mortality/aging
• mice injected with a lethal dose of lipopolysaccharide (LPS) or undergoing cecal ligation and puncture (CLP) to induce endotoxemia or polymicrobial-induced sepsis, respectively, show prolonged survival time
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immune system
• LPS-induced nitric oxide production in macrophages is blunted
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• mice injected with a lethal dose of LPS to induce endotoxemia show prolonged survival time
• mice challenged with a low dose of LPS to induce acute lung injury show reduced alveolar congestion and infiltration of inflammatory cells, attenuated cell apoptosis and macrophage infiltration, reduced pulmonary vascular hyperpermeability, and blunted nitric oxide production, indicating protection from LPS-induced acute lung inury
• mice challenged with a low dose of LPS show protection from kidney injury
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homeostasis/metabolism
• LPS-induced nitric oxide production in macrophages is blunted
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hematopoietic system
• LPS-induced nitric oxide production in macrophages is blunted
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cardiovascular system
• LPS-induced pulmonary vascular hyperpermeability is reduced
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