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Acute lung injury (ALI) is a vital pulmonary inflammatory disorder with high mortality, and it can be caused by endotoxins, hyperoxia, etc. LPS (Lipopolysaccharide) -induced acute lung injury is a commonly utilized model that characterized by excessive inflammatory response within lung, hypoxemia and pulmonary oedema. LPS was shown to activate the expression of inflammatory mediators, such as tumor necrosis factor (TNF-α) and interleukin (IL)-6, by challenging mice/rats both intratracheally and intranasally. And subsequently, readouts are analyzed at specified time point.
Creative Bioarray focuses on drug research and development services and helps customers evaluate the drug efficacy and study the associated pathological mechanisms of ALI by LPS-induced acute lung injury model.
With extensive experience in the field of ALI, we are confident to help you to overcome any upcoming challenges. Our experts are fully capable of customizing our protocols and assays to meet your specific needs. With our help, we wish to facilitate your research with high efficiency.
Figure. 1. Effects of alliin on histopathological changes in lung tissues in LPS-induced ALI mice. Representative histological changes of lung obtained from mice of different groups. A: Control group, B: alliin (100 mg/kg) alone group, C: LPS group, D: LPS+ alliin (25 mg/kg) group, E: LPS + alliin (50 mg/kg) group F: LPS + alliin (100 mg/kg) group (Hematoxylin and eosin staining, magnification 200×).
Figure. 2. Effect of 4-PBA on structural damage and production of inflammatory mediators induced by LPS in mice. (A) Lung sections of the mice were stained with representative H&E for histological examination (magnification × 200). (B) BAL fluid was performed to differentially count total cells. IL-1b (C), TNF-a (D) and IL-6 (E) in BAL fluid were analyzed by ELISA.
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Inflammation & Autoimmune Disease Models: