2. Academic Validation
  3. Corilagin attenuates aerosol bleomycin-induced experimental lung injury

Corilagin attenuates aerosol bleomycin-induced experimental lung injury

  • Int J Mol Sci. 2014 May 30;15(6):9762-79. doi: 10.3390/ijms15069762.
Zheng Wang 1,  Qiong-Ya Guo 2,  Xiao-Ju Zhang 3,  Xiao Li 4,  Wen-Ting Li 5,  Xi-Tao Ma 6,  Li-Jun Ma 7
Affiliations

Affiliations

  • 1 Department of Respiratory and Critical Medicine, the People's Hospital of Zhengzhou University, Zhengzhou 450003, China. santawang99@163.com.
  • 2 Department of Gastroenterology, the People's Hospital of Zhengzhou University, Zhengzhou 450003, China. santawang@outlook.com.
  • 3 Department of Respiratory and Critical Medicine, the People's Hospital of Zhengzhou University, Zhengzhou 450003, China. zhangxiaoju1010@hotmail.com.
  • 4 Department of Respiratory and Critical Medicine, the People's Hospital of Zhengzhou University, Zhengzhou 450003, China. lesslazy_lx@163.com.
  • 5 Department of Infectious Disease, Anhui Provincial Hospital, Hefei 230001, China. wtl9911002@163.com.
  • 6 Department of Respiratory and Critical Medicine, the People's Hospital of Zhengzhou University, Zhengzhou 450003, China. maxitao@163.com.
  • 7 Department of Respiratory and Critical Medicine, the People's Hospital of Zhengzhou University, Zhengzhou 450003, China. malijun0401@163.com.
PMID: 24886817 DOI: 10.3390/ijms15069762
Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF. Here, we investigated the effect of corilagin on lung injury following bleomycin exposure in an animal model of pulmonary fibrosis. Corilagin abrogated bleomycin-induced lung fibrosis as assessed by H&E; Masson's trichrome staining and lung hydroxyproline content in lung tissue. Corilagin reduced the number of apoptotic lung cells and prevented lung epithelial cells from membrane breakdown, effluence of lamellar bodies and thickening of the respiratory membrane. Bleomycin exposure induced expression of MDA, IKKα, phosphorylated IKKα (p-IKKα), NF-κB P65, TNF-α and IL-1β, and reduced I-κB expression in mice lung tissue or in BALF. These changes were reversed by high-dose corilagin (100 mg/kg i.p) more dramatically than by low dose (10 mg/kg i.p). Last, corilagin inhibits TGF-β1 production and α-SMA expression in lung tissue samples. Taken together, these findings confirmed that corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-β1 signaling. Corilagin may serve as a promising therapeutic agent for pulmonary fibrosis.

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