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      The protective effect of Trillin LPS-induced acute lung injury by the regulations of inflammation and oxidative state.

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          Abstract

          Inflammation response and oxidative stress have been reported to be involved in the pathogenesis of acute lung injury (ALI). Accordingly, anti-inflammatory treatment is proposed to be a possible efficient therapeutic strategy for ALI. The purpose of our present study was to evaluate the anti-inflammatory efficacy of trillin (Tr) on ALI induced by lipopolysaccharide (LPS) in mice and explore the underlying mechanism. BALB/c mice received Tr (50, 100 mg/kg) intraperitoneally 1 h prior to the intratracheal instillation of lipopolysaccharide (LPS) challenge. Pretreatment with Tr at the dose of 50, 100 mg/kg markedly ameliorated lung wet-to-dry weight (W/D) ratio, myeloperoxidase (MPO) activity and pulmonary histopathological conditions. In addition, the protective efficacy of Tr might be attributed to the down-regulations of neutrophil infiltration, malondialdehyde (MDA), inflammatory cytokines and the up-regulations of super-oxide dismutase (SOD), catalase(CAT), glutathione(GSH), Glutathione Peroxidase(GSH-Px) in bronchoalveolar lavage fluid (BALF). Meanwhile, our study revealed some correlations between (NF-E2-related factor 2) Nrf2/heme oxygenase (HO)-1/nuclear factor-kappa B (NF-κB) pathways and the beneficial effect of Tr, as evidenced by the significant up-regulations of HO-1 and Nrf2 protein expressions as well as the down-regulations of p-NF-κB and p-inhibitor of NF-κB (IκB) in lung tissues. Taken together, our results indicated that Tr exhibited protective effect on LPS-induced ALI by the regulations of related inflammatory events via the activations of Nrf2, HO-1 and NF-κB pathway. The current study indicated that Tr could be a potentially effective candidate medicine for the treatment of ALI.

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          Author and article information

          Journal
          Chem. Biol. Interact.
          Chemico-biological interactions
          1872-7786
          0009-2797
          Jan 5 2016
          : 243
          Affiliations
          [1 ] State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.
          [2 ] Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China.
          [3 ] School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China.
          [4 ] The Fourth Affiliated Hospital of Zhejiang University School of Medicine, Yiwu 322000, China.
          [5 ] State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China; Department of Physiology and Pharmacology, China Pharmaceutical University, Tongjiaxiang 24, Nanjing, China. Electronic address: Yantianhuabest@126.com.
          [6 ] State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China; Department of Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, China. Electronic address: dxs0162@sina.com.
          Article
          S0009-2797(15)30063-6
          10.1016/j.cbi.2015.09.010
          26363199
          2e46d782-5e40-43e4-aeb7-4b587762c793
          Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
          History

          Acute lung injury,HO-1,NF-κB,Nrf2,Trillin
          Acute lung injury, HO-1, NF-κB, Nrf2, Trillin

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