Auricularia auricular-judae polysaccharide attenuates lipopolysaccharide-induced acute lung injury by inhibiting oxidative stress and inflammation

• Published in: Biomedical reports Vol. 3; no. 4; pp. 478 - 482
• Main Authors: ZHUAN-YUN, LI, XUE-PING, YAO, BIN, LIU, REHEMAN, HA NIZAIER, YANG, GAO, ZHAN, SUN, QI, MA
• Format: Journal Article
• Language: English
• Published: England D.A. Spandidos 01.07.2015; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: acute lung injury; Acute respiratory distress syndrome; Alveoli; Antioxidants; Assaying; Auricularia auricular-judae polysaccharide; Bronchus; Cytokines; Edema; Enzyme-linked immunosorbent assay; Fungi; Gram-negative bacteria; Hypoxia; Inflammation; Injury analysis; Interleukin 6; Laboratory animals; Life sciences; Lipid peroxidation; Lipids; lipopolysaccharide; Lipopolysaccharides; Lungs; Malondialdehyde; Neutrophils; Oxidative stress; Pathogenesis; Permeability; Peroxidase; Pharmacology; Proteins; Pulmonary hypertension; Rats; Reactive oxygen species; Rodents; Staining; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Weight reduction; United Kingdom; China; Auricularia auricular-judae polysaccharide; lipopolysaccharide; inflammation; acute lung injury; oxidative stress
• ISSN: 2049-9434; 2049-9442
• DOI: 10.3892/br.2015.470

Auricularia auricular-judae polysaccharide (AAP) has shown a variety of pharmacological properties. In the present study, the role of AAP in acute lung injury (ALI) induced by lipopolysaccharide (LPS) was analyzed in rats to further explore the possible underlying mechanisms. Adult Sprague-Dawley rats were randomly assigned into the control, AAP, LPS and LPS plus AAP groups. Rats were injected with LPS (10 mg/kg, intraperitoneal) to induce ALI. Rats in the LPS plus AAP group were treated with AAP for 7 days before the induction of ALI. The protein concentration in the bronchoalveolar lavage fluid (BALF) was measured. The animal lung edema degree was evaluated by the wet/dry (W/D) weight ratio. The myeloperoxidase (MPO) activity and malondialdehyde (MDA) level were assayed by MPO and MDA kits, respectively. The levels of inflammatory mediators, tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, were assayed by the enzyme-linked immunosorbent assay method. Pathological changes of lung tissues were observed by hematoxylin and eosin staining. The data showed that treatment with AAP significantly improved LPS-induced lung pathological changes, attenuated protein concentration in the BALF, inhibited MPO activity and reduced the MDA level and lung W/D weight ratio. AAP also inhibited the release of TNF-α and IL-6 in blood. The results indicated that AAP has a protective effect on LPS-induced ALI in rats.