Oleanolic acid acetate attenuates polyhexamethylene guanidine phosphate-induced pulmonary inflammation and fibrosis in mice

Respir Physiol Neurobiol. 2018 Jun:252-253:1-9. doi: 10.1016/j.resp.2018.03.001. Epub 2018 Mar 2.

Abstract

Oleanolic acid acetate (OAA), triterpenoid compound isolated from Vigna angularis (azuki bean), has been revealed anti-inflammatory in several studies. We investigated the effects of OAA against polyhexamethylene guanidine phosphate (PHMG-P)-induced pulmonary inflammation and fibrosis in mice. OAA treatment effectively alleviated PHMG-P-induced lung injury, including the number of total and differential cell in BAL fluid, histopathological lesions and hydroxyproline content in a dose dependent manner. Moreover, OAA treatment significantly decreased the elevations of IL-1β, IL-6, TNF-α, TGF-β1, and fibronectin, and the activation of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome in the lungs of PHMG-P-treated mice. Cytokines are known to be key modulators in the inflammatory responses that drive progression of fibrosis in injured tissues. The activation of NLRP3 inflammasome has been reported to be involved in induction of inflammatory cytokines. These results indicate that OAA may mitigate the inflammatory response and development of pulmonary fibrosis in the lungs of mice treated with PHMG-P.

Keywords: Cytokine; Inflammasome; Lung injury; Oleanolic acid acetate; Polyhexamethylene guanidine phosphate; Vigna angularis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Bronchoalveolar Lavage Fluid / immunology
  • Cytokines / metabolism
  • Disease Models, Animal
  • Fibronectins / metabolism
  • Guanidines
  • Inflammasomes / drug effects
  • Inflammasomes / metabolism
  • Lung / drug effects
  • Lung / immunology
  • Lung / pathology
  • Male
  • Mice, Inbred C57BL
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism
  • Oleanolic Acid / pharmacology*
  • Pneumonia / drug therapy*
  • Pneumonia / metabolism
  • Pneumonia / pathology
  • Pulmonary Fibrosis / drug therapy*
  • Pulmonary Fibrosis / immunology
  • Pulmonary Fibrosis / pathology
  • Random Allocation
  • Transforming Growth Factor beta1 / metabolism
  • Triterpenes / pharmacology*

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Fibronectins
  • Guanidines
  • Inflammasomes
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Nlrp3 protein, mouse
  • Transforming Growth Factor beta1
  • Triterpenes
  • polyhexamethyleneguanidine
  • Oleanolic Acid