IntestiCult™ 类器官生长培养基 (小鼠)

用于建立和维持小鼠肠道类器官的培养基

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产品号 #（选择产品）

产品号 #06005_C

用于建立和维持小鼠肠道类器官的培养基

产品优势

简便的体外系统，可重现成年肠上皮的特征与结构，包括细胞内及细胞间的信号传导、自我维持的干细胞微环境以及腔道内外物质的功能性转运；
无血清、成分明确的培养基配方，确保实验结果的一致性；
一周内即可生成肠道类器官；
形式简单和易于操作的实验方案

产品组分包括

IntestiCult™ 类器官生长基础培养基(小鼠)，90 mL；
IntestiCult™ 类器官生长补充剂1(小鼠)，5 mL；
IntestiCult™ 类器官生长补充剂2(小鼠), 5 mL

立即询价

总览

IntestiCult™类器官生长培养基（小鼠）是一种成分明确的无血清细胞培养基，用于高效建立和长期维持培养小鼠肠道类器官。这些类器官，或称“迷你肠道”，为研究小肠和大肠上皮及相关的干细胞动力学提供了一个方便的体外器官型培养系统。在IntestiCult™中生长的类器官具有极性的上皮，包含所有已知的成年肠道上皮细胞类型。每个独立的肠隐窝在IntestiCult™类器官生长培养基（小鼠）中培养时可快速形成类器官。这些类器官的应用包括研究正常和肿瘤肠道上皮的发育和功能、构建肠道疾病模型以及研究干细胞特性和再生疗法。类器官培养使得在体外方便地表征与成年肠道高度生理相关的体系成为可能。

如果您打算将本产品用于商业目的，请通过www.huborganoids.nl与HUB联系，以获取商业用途许可或HUB许可相关的说明。

产品说明书及文档

请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。

应用领域

本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。

文献 (112)

The CBS/H2S axis regulates intestinal stem cell homeostasis and radiation-induced intestinal damage T. Wu et al. Stem Cell Research & Therapy 2025 Oct

Abstract

BackgroundThe cycling intestinal stem cells (ISCs) exhibit radiosensitivity, and their death or impaired regenerative capacity following irradiation may result in intestinal barrier dysfunction. The cystathionine-β-synthase (CBS)/H2S axis plays a critical role in regulating cell proliferation, reactive oxygen species scavenging, and the DNA damage response. However, it remains unclear whether the CBS/H2S axis modulates ISC homeostasis and tissue radiosensitivity. Methods: Intestinal epithelium specific conditional CBS knockout mice were generated by crossing CBSfl/+ mice with Villin-CreERT2 mice. CAGGCre-ER™ mice were crossed with CBSfl/fl mice to achieve CBS knockout in multiple tissues and cell types. The Lgr5-Tdtaomato-Flag mice were generated by CRISPR/Cas9 system. The CBS inhibitor AOAA or the H2S donor GYY4137 was used to treat mice or intestinal crypt organoids. Hematoxylin and eosin, immunohistochemistry, immunofluorescence, Western blot, qRT-PCR, et al. were employed to investigate the role of the CBS/H2S axis in ISCs homeostasis and radiation-induced intestinal damage. Results: Lgr5 + ISCs and progenitor cells expressed higher levels of CBS than differentiated cells. The cecum and colon expressed significant higher CBS levels than the small intestine. Treatment with the H2S donor GYY4137 enhanced the proliferation of intestinal organoids in vitro, while inhibition of CBS by AOAA reduced this effect. Genetic knockout of CBS in the intestinal epithelium or global downregulation of CBS driven by CAGG-CreER™ in vivo did not affect ISC proliferation or differentiation under physiological conditions. Pharmacological regulation of the CBS/H2S axis in vitro failed to protect organoids from radiation-induced damage. Interestingly, administration of AOAA in vivo reduced radiation-induced atrophy of the intestinal mucosa. Furthermore, global downregulation of CBS significantly promoted ISC recovery after irradiation exposure. However, intestinal epithelium-specific CBS knockout did not confer radioprotective effects. Conclusions: Our findings suggest that the CBS/H2S axis contributes to the regulation of ISC homeostasis and represents a potential target for radiation protection, mediated through the intervention of non-epithelial cells.

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Nylon mesh chip promotes three-dimensional visualization of intestinal organoids J. Tan et al. Scientific Reports 2025 Jul

Abstract

Organoids are pivotal for bridging cellular-level and organism-level biological studies; however, significant challenges persist in their three-dimensional (3D) visualization. This study presents a nylon mesh chip designed to overcome these obstacles specifically for intestinal organoids (IOs). The chip, meticulously fabricated and assembled, comprises an upper glass layer, a nylon mesh, and a lower glass layer. We cultured IOs from mouse intestinal crypts and performed fluorescent labeling on the chip. For enhanced visualization, fluorescent labeling combined with 3D reconstruction techniques was employed. Results demonstrate that the chip’s structure stabilizes IOs in liquid environments. While conventional fluorescence imaging is limited by mesh interference, laser confocal 3D reconstruction achieves high-quality visualization by effectively filtering out redundant signals. The nylon mesh chip is a robust tool for 3D visualization of IOs and holds potential for other budding organoid types. This innovation is poised to advance organoid 3D visualization research. The online version contains supplementary material available at 10.1038/s41598-025-12015-5.

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Paneth cells inhibit intestinal stem cell proliferation through the bone morphogenic protein 7 pathway under rotavirus-mediated intestinal injury Bu et al. World Journal of Gastroenterology 2025 Jul

Abstract

Rotavirus (RV), a primary cause of diarrhea-related mortality in 2021, has been shown to damage intestinal epithelial cells while upregulating intestinal stem cells (ISCs) activities. ISCs within the crypt niche drive the continuous self-renewal of intestinal epithelium, preserving its barrier functions. Paneth cells secrete antimicrobial peptide and signaling molecules within the intestine crypt, thereby playing a crucial role in intestinal immune defense and providing ISCs functional support. However, the regulatory function of Paneth cells under pathological conditions, such as RV infection, remains unclear. To determine the impact of RV infection on Paneth cells and how Paneth cells regulate ISCs during intestinal injury repair. We constructed a reference genome for the RV enteric cytopathogenic human orphan virus strain and reanalyzed published single-cell RNA sequencing data to investigate Paneth cell responses to RV-induced intestinal injury. We derived Paneth-ISC communication networks using CellChat, tracked ISC differentiation with pseudotime analysis, and validated our findings in leucine-rich repeat-containing G protein-coupled receptor 5-enhanced green fluorescent protein-internal ribosomal entry site-Cre recombinase estrogen receptor variant 2 mice and organoids via immunofluorescence, flow cytometry, and reverse transcription quantitative polymerase chain reaction. We found that RV directly infects Paneth cells, leading to a reduction in mature Paneth cells and an increase in kallikrein 1-high immature Paneth cells. Paneth-ISC communication was significantly enhanced. In particular, the bone morphogenic protein 7 (BMP7)-activin A receptor type 2B/BMP receptor type 1A-Smad pathway was upregulated post-infection, suggesting that Paneth cells suppress excessive ISC proliferation. Functional validation confirmed activation of this pathway. Paneth cells regulate ISC proliferation during RV infection by activating BMP7 signaling, limiting excessive stem cell expansion and preserving crypt homeostasis for effective epithelial repair.

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物种	小鼠
配方	无血清

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物种

小鼠

配方

无血清

IntestiCult™ 类器官生长培养基 (小鼠)

产品号 #06005

产品号 #（选择产品）

产品号 #06005_C

产品优势

产品组分包括

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产品说明书及文档

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IntestiCult™ 类器官生长培养基 (小鼠)

产品号 #06005

产品号 #（选择产品）

产品号 #06005_C

产品优势

产品组分包括

总览

产品说明书及文档

应用领域

相关材料与文献

技术资料 (40)

文献 (112)

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