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- 询价记录
- 文献和实验
- 技术资料
- 英文名：
BV2
- 库存：
100万
- 供应商：
欣润生物
- 肿瘤类型：
否
- 细胞类型：
细胞系
- ATCC Number：
CL1333
- 品系：
小鼠
- 组织来源：
脑胶质
- 相关疾病：
正常
- 物种来源：
小鼠
- 免疫类型：
不详
- 细胞形态：
不规则
- 是否是肿瘤细胞：
否
- 器官来源：
脑
- 运输方式：
新鲜或干冰
- 年限：
成年
- 生长状态：
贴壁生长
- 规格：
T25方瓶
- 细胞名称：BV2细胞（小鼠小胶质细胞）
- 形态：不规则，贴壁生长
- 含量：>1x106 个/瓶
- 污染：支原体、细菌、酵母和真菌检测为阴性
- 规格：T25瓶或者1mL冻存管包装
二、细胞接收后的处理：
1、贴壁细胞
- 收到T25方瓶细胞后，请检查是否漏液，如果漏液，请拍照片发给我们（冻存管细胞收到后直接37℃水浴复苏或直接放置于液氮中长期储存）。
- 请先在显微镜下确认细胞生长状态，去掉封口膜并将T25瓶置于37℃培养约2-3h。
- 弃去T25瓶中的培养基，换用新鲜的完全培养基。
- 如果细胞长满（90%以上）请及时进行细胞传代。
- 接到细胞次日，请检查细胞是否污染，若发现污染或疑似污染，请及时与我们取得联系。
2、悬浮细胞
- 收到细胞后，请检查是否漏液，如果漏液，请拍照片发给我们。
- 请先在显微镜下确认细胞生长状态，去掉封口膜并将15ml离心管置于37℃培养约2-3h。
- 1200rpm离心5min，弃去15ml离心管中的培养基，细胞沉淀用新鲜的完全培养基重悬并培养。
- 如果细胞长满（90%以上）请及时进行细胞传代。
- 接到细胞次日，请检查细胞是否污染，若发现污染或疑似污染，请及时与我们取得联系。
本公司的细胞培养操作规程，供参考
一、培养基及培养冻存条件准备：
- 准备H-DMEM培养基，90%；优质胎牛血清，10%。
- 培养条件： 气相：空气，95%；二氧化碳，5%。 温度：37℃，培养箱湿度为70%-80%。
- 冻存液：90%血清，10%DMSO，现用现配。液氮储存。
对于贴壁细胞，传代可参考以下方法：
- 弃去培养上清，用不含钙、镁离子的PBS润洗细胞1-2次。
- 加2ml消化液（0.25%Trypsin-0.53mM EDTA）于培养瓶中，置于37℃培养箱中消化2-3分钟，然后在显微镜下观察细胞消化情况，若细胞大部分变圆并脱落，迅速拿回操作台，轻敲几下培养瓶后加入3ml此细胞的培养基终止消化。
- 轻轻吹打后吸出，移入15ml离心管中，在1200RPM条件下离心5分钟，弃去上清液，加入1mL培养液后吹匀。
- 移入到事先准备好的含有5ml培养基的T-25培养瓶中或含有14ml培养基的T-75培养瓶中培养。
3）细胞冻存：待细胞生长状态良好时，可进行细胞冻存。贴壁细胞冻存时，先要消化处理并进行细胞计数。消化方法按照细胞传代方法的1-3步骤进行，最后的重悬液使用血清。悬浮细胞直接计数后离心，用血清重悬浮，加DMSO至最终浓度为10%。加入DMSO后迅速混匀，按每1ml的数量分配到冻存管中。本公司按每个冻存管细胞数目大于1X106个细胞冻存。
注意事项：
1. 收到冻存管细胞后，若发现干冰已挥发干净、冻存管瓶盖脱落、破损及细胞有污染，请立即与我们联系。
2. 所有动物细胞均视为有潜在的生物危害性，必须在二级生物安全台内操作，并请注意防护，所有废液及接触过此细胞的器皿需要灭菌后方能丢弃。
3. 细胞用途：仅供科研使用。
发货方式：
复苏后发货：我们复苏细胞后发货，货期一周左右，免运费。（气温较好建议复苏后发货）
冻存发货(干冰运输）：需额外增加干冰运费，选择干冰运输的我们发两管细胞，为了保证客户接种可靠性多发一管。（气温低于0℃须冻存发货）
细胞发货采取专业的运输包装，并选择最快捷的运输方式（顺丰速运或其他空运快递）
Effects of Microenvironment on Morphology and Function of the Microglial Cell Line BV-2
ffects of microenvironmental changes were examined in the microglial cell line BV-2. In serum supplemented medium cells were ameboid shaped and exhibited thin cytoplasmatic processes at lower concentration or in absence of serum. High levels of acetylated low-density lipoprotein (LDL) receptor and of phagocytic and proliferative activity were detected. Lipopolysaccharide (LPS) and the neuropeptide substance P (SP) induced secretion of interleukin-6. Low interleukin-3 secretion was detected only occasionally and was not influenced by LPS and SP. In defined medium, "process-bearing" cells were evident. Compared to cultures in serum supplemented medium, the cells expressed lower acetylated LDL-binding and phagocytic activity while actively proliferated, the response to LPS was reduced and to SP absent. Granulocyte/macrophage colony-stimulating factor increased the number of process-bearing cells, of acetylated LDL-binding and of IL-6 secretion induced by LPS. Cell morphology was not influenced by neurotrophins like nerve growth factor and brain-derived neurotrophic factor. The described phenotypical and functional plasticity makes the BV-2 cell line a useful model to investigate mechanisms of microglial activation.
Rotenone Directly Induces BV2 Cell Activation via the p38 MAPK Pathway
Parkinson's disease (PD) is the second most common neurodegenerative disease. Although its pathogenesis is still unclear, increasing evidence suggests that mitochondrial dysfunction induced by environmental toxins, such as mitochondrial complex I inhibitors, plays a significant role in the disease process. The microglia in PD brains are highly activated, and inflammation is also an essential element in PD pathogenesis. However, the means by which these toxins activate microglia is still unclear. In the present study, we found that rotenone, a mitochondrial complex I inhibitor, could directly activate microglia via the nuclear factor kappa B (NF-κB) signaling pathway, thereby inducing significantly increased expression of inflammatory cytokines. We further observed that rotenone induced caspase-1 activation and mature IL-1β release, both of which are strictly dependent on p38 mitogen-activated protein kinase (MAPK). The activation of p38 is associated with the presence of reactive oxygen species (ROS) produced by rotenone. Removal of these ROS abrogated the activation of the microglia. Therefore, o
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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.
Elabscience | BV2细胞M1极化造模与流式检测，这份Protocol请收好
小胶质细胞，使其向M1表型倾斜，而M2保护性表型则相对不足，形成"促炎-神经损伤-更多DAMPs释放"的恶性循环[2,4]。因此，促进小胶质细胞从M1向M2表型的转化，已成为神经退行性疾病治疗策略的重要研究方向。 图2. 小胶质细胞的激活表型[3] 图中分别标明了诱导经典（M1）或替代（M2）激活途径的分子，并展示了不同极化细胞（M1、M2a、M2b、M2c 和 M2d）所表达的分子。 三、BV2细胞——研究小胶质细胞的“利器” BV2细胞系是源自新生小鼠小胶质细胞、经v-raf/v-myc逆转
阿尔茨海默病（AD）研究・体外篇| 从细胞到类器官，体外模型选型手册
在原代细胞或体内模型中验证。 2. PC12细胞 模型来源： PC12来源于大鼠肾上腺嗜铬细胞瘤，可在神经生长因子作用下形成神经突样结构。 常见用途： 主要用于研究神经突生长、氧化应激、线粒体损伤和细胞死亡。 主要优势： 培养相对简单，神经生长因子诱导后的形态变化明显。 主要局限： PC12并不是中枢神经元，与成熟皮质或海马神经元存在明显差异。 模型定位： 适合神经元样分化和一般神经毒性研究，不能直接替代原代中枢神经元。 3. BV2细胞 模型来源： BV2是常用的小鼠小胶质细胞系。 常见
体的功能阐述： 上海交通大学医学院附属瑞金医院神经科、Med-X 研究院神经科学与神经工程中心的杨国源课题组在《Theranostics》杂志上发表了重要工作[3]，文中阐述 M2 型小胶质细胞 BV2 来源的外泌体（M2-EXO）通过将外泌体中 miR-124 转移到神经元并调控其下游基因 USP14 表达，从而促进神经细胞存活和减弱缺血性脑损伤，对缺血小鼠的大脑发挥神经保护作用。 图六 M2-EXO 可减轻脑卒中后神经元凋亡和促进神经行为恢复 同济大学和美国内布拉斯加大学医学中心联合
技术资料
