title: Ginsenoside Rg3 ameliorates lipopolysaccharide-induced acute lung injury in mice through inactivating the nuclear factor-κB (NF-κB) signaling pathway.
abstract: Ginsenoside Rg3 (GRg3), one of the major active saponins isolated from ginseng (the root of Panax ginseng C.A. Meyer, Araliaceae), has been reported with many health benefits. Currently, the protective effect of GRg3 on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice was investigated. The results indicated that GRg3 treatment could greatly attenuate LPS-induced histopathological alterations in the lung in a concentration-dependent manner. LPS-induced increase of lung wet-to-dry weight ratio (W/D ratio) was also dose-dependently reduced by GRg3 treatment. LPS-induced increases of the total cells, neutrophils and macrophages in the bronchoalveolar lavage fluids (BALFs) were significantly inhibited by GRg3 treatment in a dose-dependent fashion. The levels of pro-inflammatory cytokines including TNF-α, IL-1β and IL-6 in BALFs increased after LPS-induced ALI, which was inhibited by GRg3. Western blot results showed that during ALI LPS activated NF-κB pathway in the lung tissues by upregulating NF-κB p65 phosphorylation and its downstream COX-2 expression; however, these effects of LPS were inhibited by GRg3 treatment. Taken together, these findings in present study suggested that GRg3 provided protective effects against LPS-induced ALI in animal model and might harbor the potential to be considered as drug for the treatment of ALI in clinic.
authors.affiliation: Department of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, People's Republic of China. Electronic address: chengzhiqiang07@sina.com.
authors.forename: Zhiqiang
authors.initials: Z
authors.lastname: Cheng
authors.affiliation: Department of Emergency Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, People's Republic of China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000188:drug therapy*; D000818:Animals; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D036145:Ginsenosides / Q000627:therapeutic use*; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology; D008168:Lung / Q000187:drug effects* / Q000502:physiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D005894:Panax / Q000276:immunology; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D016207:Cytokines; D036145:Ginsenosides; D008070:Lipopolysaccharides; D016328:NF-kappa B; C097367:ginsenoside Rg3; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2
keywords: Acute lung injury (ALI); Cyclooxygenase 2 (COX-2); Ginsenoside Rg3 (GRg3); Lipopolysaccharide (LPS); Nuclear factor-κB (NF-κB)