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Protective effect of baicalin against lipopolysaccharideinduced acute lung injury in rats, and the mechanism of action
Abstract
Purpose: To study the protective influence of baicalin (BA) against LPS-mediated acute lung injury (ALI) in a rat model.
Methods: Twenty-seven Sprague-Dawley (SD) rats were assigned (9 rats each) to groups as follows: normal control (NC) treated intraperitoneally with normal saline; lipopolysaccharide (LPS) group treated with 10 mg/kg LPS; and lipopolysaccharide and baicalin (LPS + Ba) group treated with 100 mg/kg LPS, followed 15 min later by 10 mg/kg of baicalin. Pathological changes were assessed by H & E staining. Different types of cells were identified and counted using Rayleigh Giemsa staining. Levels of IL-6 and TNF-α and IL-1β in pulmonary tissue were determined by enzyme-linked immunosorbent assay (ELISA). Matute-Bello scoring method was applied to evaluate the extent of lung injury, while pulmonary expression levels of Nrf2, HO-1 and NQO1 were assayed with Western blot.
Results: Lung injury score, and numbers of neutrophils and macrophages were significantly higher in LPS than in NC group. Inflammatory score, and numbers of neutrophils and macrophages in LPS + BA group were significantly lower than those in LPS group (p < 0.05). Compared with NC group, lung tissue levels of IL-6, TNF-α and IL-1β in LPS group were significantly increased, but were significantly reduced in LPS + BA rats, relative to LPS rats (p < 0.05). Expression levels of Nrf2, HO-1 and NQO1 in lung tissue were significantly lower in LPS group than in NC group (p < 0.05) but higher in lung tissue of LPS + BA group, relative to LPS group.
Conclusion: Baicalin (BA) protects rats from LPS-induced ALI by enhancing the expressions of Nrf2 and HO-1 through activation of Nrf2/ARE signal pathway. These findings may be useful in developing novel BA-based anti-inflammatory drugs.
