| Description | Lipopolysaccharides (LPS) is a unique component of the cell wall of Gram-negative bacteria and consists of three regions: lipid A, oligosaccharide core, and O-specific polysaccharide (O-antigen). Lipopolysaccharides help maintain the integrity of the outer cell membrane and protect bacteria from damage by bile salts and lipid antibiotics. Lipopolysaccharides is a highly immunogenic antigen that can enhance immune responses and can be used for inflammation model construction. |
| 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 |
| 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. |