| Description | Lipopolysaccharides (LPS) derived from Escherichia coli 055:B5, are a unique component of the cell wall of Gram-negative bacteria. They are composed of three regions: lipid A, oligosaccharide core, and O-specific polysaccharide (O-antigen). Lipopolysaccharides help maintain the integrity of the cell outer membrane and protect bacteria from damage by bile salts and lipid antibiotics. Lipopolysaccharides are highly immunogenic antigens that can enhance immune responses and can be used to construct inflammatory models. |
| In vitro | 方法：人肺粘液表皮样癌细胞 H292 和单核细胞 THP-1 用 Lipopolysaccharides (1-20 µg/mL) 处理 6-48 h，使用 MTT 方法检测细胞毒性。结果：用 1 和 2.5 µg/mL Lipopolysaccharides 处理的 H292 细胞及用 1 和 2 µg/mL Lipopolysaccharides 处理的 THP-1 细胞的活力没有观察到显著变化。用更高浓度 (5–20 µg/mL) 的 Lipopolysaccharides 对 H292 和 THP-1 细胞都具有显著的细胞毒性。[1]方法：人诱导多能干细胞来源的心肌细胞 hiPSC-CMs 用 Lipopolysaccharides (0.1-100 µg/mL) 处理 6-48 h，使用 qRT-PCR 方法检测炎性细胞因子表达情况。结果：IL-1β 的 mRNA 表达水平在 Lipopolysaccharides 处理 6 h 时增加，IL-10 仅在 48 h 时增加，TNF-α 和 IL-6 在 6 h 和 48 h 时均增加。[2]方法：中性粒细胞用 Lipopolysaccharides (10 mg/ml) 处理 4 h，使用 Western Blot 方法检测靶点蛋白表达水平。结果：Lipopolysaccharides 处理后 H3-cit 和 TLR4 的表达增加。Lipopolysaccharides 诱导中性粒细胞胞外诱捕网 NETs 的形成。[3] |
| In vivo | 方法：为构建败血症小鼠模型，将 Lipopolysaccharides (25 mg/kg) 单次腹腔注射给 C57/BL 小鼠。结果：Lipopolysaccharides 诱导炎症因子 TNF-α 和 IL-1β 显著上调。Lipopolysaccharides 诱导小鼠败血症模型。[4]方法：为研究 Lipopolysaccharides 对认知障碍和神经炎症的影响，将 Lipopolysaccharides (500-750 μg/kg in saline) 腹腔注射给 C57BL/6J 小鼠，每天一次，持续七天。结果：Lipopolysaccharides 治疗会导致小鼠的疾病行为和认知障碍，这些影响伴随着海马中的小胶质细胞活化和神经元细胞损失。Lipopolysaccharides 处理可降低血清和脑匀浆中 IL-4、IL-10 的水平，而 TNF-α、IL-1β、PGE2 和 NO 的水平升高。[5] |
| Synonyms | 脂多糖, LPS |
| molecular weight | 4899.92 |
| Molecular formula | C205H366N3O117P5 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility | H2O: 5 mg/mL (Need ultrasonic) |
| References | 1. Liu X, et al. LPS‑induced proinflammatory cytokine expression in human airway epithelial cells and macrophages via NF‑κB, STAT3 or AP‑1 activation. Mol Med Rep. 2018 Apr;17(4):5484-5491. 2. Yücel G, et al. Lipopolysaccharides induced inflammatory responses and electrophysiological dysfunctions in human-induced pluripotent stem cell derived cardiomyocytes. Sci Rep. 2017 Jun 7;7(1):2935. 3. Chen J, et al. Aβ1-40 Oligomers Trigger Neutrophil Extracellular Trap Formation through TLR4- and NADPH Oxidase-Dependent Pathways in Age-Related Macular Degeneration. Oxid Med Cell Longev. 2022 Jun 18;2022:6489923. 4. Wang Z, et al. BmKK2, a thermostable Kv1.3 blocker from Buthus martensii Karsch (BmK) scorpion, inhibits the activation of macrophages via Kv1.3-NF-κB- NLRP3 axis. J Ethnopharmacol. 2023 Oct 5;314:116624. 5. Zhao J, et al. Neuroinflammation induced by lipopolysaccharide causes cognitive impairment in mice. Sci Rep. 2019 Apr 8;9(1):5790. |
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