Naja naja atra venom ameliorates pulmonary fibrosis by inhibiting inflammatory response and oxidative stress

BMC Complementary and Alternative Medicine

Research Article

Jin-Hua Gu¹  Jian-Qun Kou¹  Rong Han¹  Zheng-Hong Qin¹  Kui Cui¹  Guanghui Wang²  Xuechu Zhen³ 

[1] Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University School of Pharmaceutical Science, 215123, Suzhou, China;Department of Pharmacology and Laboratory of Molecular Neuropathology, Soochow University School of Pharmaceutical Science, 215006, Suzhou, China;Department of Pharmacology and Laboratory of Neuropsychopharmacology, Soochow University School of Pharmaceutical Science, 215006, Suzhou, China;

关键词: Naja naja atra venom;    Pulmonary fibrosis;    Hydroxyproline;    NF-κB;    TGF-βm;    Oxidative stress;   

DOI  :  10.1186/1472-6882-14-461

 received in 2013-09-05, accepted in 2014-11-14,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundNaja naja atra venom (NNAV) displays diverse pharmacological actions including analgesia, anti-inflammation and immune regulation.In this study, we investigated the effects of NNAV on pulmonary fibrosis and its mechanisms of action.MethodsTo determine if Naja naja atra venom (NNAV) can produce beneficial effects on pulmonary fibrosis, two marine models of pulmonary fibrosis were produced with bleomycin (BLM) and lipopolysaccharide (LPS). NNAV (30, 90, 270 μg/kg) was orally administered once a day started five days before BLM and LPS until to the end of experiment. The effects of NNAV treatment on pulmonary injury were evaluated with arterial blood gas analysis, hydroxyproline (HYP) content assessment and HE/Masson staining. The effects of NNAV treatment on inflammatory related cytokines, fibrosis related TGF-β/Smad signaling pathway and oxidative stress were examined.ResultsThe results showed that NNAV improved the lung gas-exchange function and attenuated the fibrotic lesions in lung. NNAV decreased IL-1β and TNF-α levels in serum in both pulmonary fibrosis models. NNAV inhibited the activation of NF-κB in LPS-induced and TGF-β/Smad pathway in BLM-induced pulmonary fibrosis. Additionally, NNAV also increased the levels of SOD and GSH and reduced the levels of MDA in BLM-induced pulmonary fibrosis model.ConclusionsThe present study indicates that NNAV attenuates LPS- and BLM-induced lung fibrosis. Its mechanisms of action are associated with inhibiting inflammatory response and oxidative stress. The study suggests that NNAV might be a potential therapeutic drug for treatment of pulmonary fibrosis.

【 授权许可】

Unknown   
© Cui et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.