04 November 2019 : Animal Research
Eupatilin Alleviates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting Inflammation and Oxidative StressHaiying Liu12BCDEF, Jindou Hao2BCDE, Chunyuan Wu2BCD, Guosheng Liu1ABCDEF*, Xing Wang2BCE, Jieming Yu2BE, Yu Liu2BF, Hongxia Zhao2ABCDEFG
Med Sci Monit 2019; 25:8289-8296
BACKGROUND: Eupatilin, an active flavone separated from Artemisia species, has various biological activity such as anti-inflammatory activity. The aim of the present study was to find out the influence of eupatilin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats.
MATERIAL AND METHODS: The administration of LPS was used to induce ALI; eupatilin was given 1 hour before the LPS administration. Lung structural damage of rats was analyzed by hematoxylin and eosin staining and the wet/dry lung ratio. The related inflammatory factors and lung injury markers were examined by enzyme-linked immunosorbent assay. The oxidative stress factors were analyzed by corresponding kits. The expression of peroxisome proliferator-activated receptor-α (PPAR-α) was assayed by western blot and immunohistochemical staining.
RESULTS: The results showed that eupatilin alleviated LPS-induced structural damage and decreased the wet/dry lung ratio concentration-dependently. Eupatilin decreased the level of surfactant protein (SP)-A, SP-D, and inflammatory factors such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and monocyte chemo-attractant protein (MCP)-1. LPS trigged nitric oxide (NO) generation, improved the production of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and decreased the activity of superoxide dismutase (SOD), which were reversed when rats treated with eupatilin in a concentration-dependent way. Besides, the expression of PPAR-a was increased under the treatment of eupatilin.
CONCLUSIONS: Collectively, eupatilin alleviated LPS-induced ALI through inhibiting inflammation and oxidative stress in a concentration-dependent way, which was likely to be closely related with the activation of PPAR-α.
Keywords: acute lung injury, Eupatorium, Lipopolysaccharides, Oxidative Stress, PPAR alpha, Bronchoalveolar Lavage Fluid, Flavonoids, Interleukin-6, Lung, Malondialdehyde, Nitric Oxide, Superoxide Dismutase
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