Efficacy of silymarin in treatment of COPD via P47phox signaling pathway

Lin Xu,Qingying Song,Cheng Zhang,Zhanghong Ouyang,Mengning Zheng,Xiangyan Zhang

doi:10.1590/fst.52821

Abstract

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. To investigate effect of silymarin on chronic obstructive pulmonary disease (COPD). The serum samples of 20 healthy controls, 20 patients with acute exacerbation of COPD and 20 patients with stable COPD were collected. LPS and smoking were used to induce COPD mouse model. Our results showed that in patients with acute exacerbation of COPD, O2-level release from peripheral blood neutrophils were negatively correlated with forced expiratory volume in the first second (FEV1), FEV1 in predicted value, FEV1/forced vital capacity (FVC), and arterial partial pressure (PaO2). (r=-0.898, -0.878, -874, -0.890, all P<0.01). Compared with that in the control group, the phosphorylation of NADPH oxidase p47phox factor and peripheral blood neutrophil membrane protein in the stable COPD group and the acute exacerbation COPD group were significantly stronger. Silymarin can inhibit the inflammatory response and oxidative stress. In conclusion, silymarin reduces oxidative stress in phagocytic and non-phagocytic cells, thus decreasing the oxidative stress in COPD patients

Highlights

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide (World Health Organization 2014)
NADPH oxidase in the phagocytic cells is inactive at rest or produces merely a small amount of physiologically active reactive oxygen species (ROS)
Previous studies have confirmed that in the ischemic state of cardiomyocytes, intracellular ROS are significantly increased, and the expression of p47phox protein is consistent with the increase of reactive oxygen species (Hahn et al, 2011)

Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide (World Health Organization 2014). COPD mainly affects the lung parenchyma and peripheral airways, eventually leading to progressive and irreversible damage of the lung tissues, and even more severe complications, such as gastric ulcer, respiratory failure, pulmonary heart disease and right heart failure, etc. Environmental pollution, smoking and radiation can cause oxidative stress in the body (Thomson, 2018) mainly due to excessive accumulation of free radicals / reactive oxygen species (ROS) and nitrogen oxides (RNS) or antioxidant levels and antioxidants. Enzyme activity is low, resulting in DNA damage in respiratory airway cells causing COPD and other related complications. Effective interventions for oxidative stress may be a novel target for the treatment of COPD

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Conclusion