acteoside and Acute-Lung-Injury

In recent years, cistanche tea has been increasingly used as a major herbal supplement in functional drinks, and it has attracted a growing number of consumers because of its excellent tonic effects and medicinal properties. Acteoside (ACT), which is the principal bioactive component of Chinese cistanche tea, possesses various pharmacological effects. This study profiled, isolated, identified, and investigated the hepatoprotective capacities of metabolites in rat urine after the administration of ACT. Eleven metabolites, including one new compound (M8), were obtained and identified by nuclear magnetic resonance (NMR) spectroscopy for the first time. Compared with native ACT, ACT metabolites such as hydroxytyrosol (HT), 3-hydroxyphenylpropionic acid (3-HPP), and caffeic acid (CA) exhibited higher hepatoprotective activities by regulating oxidative stress, lipid peroxidation, and inflammatory responses in a GalN/LPS-induced-acute-hepatic-injury mouse model. The HT treatment markedly reduced the levels of TNF-α to 280 ± 14.3 ng/L compared with the model group (429 ± 9.20 ng/L, p < 0.01). The results obtained indicated that cistanche tea could be developed as a functional drink for the prevention of hepatic injuries and that ACT metabolites could be responsible for the potent hepatoprotective activity as well as the other therapeutic effects.

Topics: Acute Lung Injury; Animals; Cistanche; Glucosides; Humans; Liver; Male; Mass Spectrometry; Mice; Molecular Structure; Phenols; Plant Preparations; Protective Agents; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha

The purpose of the present study was to investigate the protective role of acteoside (AC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). BalB/c mice intraperitoneally received AC (30, and 60 mg/kg) or dexamethasone (2 mg/kg) 2h prior to or after intratracheal instillation of LPS. Treatment with AC significantly decreased lung wet-to-dry weight (W/D) ratio and lung myeloperoxidase (MPO) activity and ameliorated LPS-induced lung histopathological changes. In addition, AC increased super oxide dismutase (SOD) level and inhibited malondialdehyde (MDA) content, total cell and neutrophil infiltrations, and levels of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) in LPS-stimulated mice. Furthermore, we demonstrated that AC inhibited the phosphorylation of IκBα, nuclear factor-κB (NF-κB) p65, inhibitor of nuclear factor kappa-B kinase-α (IKK-α) and inhibitor of nuclear factor kappa-B kinase-β (IKKβ) in LPS-induced inflammation in A549 cells. Our data suggested that LPS evoked the inflammatory response in lung epithelial cells A549. The experimental results indicated that the protective mechanism of AC might be attributed partly to the inhibition of proinflammatory cytokine production and NF-κB activation.

Topics: Acute Lung Injury; Animals; Anti-Inflammatory Agents; Bronchoalveolar Lavage Fluid; Cytokines; Dexamethasone; Glucosides; Lipopolysaccharides; Lung; Male; Malondialdehyde; Mice; Mice, Inbred BALB C; NF-kappa B; Phenols; Signal Transduction; Superoxide Dismutase