In Vitro Cellular & Developmental Biology. Animal最新文献

{"title":"Dihydrocapsaicin suppresses the migration and invasion of gastric cancer cells by upregulating TRPV1 expression.","authors":"Yongan Fu, Yangqiang Wang, Zongda Cai, Shurong Huang, Jinping Chen","doi":"10.1007/s11626-026-01226-3","DOIUrl":"https://doi.org/10.1007/s11626-026-01226-3","url":null,"abstract":"<p><p>Gastric cancer is a common digestive system malignancy worldwide, and its high metastatic potential is one of the main reasons for poor patient prognosis. Dihydrocapsaicin, a natural derivative of capsaicin found in chili peppers, has recently been shown to possess anti-tumor potential. However, the effects and underlying mechanisms of dihydrocapsaicin on gastric cancer cell migration and invasion remain unclear. This study aims to investigate the impact of dihydrocapsaicin on the migratory and invasive abilities of gastric cancer cells and to elucidate the regulatory role of TRPV1 in this process. Human gastric cancer cell lines NCI-N87 and HGC-27 were treated with different concentrations of dihydrocapsaicin. The changes in the migration and invasion abilities of gastric cancer cells were detected. Meanwhile, WB was used to detect the differential expression of TRPV1, E-cadherin, N-cadherin, Vimentin, and Snail. Subsequently, the expression of TRPV1 was interfered in the dihydrocapsaicin-treated gastric cancer cell lines, and the differential expressions of the above cell migration, invasion, and E-cadherin, N-cadherin, Vimentin, and Snail proteins were detected. Dihydrocapsaicin could significantly and dose-dependently inhibit the migration and invasion of gastric cancer cells NCI-N87 and HGC-27. In addition, dihydrocapsaicin treatment significantly increased the expression of TRPV1 and E-cadherin proteins in gastric cancer cells, and significantly inhibited the expression of N-cadherin, Vimentin, and Snail proteins in gastric cancer cells. Functional rescue experiments confirmed that when the expression of TRPV1 was inhibited, the inhibitory effect of dihydrocapsaicin on the migration and invasion of gastric cancer cells was significantly weakened. Dihydrocapsaicin can effectively inhibit the migration and invasion abilities of gastric cancer cells by upregulating the expression of TRPV1.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148602453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Daphnetin alleviates cisplatin-induced acute kidney injury by inhibiting the HIF-1α signaling pathway.","authors":"Li Wan, Congxian Lu, Chunju Xue, Xiaofeng Deng","doi":"10.1007/s11626-026-01207-6","DOIUrl":"https://doi.org/10.1007/s11626-026-01207-6","url":null,"abstract":"<p><p>Cisplatin-induced acute kidney injury (AKI) limits its clinical use, and effective renoprotective agents are lacking. Daphnetin (DAP), a natural coumarin, exhibits anti-inflammatory and antioxidant properties, but its role and mechanism in cisplatin nephrotoxicity remain unclear. This study investigates whether DAP protects against cisplatin-induced renal tubular injury and elucidates the involvement of the HIF-1α signaling pathway. A rat model of cisplatin-induced AKI and an in vitro HK-2 cell injury model were used. Renal function, histopathology, injury markers (KIM-1, NGAL), inflammatory cytokines (TNF-α, IL-1β, IL-6, TGF-β), cell viability, proliferation, apoptosis, and HIF-1α expression were assessed. Bioinformatics analysis and rescue experiments using the HIF-1α activator ML228 were performed. DAP significantly ameliorated cisplatin-induced renal dysfunction, pathological damage, and inflammatory responses in rats. In HK-2 cells, DAP enhanced viability and proliferation, reduced apoptosis, and downregulated KIM-1, NGAL, and pro-inflammatory cytokines. HIF-1α protein and mRNA level was upregulated by cisplatin, and DAP reversed this effect. Bioinformatics and KEGG analysis identified the HIF-1 pathway as the most enriched. Activation of HIF-1α by ML228 abolished DAP's protective effects, confirming the pathway's critical role. DAP alleviates cisplatin-induced AKI by inhibiting the HIF-1α signaling pathway. This natural compound represents a promising candidate for preventing chemotherapy-related renal injury.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Total flavonoids of Rhizoma Drynariae promote osteogenic differentiation of tendon-derived stem cells through the TGF-β/BMP signaling pathway, thereby improving bone regeneration after anterior cruciate ligament reconstruction in rats.","authors":"ShangYi Dai, LiXin Cao, XueFeng Wang","doi":"10.1007/s11626-026-01210-x","DOIUrl":"https://doi.org/10.1007/s11626-026-01210-x","url":null,"abstract":"<p><p>Poor tendon-bone healing is a major challenge after anterior cruciate ligament reconstruction (ACLR). TFRD, the total flavonoids of Rhizoma Drynariae, has pharmacological effects in promoting bone formation, but it remains less understood whether it accelerates tendon-bone healing by regulating the osteogenic differentiation of tendon-derived stem cells (TDSCs). TDSCs were isolated from the Achilles tendons of rats and characterized for their stem cell properties through flow cytometry and multilineage differentiation assays. The effects of TFRD on TDSC proliferation, migration, and osteogenic differentiation were evaluated using the cell counting kit-8 assay, scratch wound healing assays, Alizarin Red S staining, and Western blot analysis. Gene and protein expression levels associated with the transforming growth factor-β/bone morphogenetic protein (TGF-β/BMP) signaling pathway were assessed by real-time quantitative polymerase chain reaction and Western blot. A rat ACLR model was created and divided into four experimental groups: Sham, ACLR, TFRD, and TFRD + Noggin. Tendon-bone healing was analyzed using hematoxylin and eosin staining, Masson's trichrome staining, bone mineral density measurements, and immunohistochemistry. Noggin was used to inhibit BMP signaling for pathway validation. TFRD (50-100 μg/mL) significantly enhanced the proliferation, migration, and osteogenic differentiation of TDSCs, and increased the expression of key osteogenic markers, including runt-related transcription factor 2 (RUNX2) and alkaline phosphatase (ALP). Mechanistically, TFRD activated the TGF-β/BMP signaling pathway, leading to elevated levels of TGF-β1, BMP-2, and phosphorylated Smad1/5/8. Moreover, TGF-β1 extended the duration of BMP-2 signaling and suppressed Noggin expression. The osteogenic effects of TFRD were diminished when Noggin was applied, indicating its role in modulating the BMP pathway. In vivo, TFRD significantly improved collagen fiber alignment, calcification, and bone mineral density at the tendon-bone junction, while also upregulating RUNX2 and ALP expression. TFRD promotes osteogenic differentiation of TDSCs by activating the TGF-β/BMP signaling pathway, improves tendon-bone healing after ACLR, and provides experimental support for its clinical application.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DIRAS2 promotes the progression of oral leukoplakia via suppressing ferroptosis.","authors":"Zitong Tian, Wenjing Li, Xing Li, Min Wang, Xiaofei Tang, Min Zhang","doi":"10.1007/s11626-026-01191-x","DOIUrl":"10.1007/s11626-026-01191-x","url":null,"abstract":"<p><strong>Background: </strong>Oral leukoplakia (OLK) is the most prevalent potentially malignant oral disorder (OPMD). Ferroptosis, a distinct form of regulated cell death, has recently garnered significant attention in a variety of diseases. DIRAS2 is a member of the DIRAS family within the RAS protein superfamily and is highly expressed in OLK tissues. Nevertheless, the precise mechanism through which DIRAS2 modulates ferroptosis in OLK remains elusive.</p><p><strong>Methods: </strong>Immunohistochemical staining was used to assess the expression of GPX4 in human normal oral mucosa and OLK tissues. DIRAS2 knockdown and control Leuk-1 cell were treated with Erastin to induce ferroptosis, and EDU, Mito Tracker green and MitoSOX probes were utilized to evaluate cell proliferation and mitochondrial changes. Additionally, the expression of ferroptosis-associated proteins and PI3K-AKT pathway in Leuk-1 cells and 4-nitroquinoline-1-oxide (4NQO)-induced DIRAS2^flox/flox mouse and DIRAS2^{flox/flox:Cre+} mouse tongue tissues was examined via western blotting and immunohistochemistry, respectively.</p><p><strong>Results: </strong>GPX4 was abnormally highly expressed in human OLK tissues than in normal mucosa tissues. Erastin significantly elevated Reactive Oxygen Species (ROS) level in Leuk-1 cells, concurrently downregulating cell proliferation and GPX4, PI3K, AKT and pAKT expression. DIRAS2 knockdown further potentiated Erastin-induced ferroptosis. Additionally, compared with the control group, DIRAS2-knockdown cells presented significant alterations in mitochondrial morphology. Compared to control mice, the expression of GPX4, PI3K, AKT and pAKT in the 4NQO-induced mouse tongue tissues was markedly upregulated. The expression of these proteins in DIRAS2^{flox/flox:Cre +} mouse tongue tissues demonstrated a notable reduction compared with DIRAS2^flox/flox mouse tongue tissues.</p><p><strong>Conclusion: </strong>DIRAS2 may affect OLK development by repressing ferroptosis through the PI3K/AKT pathway.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated intravesical pressure promotes circulating tumor cell release in an orthotopic mouse model of bladder cancer.","authors":"Ling Yi, Qing Chen, Min Zeng, Zongxin Xiao, Hua Chen, Leming Song, Xianxin Zhu","doi":"10.1007/s11626-026-01176-w","DOIUrl":"10.1007/s11626-026-01176-w","url":null,"abstract":"<p><p>Elevated intravesical pressure during transurethral resection of bladder tumor (TURBT) is hypothesized to facilitate the release of circulating tumor cells (CTCs), potentially increasing the risk of hematogenous metastasis. However, the causal relationship between intravesical pressure and CTC dissemination remains unclear. This study aimed to investigate the effect of different intravesical pressure levels on the release of CTCs in an orthotopic mouse model of bladder cancer. An orthotopic bladder cancer model was established in female C57BL/6 mice by implanting MB49-luc cells. Tumor-bearing mice were randomly assigned to three groups (n = 6 per group) subjected to different intravesical pressures for 20 min: 0 cmH₂O, 40 cmH₂O, and 80 cmH₂O. Peripheral blood was collected 24 h post-intervention for CTC detection. CTCs were isolated and identified as CD45⁻/EpCAM⁺ cells using flow cytometry. The release of CTCs into the peripheral blood was significantly promoted by elevated intravesical pressure. Mice in the 40 cmH₂O and 80 cmH₂O groups showed a significantly higher proportion of CTCs compared to the 0 cmH₂O control group. Furthermore, the 80 cmH₂O group demonstrated a significantly greater increase in CTCs than the 40 cmH₂O group, indicating a pressure-dependent effect. Increased intravesical pressure directly promotes the release of CTCs in bladder cancer in a pressure-dependent manner. These findings provide experimental evidence supporting the \"pressure-driven CTC dissemination\" hypothesis and highlight the potential clinical importance of monitoring and controlling intravesical pressure during surgical procedures to minimize the risk of tumor cell spread.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"745-753"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RYK silencing-modified bone marrow-derived mesenchymal stem cells suppress gastric cancer progression.","authors":"Yongan Fu, Zongda Cai, Yangqiang Wang, Mingjin Huang, Jinghua Huang","doi":"10.1007/s11626-026-01175-x","DOIUrl":"10.1007/s11626-026-01175-x","url":null,"abstract":"<p><p>Gastric cancer (GC) is a prevalent malignant tumor threatening human health. This study aimed to explore the potential mechanism of receptor-like tyrosine kinase (RYK) silencing-modified bone marrow-derived mesenchymal stem cells (BMSCs) in the progression of GC. BMSCs were transfected with the RYK siRNA and negative controls. Cell co-culture experiments were used to explore the interaction between different BMSCs and human gastric carcinoma cell line NCI-N87. Cancer cell proliferation, cell cycle, apoptosis, colony formative ability, and invasive ability were assessed. Western blot analysis was performed to determine the protein levels of cyclinA, Bcl-xL, Bcl-2, cleaved caspase 3, cleaved caspase 7, cleaved caspase 9, and cleaved PARP1 in NCI-N87 cells. Compared with NCI-N87 cells, co-culture of si-NC-modified BMSCs with NCI-N87 cells promoted the proliferation, colony formative ability, and invasion of NCI-N87 cells, inhibited the apoptosis of NCI-N87 cells, and reduced the proportion of NCI-N87 cells present in G2/M phase cells. In addition, compared with the si-NC-BMSCs + N87 group, the si-RYK-BMSCs + N87 group inhibited the proliferation, colony formative ability, and invasion of NCI-N87 cells, promoted the apoptosis of NCI-N87 cells, and increased the proportion of G2/M phase cells. Thus, RYK silencing-modified BMSCs can inhibit the proliferation, colony formative ability, and invasion of NCI-N87 cells, while inducing apoptosis and G2/M phase arrest.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"789-800"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147654039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ex vivo engineering of neural tissue structure and growth using sequential 2D and 3D solid scaffolds.","authors":"Orly E Weiss, Danny Baranes","doi":"10.1007/s11626-026-01182-y","DOIUrl":"10.1007/s11626-026-01182-y","url":null,"abstract":"<p><p>Brain injury disrupts tissue integrity, creating wounds with complex boundaries that hinder effective repair. Regeneration and reconnection require guiding deformed tissue along proper growth pathways. Pre-engineered scaffold implants made from biomaterials offer promise; however, while hydrogel-based scaffolds are common for brain repair, their low mechanical strength and slow cell growth limit effectiveness. This study examined solid scaffolds, which provide superior mechanical support and promote rapid cell growth, to modulate the growth behavior of injured hippocampal tissue. Three scaffold types were used: planar bioactive glass, planar aragonite (promoting neuronal and astrocytic growth), and three-dimensional glass beads. The scaffolds were applied in two steps. First, hippocampal tissue chunks from postnatal rat brains were cultured on the planar substrates; then, glass beads were added. On glass, tissue adopted a round/oval shape with pronounced vertical growth, while on aragonite it flattened and spread irregularly, reaching lengths twice as large and an area 3.8 times greater than on glass. In the second step, adding glass beads led to vertical growth on glass, with tissue encapsulating beads to form a complex 3D structure. In contrast, aragonite-supported tissue formed bump-like structures when encapsulating the beads, remaining largely planar. Also, they showed a tenfold lower bead density and twofold greater inter-bead distances than tissue on glass. In both cases, cellular outgrowth occurred. These findings show that sequential application of solid scaffolds with distinct structural properties can guide diverse tissue growth behaviors and serve as a strategy for fabricating neural implants, with implications for treating brain trauma and disease.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"815-824"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside F1 ameliorates nonalcoholic fatty liver disease by activating the AMPK/PGC-1α pathway and autophagy.","authors":"Wenjiao Xie, Yun Lv, Zhixian Zhou, Guihui Wang, Xu Zhang, Daiping Peng, Haiyan Yang, Juan Liao, Xin Sun, Wei Lin, Zhe Ding","doi":"10.1007/s11626-026-01177-9","DOIUrl":"10.1007/s11626-026-01177-9","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases globally, and currently, there is a lack of specific effective drugs. Ginsenoside F1 (Gf1) is the main active ingredient of the traditional Cahinese medicine Sansheng Siwei Wan, but its role and mechanism in NAFLD remain unclear. This study aims to explore the ameliorative effect of Gf1 on NAFLD and clarify whether it exerts its effect by regulating the AMPK/PGC-1α signaling pathway and autophagy. An NAFLD model was established by feeding SD rats with a high-fat diet (HFD) for 8 weeks, followed by intragastric administration of different doses (25, 50, 100 mg/kg/d) of Gf1 for 4 weeks. In vitro, a lipotoxicity model was established by treating AML-12 mouse hepatocytes with a mixture of oleic acid/palmitic acid (OA/PA), and Gf1 (20, 40 μM) was applied for intervention. The efficacy of Gf1 was evaluated by detecting serum biochemical indicators, liver histopathology, inflammatory factors, cell proliferation, apoptosis, etc. Western Blot was used to detect the expression of key proteins in the AMPK/PGC-1α pathway and autophagy marker proteins in the liver and cells. Mechanistic verification was carried out by using the AMPK inhibitor BML-275 and the PGC-1α inhibitor SR-18292. Gf1 intervention significantly reduced the liver weight, liver index, serum levels of ALT, AST, TG, TC, and the expression of inflammatory factors TNF-α, IL-6, IFN-γ in NAFLD rats, and improved liver fat accumulation and glycogen storage. In AML-12 cells, Gf1 promoted cell proliferation inhibited by FFA, inhibited cell apoptosis and the release of inflammatory factors. Mechanistic studies showed that Gf1 significantly upregulated the protein expression of p-AMPK and PGC-1α in liver tissues and cells, and simultaneously activated autophagy (increased LC3-II/I and Beclin-1, decreased p62). The promoting effects of Gf1 on cell proliferation, apoptosis, inflammation, and autophagy could be reversed by the AMPK or PGC-1α inhibitor. Gf1 can effectively improve liver steatosis, inflammatory response, and cell damage in NAFLD models in vivo and in vitro. Its protective effect may be related to the activation of the AMPK/PGC-1α signaling pathway and the subsequent enhancement of autophagy. This study reveals for the first time the potential value of Gf1 in the treatment of NAFLD and its molecular mechanism, providing new experimental evidence for the development of NAFLD drugs targeting the AMPK/PGC-1α/autophagy axis.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"754-767"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pro-myogenic and anti-atrophic effects of Padina arborescens extract through Akt/mTOR signaling in dexamethasone-induced C2C12 cells and zebrafish model.","authors":"Kyeong Min Lee, Wook-Chul Kim, Yun-Su Lee, Ji-Won Park, Bohyun Yun, WonWoo Lee, Kyung-Min Choi, Seung Tae Im, Seung-Hong Lee","doi":"10.1007/s11626-026-01181-z","DOIUrl":"10.1007/s11626-026-01181-z","url":null,"abstract":"<p><p>Muscle atrophy, which is characterized by the loss and dysfunction of skeletal muscle proteins, is a major degenerative condition that is associated with aging and glucocorticoid therapy. Marine-derived compounds, particularly polyphenols, have recently potential in modulating muscle metabolism and regeneration. This study aimed to investigate the effects of the ethanolic extract from Padina arborescens (PAE) on myogenic differentiation and dexamethasone (DEXA)-induced muscle atrophy using C2C12 myotubes and a zebrafish model. PAE treatment significantly promoted myotube differentiation by modulating the Akt/mTOR signaling pathway and enhancing the expression level of myogenic regulatory factors (MyoD and myogenin). In DEXA-treated myotubes, PAE effectively suppressed the ubiquitin proteasome system, restored myosin heavy chain protein synthesis, and recovered myotube morphology. In vivo, PAE supplementation ameliorated the DEXA-induced locomotor dysfunction in zebrafish without causing developmental or neurotoxic abnormalities, as confirmed by the normal survival rate, body length, and heart rate. Collectively, these findings indicated that polyphenol-rich PAE exerts protective and anabolic effects by promoting myogenesis and preventing glucocorticoid-induced muscle degradation. Therefore, PAE may be used as a promising marine-derived therapeutic agent for maintaining skeletal muscle health and preventing muscle atrophy.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"801-814"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Establishment of a novel immortalized cell line derived from porcine plasmacytoid dendritic cells.","authors":"Shunichi Suzuki, Takato Takenouchi, Hirohide Uenishi","doi":"10.1007/s11626-026-01186-8","DOIUrl":"10.1007/s11626-026-01186-8","url":null,"abstract":"","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"738-744"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}