SVneo cells. Functional roles were assessed through cell migration, invasion, cytokine secretion, and NF-κB signaling assays.

Results

TPM2 and DAW1 were significantly downregulated in inflammatory conditions, with TPM2 showing stronger involvement (P < 0.01). TPM2 overexpression enhanced trophoblast migration and invasion as well as suppressed IL-6, IL-1β, and IL-8 production (P < 0.01). Mechanistically, TPM2 inhibited IκBα degradation and blocked nuclear translocation of p65 (P < 0.01), thereby suppressing NF-κB signaling.

Conclusion

TPM2 is a novel modulator of inflammation in severe obstetric disorders. These findings offer mechanistic insights and highlight TPM2's potential as a diagnostic biomarker and therapeutic target in inflammatory pregnancy complications.

背景和目的严重的产科疾病，如先兆子痫和严重的孕产妇感染，是孕产妇和围产期发病率的主要原因。炎症在其发病机制中起着核心作用，但潜在的分子调节因子仍不明确。我们试图通过综合生物信息学和功能验证来揭示涉及严重产科疾病炎症反应的关键基因和信号通路。方法通过整合转录组数据集（GSE131411和GSE233557）鉴定差异表达基因（deg），随后进行一系列分析，如蛋白质-蛋白质相互作用（PPI）网络开发、富集分析和单样本基因集富集分析（ssGSEA）。在胎盘组织和lps处理的HTR-8/SVneo细胞中，采用qRT-PCR和Western blot验证关键基因。通过细胞迁移、侵袭、细胞因子分泌和NF-κB信号分析来评估功能作用。结果炎症状态下，stpm2和DAW1明显下调，其中TPM2的参与程度更强（P <； 0.01）。TPM2过表达增强滋养细胞迁移和侵袭，抑制IL-6、IL-1β和IL-8的产生（P <； 0.01）。机制上，TPM2抑制i -κB α降解，阻断p65核易位（P <； 0.01），从而抑制NF-κB信号传导。结论tpm2是一种新型的严重产科疾病炎症调节剂。这些发现提供了机制见解，并突出了TPM2作为炎症性妊娠并发症的诊断生物标志物和治疗靶点的潜力。

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引用次数: 0

Niaodukang for the treatment of chronic kidney disease: Regulation of the TRAF3/NF-κB2 signaling pathway and its improvement of the intestinal barrier 尿毒康治疗慢性肾病：调节TRAF3/NF-κB2信号通路及其改善肠屏障的作用

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-12-09 DOI: 10.1016/j.tice.2025.103271

Juan Xu , Lei Wang , Hong Wang , Jie Pang , Linna Liu , Ting Zhang , Ling Yuan , Xiaoxue Cui , Qian Jiang , Yanlin Li

Background

Niaodukang (NDK) mixture is a traditional Chinese herbal formula clinically used for chronic kidney disease (CKD). However, its bioactive components and molecular mechanisms remain unclear.

Objective

To explore the protective effect of NDK on CKD-associated intestinal barrier dysfunction and identify its key active compound targeting the TRAF3/NF-κB2 pathway.

Methods

A 5/6 nephrectomy rat model and indole-induced Caco-2 cell injury model were established. Renal function, intestinal tight junction integrity, and inflammatory signaling were evaluated by histological, molecular, and ultrastructural analyses. Network pharmacology and molecular docking were applied to predict bioactive compounds, followed by in vitro validation.

Results

NDK significantly improved renal function (reduced Scr, BUN, and urine protein; P < 0.01) and restored intestinal epithelial barrier integrity, as indicated by increased ZO-1 and occludin expression and improved ultrastructure. Among 126 candidate compounds, formononetin from Astragalus membranaceus exhibited strong binding affinity to TRAF3. Functional assays confirmed that formononetin suppressed TRAF3/NF-κB2 signaling, restored tight junction proteins, and alleviated epithelial injury, whereas TRAF3 overexpression abolished these protective effects.

Conclusion

NDK ameliorates CKD-associated intestinal barrier dysfunction by suppressing the TRAF3/NF-κB2 pathway. Formononetin serves as a principal active compound mediating this effect, elucidating the pharmacological basis of NDK and supporting its therapeutic potential for CKD.

背景：尿毒康（NDK）合剂是临床上用于治疗慢性肾脏病（CKD）的传统中药方剂。然而，其生物活性成分和分子机制尚不清楚。目的：探讨NDK对ckd相关肠屏障功能障碍的保护作用，并鉴定其靶向TRAF3/NF-κB2通路的关键活性化合物。方法：建立5/6肾切除大鼠模型和吲哚诱导Caco-2细胞损伤模型。通过组织学、分子和超微结构分析评估肾功能、肠紧密连接完整性和炎症信号。应用网络药理学和分子对接技术预测活性化合物，并进行体外验证。结果：NDK可显著改善肾功能（降低Scr、BUN和尿蛋白）；P 结论：NDK可通过抑制TRAF3/NF-κB2通路改善ckd相关肠屏障功能障碍。刺芒柄花素是介导这一作用的主要活性化合物，阐明了NDK的药理学基础，并支持其治疗慢性肾病的潜力。

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引用次数: 0

The oxidative stress regulatory mechanism of autophagy and apoptosis in lens epithelial cells 氧化应激对晶状体上皮细胞自噬和凋亡的调控机制

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2026-01-02 DOI: 10.1016/j.tice.2025.103308

Mengyi Lin , Yalan Chen , Gangjin Kang

Cataract is the leading cause of blindness worldwide, and its incidence rate is still on the rise. Oxidative stress plays a key role in the formation of cataracts. Oxidative stress not only causes damage to lens epithelial cells (LECs) but also activates autophagy and apoptosis. Specifically, under oxidative stress conditions, the apoptosis of LECs is significantly activated, which in turn leads to accelerated lens opacity and cataract development. Meanwhile, autophagy, as a cellular self-protection mechanism, exhibits bidirectional regulatory characteristics in response to oxidative stress. In addition, in diabetic cataracts, high glucose levels can disrupt the balance between autophagy and oxidative stress, exacerbating LECs damage. This cross-effect of apoptosis and autophagy highlights the core position of both in the pathogenesis of cataracts, but the specific molecular mechanism still needs to be further clarified. Although antioxidants can alleviate apoptosis and autophagy damage induced by oxidative stress, the clinical treatment of cataracts still urgently needs prevention and treatment strategies targeting molecular mechanisms.

白内障是全球致盲的主要原因，其发病率仍在上升。氧化应激在白内障的形成中起着关键作用。氧化应激不仅会导致晶状体上皮细胞损伤，还会激活晶状体上皮细胞的自噬和凋亡。在氧化应激条件下，lec细胞的凋亡被显著激活，从而加速晶状体混浊和白内障的发生。同时，自噬作为细胞的一种自我保护机制，在氧化应激反应中表现出双向调节的特点。此外，在糖尿病性白内障中，高葡萄糖水平会破坏自噬和氧化应激之间的平衡，加剧LECs损伤。细胞凋亡与细胞自噬的交叉作用凸显了两者在白内障发病中的核心地位，但具体的分子机制仍需进一步阐明。虽然抗氧化剂可以减轻氧化应激引起的细胞凋亡和自噬损伤，但临床治疗白内障仍迫切需要针对分子机制的预防和治疗策略。

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引用次数: 0

Mast cell characterization, density, and distribution in placenta accreta spectrum: A histological, histochemical and immunohistochemical analysis 肥大细胞的特征，密度和分布在胎盘增生光谱：组织学，组织化学和免疫组织化学分析。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-12-11 DOI: 10.1016/j.tice.2025.103273

Thaer Bahjat , Malak AL-Yawer , Haydar Al- Shamaa

The placenta accreta spectrum (PAS) is a group of disorders characterized by abnormal trophoblastic invasion, often associated with decidual defects, stromal remodeling, and immune dysregulation, resulting in serious obstetric complications. Mast cells (MCs), known for their roles in tissue remodeling, angiogenesis, and inflammation, have not been fully explored in the context of PAS. This study aimed to investigate the morphological, phenotypic, and quantitative alterations of MCs in PAS compared to normal placentas using a multimodal histopathological approach. Placental tissues from PAS cases and gestational age-matched controls were examined using hematoxylin and eosin (H&E), toluidine blue (TB), Alcian blue/safranin (A/S), and immunohistochemistry (IHC) with anti-tryptase antibodies. MC density, distribution, morphology, and activation status were assessed in the decidual, villous, and myometrial compartments and statistical comparisons were made using t-tests and two-way ANOVA. The results showed a significant increase in MC density in PAS placentas across all staining methods (p < 0.05). Histochemical stains revealed a greater number of morphologically activated MCs, particularly connective tissue-type mast cells (CTMCs), in PAS tissues. IHC confirmed elevated counts of tryptase-positive MCs exhibiting features of degranulation, especially in areas adjacent to trophoblastic invasion and stromal disruption. Statistical analysis indicated a significant effect of both diagnosis and staining technique on MC counts (p < 0.001). These findings suggest that MCs are increased and activated in PAS, with potential roles in extracellular matrix (ECM) degradation, inflammation, and abnormal implantation. The predominance of CTMCs and their spatial association with invasive extravillous trophoblasts point to a contributory role in PAS pathophysiology. Further research using expanded immunomarker panels, functional assays, and more diverse study populations is needed to determine whether MCs are causal agents or secondary responders in PAS and to assess their potential as diagnostic or therapeutic targets.

胎盘增生谱（PAS）是一组以滋养细胞异常侵袭为特征的疾病，常伴有蜕膜缺陷、间质重塑和免疫失调，可导致严重的产科并发症。肥大细胞（MCs）以其在组织重塑、血管生成和炎症中的作用而闻名，但在PAS的背景下尚未得到充分的探讨。本研究旨在利用多模态组织病理学方法研究PAS中MCs与正常胎盘的形态学、表型和定量变化。采用苏木精和伊红（H&E）、甲苯胺蓝（TB）、阿利新蓝/红花红（A/S）和抗胰蛋白酶抗体免疫组化（IHC）检测PAS病例和胎龄匹配对照组的胎盘组织。在蜕膜室、绒毛室和肌层室中评估MC密度、分布、形态和激活状态，并使用t检验和双向方差分析进行统计比较。结果显示，在所有染色方法中，PAS胎盘的MC密度都显著增加(p

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引用次数: 0

Granzyme B knockdown inhibits NLRP3-mediated pyroptosis and the JAK2/STAT3 signaling in renal fibrosis 颗粒酶B敲低抑制nlrp3介导的肾纤维化和JAK2/STAT3信号传导。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-11-04 DOI: 10.1016/j.tice.2025.103216

Minhui Wang, Daojun Chen, Daofa Zhang, Hui Han, Maowei Xie, Ying Zhang, Yun Cao, Jiali Wei

Background

Renal fibrosis (RF) is a common histopathological feature of chronic kidney disease (CKD) and is closely associated with persistent inflammation and regulated cell death. However, the underlying molecular mechanisms of pyroptosis in RF are unclear.

Methods

Pyroptosis-related hub genes in RF were identified through bioinformatics analysis. Granzyme B (GZMB) was knocked down in transforming growth factor (TGF-β)-stimulated HK-2 cells and in a folic acid (FA)-induced nephropathy mouse model. Western blot and enzyme-linked immunosorbent assays were performed to detect the expression of fibrosis and pyroptosis-related markers. Cell viability was assessed by the Cell Counting Kit-8 assay. Hematoxylin and eosin (HE) and Masson's staining were used to evaluate tubular injury and collagen deposition in renal tissues.

Results

GZMB was identified as a pyroptosis-associated hub gene. It was significantly upregulated in RF and exhibited high diagnostic performance. In TGF-β-stimulated HK-2 cells, GZMB knockdown enhanced cell viability and reduced lactate dehydrogenase release. In vivo, GZMB silencing ameliorated tubular injury, reduced collagen deposition, and improved renal function. The expression levels of pyroptosis-related proteins, including the N-terminal fragment of gasdermin D, cleaved caspase-1, and NOD-like receptor family pyrin domain containing 3 (NLRP3), as well as fibrotic markers alpha-smooth muscle actin and collagen type I, were downregulated after GZMB knockdown. Mechanically, GZMB knockdown inhibited NLRP3 inflammasome activation and suppressed the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway.

Conclusion

GZMB deficiency inhibits pyroptosis and dampens the JAK2/STAT3 pathway, representing a potential approach for RF treatment.

背景：肾纤维化（RF）是慢性肾脏疾病（CKD）的常见组织病理学特征，与持续炎症和调节细胞死亡密切相关。然而，RF中焦亡的潜在分子机制尚不清楚。方法：通过生物信息学分析，鉴定RF中与热释相关的中枢基因。在转化生长因子（TGF-β）刺激的HK-2细胞和叶酸（FA）诱导的肾病小鼠模型中，颗粒酶B （GZMB）被下调。采用Western blot和酶联免疫吸附法检测纤维化和焦热相关标志物的表达。采用细胞计数试剂盒-8测定细胞活力。苏木精伊红（HE）染色及马松染色评价肾小管损伤及肾组织胶原沉积。结果：GZMB被鉴定为一个与焦热相关的枢纽基因。它在RF中显著上调，并表现出很高的诊断性能。在TGF-β刺激的HK-2细胞中，GZMB敲低可提高细胞活力，减少乳酸脱氢酶的释放。在体内，GZMB沉默可改善肾小管损伤，减少胶原沉积，改善肾功能。GZMB敲低后，胃粘膜蛋白D n端片段、cleaved caspase-1、nod样受体家族pyrin domain containing 3 （NLRP3）、纤维化标志物α -平滑肌肌动蛋白、I型胶原蛋白等与热降解相关的蛋白表达水平下调。机械上，GZMB敲低抑制NLRP3炎性体的激活，抑制Janus激酶2/信号转导和转录激活因子3 （JAK2/STAT3）通路。结论：GZMB缺乏抑制焦亡并抑制JAK2/STAT3通路，是一种潜在的RF治疗方法。

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引用次数: 0

CRViT-YOLO: A method for multi-morphological blood cell detection using convolution-restructured vision transformer crvityolo：一种基于卷积重构视觉变压器的多形态血细胞检测方法。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2026-01-06 DOI: 10.1016/j.tice.2026.103312

Yaning Du , Yuliang Ma , Qingshan She , Xugang Xi

Complete blood cell counting plays a critical role in medical diagnostics; however, conventional manual examination is time-consuming and prone to errors due to variations in data sources, image quality, cell morphology, and staining characteristics. Deep learning has emerged as a promising solution to enhance both the accuracy and efficiency of blood cell detection. In this study, we present CRViT-YOLO, a novel detection framework built upon the YOLOv9 architecture. The proposed framework incorporates a Convolutional-Reconstructed Vision Transformer (CRViT) module to improve feature extraction by effectively capturing both local and global contextual information. Furthermore, a Feature Enhancement Module (FEM) is introduced to refine local feature representations, while the integration of the EIoU loss function enhances localization accuracy, particularly for densely packed or overlapping cells across diverse scales and types, and demonstrates robust performance in detecting polymorphic, healthy, and pathological cells. Extensive experiments conducted on four publicly available datasets—BCCD, BCDD, LISC, and BBBC041—validate the effectiveness and generalizability of the proposed approach, achieving mean average precision (mAP@50) scores of 93.9 %, 99.4 %, 98.8 %, and 76.0 %, respectively, in multi-class blood cell detection tasks.

全血细胞计数在医学诊断中起着至关重要的作用；然而，由于数据源、图像质量、细胞形态和染色特征的变化，传统的人工检查既耗时又容易出错。深度学习已经成为一种很有前途的解决方案，可以提高血细胞检测的准确性和效率。在本研究中，我们提出了一种基于YOLOv9架构的新型检测框架crviti - yolo。该框架结合了卷积重建视觉变换（CRViT）模块，通过有效捕获局部和全局上下文信息来改进特征提取。此外，引入了一个特征增强模块（FEM）来细化局部特征表示，而EIoU损失函数的集成提高了定位精度，特别是对于不同尺度和类型的密集排列或重叠细胞，并在检测多态、健康和病理细胞方面表现出强大的性能。在四个公开可用的数据集（bccd， BCDD， LISC和bbbc041）上进行的大量实验验证了所提出方法的有效性和可推广性，在多类别血细胞检测任务中，平均精度（mAP@50）分别达到93.9 %,99.4 %，98.8 %和76.0 %。

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引用次数: 0

Sinapic acid attenuates vancomycin-induced hepatotoxicity in rats via modulation of ER stress (CHOP, IRE1, ATF-6, PERK), apoptotic pathways (caspase-3, Bax/Bcl-2, Apaf-1, cytochrome-c), and antioxidant defenses 辛酸通过调节内质膜应激（CHOP、IRE1、ATF-6、PERK）、凋亡通路（caspase-3、Bax/Bcl-2、Apaf-1、细胞色素-c）和抗氧化防御，减轻万古霉素诱导的大鼠肝毒性。

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2025-11-29 DOI: 10.1016/j.tice.2025.103255

Cihan Gur , Mustafa Ileriturk , Nurhan Akaras , Fatih Mehmet Kandemir

The present study aimed to investigate the protective properties of sinapic acid (SNP), one of the four most common hydroxycinnamic acids, whose activity against vancomycin (VCM)-induced hepatotoxicity, a glycopeptide antibiotic, has not been previously investigated. In the presented study, the protective properties of SNP against VCM-induced liver toxicity were investigated. For this purpose, VCM (200 mg/kg) and/or SNP (10 or 20 mg/kg) were given to Sprague-Dawley rats (n = 7) for 7 days. At the end of the study, biochemical, molecular, and histological analyses were performed on liver tissues. According to the data obtained, it was determined that VCM triggered oxidative stress, endoplasmic reticulum stress, autophagy, and apoptosis in liver tissue, activated metalloproteinases, and caused histological irregularities in the liver. On the other hand, after SNP treatment, it was observed that the activities of antioxidant enzymes SOD, CAT, and GPx increased, GSH stores were renewed, and MDA levels, an important indicator of lipid peroxidation, decreased. It was observed that oxidative DNA damage was alleviated and 8-OHdG levels were downregulated by suppressing oxidative stress. After SNP treatment, with the alleviation of ER stress, a decrease occurred in the relative mRNA transcript levels of ATF-6, PERK, IRE1, GRP-7,8, and CHOP sensors. Furthermore, SNP was seen to exhibit anti-apoptotic effects by decreasing Bax, Caspase-3, Apaf-1, and cytochrome-C and up-regulating Bcl-2 in the liver. Data also indicate that SNP suppresses MAPK-14, activates AKT2, and down-regulates metalloproteinases. In conclusion, it was observed that SNP may be an important protective agent against the hepatotoxicity of VCM.

作为四种最常见的羟基肉桂酸之一，sinapic acid （SNP）对糖肽抗生素万古霉素（VCM）诱导的肝毒性的保护作用尚未得到研究。在本研究中，研究了SNP对vcm诱导的肝毒性的保护作用。为此，给Sprague-Dawley大鼠（n = 7）注射VCM（200 mg/kg）和/或SNP(10或20 mg/kg) 7天。研究结束时，对肝组织进行生化、分子和组织学分析。根据所获得的数据，我们确定VCM触发肝组织氧化应激、内质网应激、自噬和凋亡，激活金属蛋白酶，导致肝脏组织异常。另一方面，SNP处理后，抗氧化酶SOD、CAT和GPx活性升高，GSH储存更新，脂质过氧化的重要指标MDA水平下降。通过抑制氧化应激可减轻氧化DNA损伤，降低8-OHdG水平。SNP处理后，随着内质膜应激的减轻，ATF-6、PERK、IRE1、GRP-7、8和CHOP传感器的相对mRNA转录水平下降。此外，SNP通过降低肝脏中的Bax、Caspase-3、Apaf-1和细胞色素- c以及上调Bcl-2而表现出抗凋亡作用。数据还表明，SNP抑制MAPK-14，激活AKT2，下调金属蛋白酶。综上所述，SNP可能是抗VCM肝毒性的重要保护剂。

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引用次数: 0

Polystyrene microplastics impact on cardiac and pulmonary physiology and microenvironment in a mouse model: Role of taurine supplementation and molecular docking insights 聚苯乙烯微塑料对小鼠模型中心肺生理和微环境的影响：牛磺酸补充的作用和分子对接见解

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell

Pub Date : 2026-04-01 Epub Date: 2026-01-06 DOI: 10.1016/j.tice.2026.103313

Amany Abdel-Rahman Mohamed , Badriyah S. Alotaibi , Yasmina M. Abd El-Hakim , Ibrahim Jafri , Samah S. Abuzahrah , Tarek Khamis , Ahmed E. Noreldin , Ali H. El-Far , Nawal Alsubaie , Wesam K. Bakhsh , Mohamed El-Gamal

Polystyrene microplastics (PS-MPs) have recently gained attention as widespread environmental contaminants posing risks to both human and animal health. In this study, we investigated the potential protective effect of taurine (200 mg/kg b.wt) against cardiopulmonary toxicity induced by PS-MPs (10 mg/kg b.wt) in male Swiss mice following a 60-day oral exposure. Molecular docking investigation for both proteins and mRNA targets was carried out utilizing a global, flexible docking strategy that allowed for full ligand conformational freedom and binding surface exploration. We designed an experimental model comprising four groups: Control, Taurine, PS-MPs, and a combined group (PS-MPs + Taurine). The results indicated that taurine significantly protected against PS-MPs-induced biochemical, histopathological, and molecular alterations that occurred in the cardiac and pulmonary tissues of mice. PS-MPs exposure disrupted the redox balance by suppressing enzymatic antioxidants (CAT, SOD, GPx) and increasing lipid peroxidation, while elevating cardiac injury markers (LDH, CK-MB, CPK, cTnI). These oxidative changes were accompanied by increased pro-inflammatory cytokines (TNF-α, IL-1β) in both tissues, histopathological lesions in the heart and lungs, and upregulation of gene expressions of inflammatory and pyroptotic mediators (NLRP3, Caspase-1, ASC, GSDMD, NF-κB, COX-2, IL-1β, IL-18). Co-administration of taurine with PS-MPs markedly ameliorated these alterations, restoring antioxidant defenses, reducing lipid peroxidation and cytokine levels, downregulating inflammasome and pyroptosis-related gene expression, and improving tissue architecture. Molecular docking supported these findings by showing taurine’s potential interactions with inflammatory mediators, while styrene exhibited affinity for antioxidant enzymes, consistent with in vivo oxidative disruption. Collectively, the study highlights oxidative stress and inflammation as key mechanisms of PS-MPs-induced cardiopulmonary toxicity and highlights taurine’s promise as a protective agent against microplastics-related health risks.

聚苯乙烯微塑料（PS-MPs）作为一种广泛存在的环境污染物，对人类和动物的健康构成了威胁，最近引起了人们的关注。在这项研究中，我们研究了牛磺酸（200 mg/kg b.wt）对雄性瑞士小鼠口服暴露60天后PS-MPs（10 mg/kg b.wt）诱导的心肺毒性的潜在保护作用。利用全局灵活的对接策略，对蛋白质和mRNA靶点进行分子对接研究，允许完全的配体构象自由和结合表面探索。我们设计了一个实验模型，包括四组：对照组、牛磺酸组、PS-MPs组和PS-MPs +牛磺酸组。结果表明，牛磺酸对ps - mps诱导的小鼠心脏和肺组织的生化、组织病理和分子改变具有显著的保护作用。PS-MPs暴露通过抑制酶促抗氧化剂（CAT， SOD, GPx）和增加脂质过氧化作用而破坏氧化还原平衡，同时升高心脏损伤标志物（LDH, CK-MB， CPK, cTnI）。这些氧化变化伴随着两种组织中促炎细胞因子（TNF-α, IL-1β）的增加，心脏和肺部的组织病理学病变，以及炎症和焦亡介质（NLRP3, Caspase-1， ASC， GSDMD, NF-κB, COX-2, IL-1β, IL-18）基因表达的上调。牛磺酸与PS-MPs联合使用可显著改善这些改变，恢复抗氧化防御，降低脂质过氧化和细胞因子水平，下调炎性体和热缩相关基因表达，改善组织结构。分子对接显示牛磺酸与炎症介质的潜在相互作用支持了这些发现，而苯乙烯则表现出与抗氧化酶的亲和力，与体内氧化破坏一致。总的来说，该研究强调了氧化应激和炎症是ps - mps诱导的心肺毒性的关键机制，并强调了牛磺酸作为微塑料相关健康风险的保护剂的前景。

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引用次数: 0