Lipopolysaccharides

SKU: orb1309477

Description

Lipopolysaccharide (LPS) from E. coli O55:B5 is a potent immunostimulant that activates immune responses via TLR4. It is widely used to model inflammatory diseases such as arthritis, COPD, and ARDS in both in vitro cell studies and in vivo animal experiments.

Key Properties

• MW: 4899.92
• Formula: C₂₀₅H₃₆₆N₃O₁₁₇P₅
• SMILES: CCCCCCCCCCCCCCCC1[C@H](OC([C@H]([C@@H]1OC(=O)CC(CCCCCCCCCCC)O)O)CO[C@H]2[C@H](C([C@@H](C(O2)CO[C@@]3(CC([C@H](C(O3)C(CO)O)O[C@H]4[C@@H](C([C@@H](C(O4)C(CO)O)OP(=O)(O)OP(=O)(O)OCCN)O[C@@H]5[C@@H](C([C@@H](C(O5)C(CO[C@@H]6[C@@H](C([C@](CO6)(C(CO)O)O)O)O)O)OP(=O)(O)O)O[C@@H]7C(C([C@@H](C(O7)CO[C@@H]8C(C([C@H](C(O8)CO)O)O)O)O)O[C@@H]9C(C([C@H](C(O9)CO)O)O)O[C@@H]1C(C([C@@H](C(O1)CO)O[C@@H]1C(C([C@H](C(O1)CO)O)OC1[C@@H](C(C([C@@H](O1)C)O[C@@H]1C(C([C@@H](C(O1)CO)O)O[C@@H]1C(C[C@H](C(O1)C)O)O)O[C@@H]1C(C([C@H](C(O1)CO)O)O)O)O)O)O)O)O[C@@H]1[C@H](C([C@@H](C(O1)CO)O)O)NC(=O)C)O)O)O)O[C@@]1(CC([C@H](C(O1)C(CO)O)O)O[C@@]1(CC([C@H](C(O1)C(CO)O)O)O)C(=O)O)C(=O)O)C(=O)O)OP(=O)(O)O)OC(=O)CC(CCCCCCCCCCC)OC(=O)CCCCCCCCCCCCC)NC(=O)CC(CCCCCCCCCCC)OC(=O)CCCCCCCCCCC)CP(=O)(O)O
• Target: Others
• Solubility: DMSO:1 mg/mL (0.2 mM);H2O:5 mg/mL (1.02 mM)

Bioactivity

• Target IC50:
  SH-SY5Y cells viability:0.25 μg/mL (48h)|A549 cells viability:11.06 mg/L|bovine aortic endothelial cell proliferation:22 ng/mL
• In Vivo:
  METHODS: To construct a mouse model of sepsis, Lipopolysaccharides (25 mg/kg) were administered to C57/BL mice by a single intraperitoneal injection. RESULTS: Lipopolysaccharides induced significant up-regulation of inflammatory factors TNF-α and IL-1β. Lipopolysaccharides induced sepsis in a mouse model. METHODS: To investigate the effects of Lipopolysaccharides on cognitive deficits and neuroinflammation, Lipopolysaccharides (500-750 μg/kg in saline) were injected intraperitoneally into C57BL/6J mice once daily for seven days. RESULTS: Lipopolysaccharides treatment resulted in disease behavior and cognitive deficits in mice, and these effects were accompanied by microglia activation and neuronal cell loss in the hippocampus. Lipopolysaccharides treatment decreased serum and brain homogenate levels of IL-4 and IL-10, and increased levels of TNF-α, IL-1β, PGE2, and NO levels were increased.
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• In Vitro:
  METHODS: Human lung mucoepidermoid carcinoma cells H292 and monocytes THP-1 were treated with Lipopolysaccharides (1-20 µg/mL) for 6-48 h. Cytotoxicity was detected by MTT. RESULTS: No significant changes in the viability of H292 cells treated with 1 and 2.5 µg/mL Lipopolysaccharides and THP-1 cells treated with 1 and 2 µg/mL Lipopolysaccharides were observed. Lipopolysaccharides at higher concentrations (5-20 µg/mL) were significantly cytotoxic to both H292 and THP-1 cells. METHODS: Human induced pluripotent stem cell-derived cardiomyocytes hiPSC-CMs were treated with Lipopolysaccharides (0.1-100 µg/mL) for 6-48 h. Inflammatory cytokine expression was detected by qRT-PCR. RESULTS: The mRNA expression level of IL-1β was increased at 6 h of Lipopolysaccharides treatment, IL-10 was increased only at 48 h, and TNF-α and IL-6 were increased at both 6 and 48 h. METHODS: Neutrophils were treated with Lipopolysaccharides (10 mg/ml) for 4 h. The expression levels of target proteins were measured by Western Blot. RESULTS: The expression of H3-cit and TLR4 increased after treatment with Lipopolysaccharides, which induced the formation of neutrophil extracellular traps (NETs) in neutrophils.
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Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Lipopolysaccharides, LPS

Compound Identifiers

PubChem CID

11970143