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- 欣润生物
- 江苏无锡
- IM2027-1
- 2025年12月15日
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- 详细信息
- 文献和实验
- 技术资料
- 英文名：
Immortalized brown adipose precursor cells in mice
- 库存：
10
- 供应商：
欣润生物
- 肿瘤类型：
NO
- 细胞类型：
永生化
- ATCC Number：
11222
- 品系：
ICR小鼠
- 组织来源：
棕色脂肪前体
- 相关疾病：
无
- 物种来源：
小鼠
- 免疫类型：
不详
- 细胞形态：
成纤维细胞样
- 是否是肿瘤细胞：
否
- 器官来源：
/
- 运输方式：
常温
- 年限：
5年
- 生长状态：
贴壁生长
- 规格：
T25方瓶
产品介绍
细胞名称：小鼠棕色脂肪前体细胞系、永生化小鼠棕色脂肪前体细胞
背景描述：小鼠棕色脂肪前体细胞分离自小鼠肩胛处脂肪组织，体外培养的小鼠棕色脂肪前体细胞呈成纤维细胞样生长，为短梭形、小三角形以及多角形等。来源于中胚层的小鼠棕色脂肪前体细胞具有向成脂肪、成软骨、成骨、心肌细胞和神经源细胞分化的多分化潜能。因此脂肪组织可以作为干细胞库的重要来源，并可作为多种组织工程的种子细胞，有非常重要的研究和应用价值。
产品货号：IM2027
细胞类型:永生化细胞
传代能力:可传代25代左右
细胞形态:成纤维细胞样
完全培养基：小鼠棕色脂肪前体细胞系、永生化小鼠棕色脂肪前体细胞完全培养基
支原体分析鉴定：阴性
培养条件：37℃，5%CO2
发货方式：T25方瓶
货期：1-2周时间
永生化小鼠棕色脂肪前体细胞诱导成脂鉴定
The effects of short-chain fatty acid acetate on brown adipocytes differentiation and metabolism
Short-chain fatty acids (SCFA) are a sub-group of fatty acids including formic acid, acetic acid, propionic acid, isobutyric acid, butyric acid, isovaleric acid and valeric acid. Acetate, propionate and butyrate are three major shortchain fatty acids, which are mainly formed in the gastrointestinal tract via colonic bacteria fermentation of carbohydrates, especially resistant starches and dietary fibre. There has been increasing interest in the idea that the short-chain fatty acids play crucial roles in a range of physiological functions. Recently, increasing evidence suggested there is a strong link between short-chain fatty acids and energy homeostasis. Several studies highlighted the protective effects of the short-chain fatty acids on high-fat diet induced obesity and other harmful metabolic disorders in mice. However, the coherent understanding of the multi-level network in which short-chain fatty acids exert their effects still needs to be elucidated. Up to date, it has been demonstrated that short-chain fatty acids can mediate energy balance via affecting appetite control in brain, increasing
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文献和实验Chicken intestinal epithelial cells were obtained from NEWGAINBIO company. Cells were cultured on 37℃, with 5% CO2, in the Ham’s F-12 Nutrient (DMEM/12) that contained the following supplementations: fetal bovine serum (5%), in-sulin (5 µg/mL), transferrin (5 µg/mL), selenium (5 ng/mL), epidermal growth factor (5 ng/mL) and penicillin-streptomycin (100–100 U/mL) for cell culturing (full DMEM/12). Experiments were performed with chicken intestinal epithelial cells and working solutions were prepared with plain DMEM/12 without supplementation. For the investigations, cells were seeded onto 96-well, 24-well or 6-well polystyrene cell culture plates.
Primary hVICs (passage 2) were cultured to 50–60% confluence and infected with pGMLV-SV40T-puro lentivirus (NewgainBio, Wuxi, China) at a multiplicity of infection of 80 supplemented with 5 µg/mL polybrene (Sigma-Aldrich, Buchs, Switzerland).
Tissue was cultured until cells became visible around the tissue, and when the fusion reached 90% (FIGURE 1A) §ask ¦lled with the prepared culturing medium was sent to the company for further immortalisation. Cell immortalisation was done for cell stability and longer-term use. Immortalised cells were cultured with 10% FBS and 1% PS in the DMEM medium. After the cells multiplied and merged, they were routinely passed and grown ( NEWGAINBIO Inc. Wuxi, Jiangsu, China) (FIGURE 1B-C).
Mouse primary cultured renal vascular ECs and VSMCs were obtained from Newgainbio company, which were tested by Factor VIII and α-smooth muscle actin (α-SMA), the marker of ECs and VSMCs. RNeasy Mini Kit was used for RNA extraction, and the above protocols were repeated.
Porcine primary colon epithelial cells (Newgainbio company, Wuxi,China) were cultured in Dulbecco's Modified Eagle's Medium (Solarbio, Beijing, China) containing 10 % fetal bovine serum (BioInd, Kiryat shmona, Lsrael) at 37 ◦C and 5 % CO2 humidity.
为啥我的卡路里燃烧不起来？蔬菜水果中常见的它没准是你减肥路上
1）。在过去的二十年里，研究报道了很多环境毒物通过对肠道微生物群、能量摄入或脂肪生成的影响，从而与肥胖的发展有关。然而，几乎没有研究报道农药或者试剂通过抑制能量消耗和/或棕色脂肪组织产热导致肥胖的作用。研究内容CPF 抑制棕色脂肪细胞中的产热基因和线粒体呼吸首先，研究者挑选了 34 种在农业、食品加工和包装中常用的化学试剂，在带有 Ucp1-荧光素酶报告基因的小鼠永生化棕色脂肪细胞中检测了这些化学试剂对 Ucp1 表达的影响。在检测的 34 种化学物质中，只有农药 CPF 显著降低 Ucp1 启动子活性
实验材料： 1. 6-7周龄小鼠（最好为雄性鼠，因为它们的骨头比较粗大；运输后需要休息至少5天；不要使用应激或脱水的老鼠） 2. 70%乙醇 3. 冰冷的以及室温的RPMI-1640培养基（如Life Technologies） 4. 氯化铵溶液0.02mol/L Tris·Cl，pH7.2 /0.14mol/L NH4 Cl 5. 裂解淋巴细胞的抗体（杂交瘤上清）（可选）。例如，杂交瘤RA3-3A
Nat Metab：汤其群 / 郭亮团队发现半胱氨酸双加氧酶促进脂肪分解的新功能
）是催化甘油三酯分解第一步反应的限速酶。脂肪组织特异性敲除 ATGL 的小鼠更容易发生肥胖，寒冷耐受能力严重受损，同时伴随棕色脂肪的白色样改变 [1]。HSL（由 Lipe 编码）负责催化甘油三酯分解的第二步反应。增加小鼠脂肪组织 HSL 的活性抑制了高脂饮食诱导的肥胖、胰岛素抵抗以及肝脏脂肪变性 [2]。这说明脂肪组织脂解在调控机体适应性产热、能量代谢及影响肥胖发生发展中发挥重要作用。转录因子 PPARγ 可以促进 ATGL 和 HSL 的表达从而促进脂解 [3]，然而其具体调控机制尚未完全阐明
技术资料