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Chinese Journal of Natural Medicines (English Ed.) ; (6): 52-58, 2015.
Article in English | WPRIM | ID: wpr-812174

ABSTRACT

In the present study, we analyzed the role of Ginkgo biloba extract in lipopolysaccharide(LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS. G. biloba extract (12 and 24 mg·kg(-1)) and dexamethasone (2 mg·kg(-1)), as a positive control, were given by i.p. injection. The cells in the bronchoalveolar lavage fluid (BALF) were counted. The degree of animal lung edema was evaluated by measuring the wet/dry weight ratio. The superoxidase dismutase (SOD) and myeloperoxidase (MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, tumor necrosis factor-a, interleukin-1b, and interleukin-6, were assayed by enzyme-linked immunosorbent assay. Pathological changes of lung tissues were observed by H&E staining. The levels of NF-κB p65 and COX-2 expression were detected by Western blotting. Compared to the LPS group, the treatment with the G. biloba extract at 12 and 24 mg·kg(-1) markedly attenuated the inflammatory cell numbers in the BALF, decreased NF-κB p65 and COX-2 expression, and improved SOD activity, and inhibited MPO activity. The histological changes of the lungs were also significantly improved. The results indicated that G. biloba extract has a protective effect on LPS-induced acute lung injury in mice. The protective mechanism of G. biloba extract may be partly attributed to the inhibition of NF-κB p65 and COX-2 activation.


Subject(s)
Animals , Male , Mice , Acute Lung Injury , Drug Therapy , Metabolism , Bronchoalveolar Lavage Fluid , Cell Biology , Cell Count , Cyclooxygenase 2 , Genetics , Metabolism , Enzyme-Linked Immunosorbent Assay , Gene Expression , Ginkgo biloba , Chemistry , Interleukin-1beta , Interleukin-6 , Lipopolysaccharides , Lung , Allergy and Immunology , Pathology , Mice, Inbred BALB C , Peroxidase , Metabolism , Phytotherapy , Plant Extracts , Pharmacology , Pulmonary Edema , Superoxide Dismutase , Metabolism , Transcription Factor RelA , Genetics , Metabolism , Tumor Necrosis Factor-alpha
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