Preventive and therapeutic effects of Danhong injection on lipopolysaccharide induced acute lung injury in mice

Abstract

Ethnopharmacological relevance: Danhong injection (DHI), a Chinese Materia Medica standardized product extracted from Radix et Rhizoma Salviae Miltiorrhizae (Salvia miltiorrhiza Bge., Labiatae, Danshen in Chinese) and Flos Carthami (Carthamus tinctorius L., Compositae, Honghua in Chinese), has been reported to have anti-inflammatory, anti-oxidative and anti-fibrinolytic properties, which is used extensively for the treatment of cardiovascular diseases in clinic.

Aim of this study: The present study aimed to investigate the preventive and therapeutic effects of DHI on lipopolysaccharide (LPS) induced acute lung injury (ALI) in mice.

Materials and methods: Lung injury was induced by intranasal instillation with 10 μg LPS. Mice were randomly divided into four groups: Control group; LPS group; LPS+5 ml/kg DHI group and LPS+10 ml/kg DHI group. The effects of DHI on LPS-induced neutrophils influx, inflammatory cytokines release, protein leakage, myeloperoxidase (MPO) and superoxide dismutase (SOD) activities, malondialdehyde (MDA) level were examined. In addition, the NF-κB activation in lung tissues was detected by Western blot.

Results: In LPS challenged mice, DHI significantly reduced the infiltration of activated neutrophils and decreased the levels of TNF-α and IL-6 in bronchoalveolar lavage fluid (BALF). DHI also inhibited protein extravasation in BALF, attenuated edema and the pathological changes in the lung. In addition, DHI markedly prevented LPS-induced elevation of MDA and MPO levels, as well as reduction of SOD activity. Further study demonstrated that DHI effectively inhibited the NF-κB activation in lung tissues.

Conclusion: DHI has been demonstrated to protect mice from LPS induced acute lung injury by its anti-inflammatory and anti-oxidant activities.

Keywords: ALI; ARDS; Acute lung injury; Anti-inflammatory; Anti-oxidative; DHI; Danhong injection; ELISA; IL-6; LPS; MDA; MPO; NF-κB; SOD; TNF-α; acute lung injury; acute respiratory distress syndrome; enzyme-linked immunosorbent assay; interleukin-6; lipopolysaccharide; malondialdehyde; myeloperoxidase; nuclear factor-kappa B; superoxide dismutase; tumor necrosis factor-α.