Physalis peruviana L. inhibits airway inflammation induced by cigarette smoke and lipopolysaccharide through inhibition of extracellular signal-regulated kinase and induction of heme oxygenase-1

Int J Mol Med. 2017 Nov;40(5):1557-1565. doi: 10.3892/ijmm.2017.3139. Epub 2017 Sep 15.

Abstract

Physalis peruviana L. (PP) is a medicinal herb that has been confirmed to have several biological activities, including anticancer, antioxidant and anti-inflammatory properties. The aim of the present study was to evaluate the protective effect of PP on cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced pulmonary inflammation. Treatment with PP significantly reduced the influx of inflammatory cells in the bronchoalveolar lavage fluid (BALF) and lung of mice with CS- and LPS-induced pulmonary inflammation. PP also decreased the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the BALF. PP effectively attenuated the expression of monocyte chemoattractant protein-1 (MCP-1) and the activation of extracellular signal-regulated kinase (ERK) in the lung. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) activation and heme oxygenase-1 (HO-1) expression were increased by PP treatment. In an in vitro experiment, PP reduced the mRNA expression of TNF-α and MCP-1, and the activation of ERK in CS extract-stimulated A549 epithelial cells. Furthermore, PP increased the activation of Nrf2 and the expression of HO-1 in A549 cells. These findings suggest that PP has a therapeutic potential for the treatment of pulmonary inflammatory diseases, such as chronic obstructive pulmonary disease.

MeSH terms

  • Animals
  • Biomarkers
  • Bronchoalveolar Lavage Fluid / cytology
  • Cell Line, Tumor
  • Chemokine CCL2 / metabolism
  • Cytokines / metabolism
  • Disease Models, Animal
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Gene Expression Regulation
  • Heme Oxygenase-1 / genetics
  • Heme Oxygenase-1 / metabolism*
  • Humans
  • Inflammation / etiology*
  • Inflammation / metabolism*
  • Inflammation / pathology
  • Inflammation Mediators
  • Leukocytes / metabolism
  • Leukocytes / pathology
  • Lipopolysaccharides / adverse effects*
  • Male
  • Mice
  • Neutrophil Infiltration
  • Neutrophils / metabolism
  • Neutrophils / pathology
  • Physalis / chemistry*
  • Plant Extracts / chemistry
  • Plant Extracts / pharmacology*
  • Reactive Oxygen Species
  • Respiratory Mucosa / metabolism
  • Respiratory Tract Diseases / etiology
  • Respiratory Tract Diseases / metabolism
  • Respiratory Tract Diseases / pathology
  • Smoking / adverse effects*

Substances

  • Biomarkers
  • Chemokine CCL2
  • Cytokines
  • Inflammation Mediators
  • Lipopolysaccharides
  • Plant Extracts
  • Reactive Oxygen Species
  • Heme Oxygenase-1
  • Extracellular Signal-Regulated MAP Kinases