Herbal Medication, Macmoondong Decoction, Attenuates LPS-Induced COPD in Small Airways via TGF-β, CCL-2, and CXCL1

Abstract

Chronic obstructive pulmonary disease (COPD) is an incurable disease related to the respiratory system. A 2017 report by the World Health Organization stated that it was the third most common cause of death in 2015. Macmoondong decoction is a prescription that has been used widely in Korea for the treatment of respiratory diseases, but there have been few investigations into the therapeutic mechanism. To investigate the anti-COPD effect of macmoondong decoction, the animals were divided into five treatment groups: control; COPD-induced control; Spiriva; 150 mg/kg macmoondong decoction; and 1500 mg/kg macmoondong decoction. Changes typically observed in COPD, such as the populations of WBC and neutrophils in BALF, the level of IgE in serum, morphological changes, the DNA levels, and the protein expression of cytokines and chemokines (TGF-β, CCL-2, CXCL1, and CXCL11) in the pulmonary system, were evaluated. Macmoondong decoction inhibited the populations of WBC and neutrophils in BALF and the level of IgE in serum. Dose-dependent prevention of the pulmonary morphological changes, such as emphysema and airway fibrosis, was observed. Macmoondong decoction suppressed the expression of DNA and proteins related to the occurrence of COPD, such as TGF-β, CCL-2, CXCL1, and CXCL11. In particular, the expression of TGF-β, CCL-2, and CXCL1 was significantly suppressed by 1500 mg/kg macmoondong decoction treatment compared with Spiriva treatment. Macmoondong decoction exerted an anti-COPD effect, and the mechanism of its action may be the suppression of TGF-β, CCL-2, CXCL1, and CXCL11 expression, which occurred in a dose-dependent manner. The mechanism of action of macmoondong decoction may be the dose-dependent suppression of TGF-β, CCL-2, CXCL1, and CXCL11, with TGF-β, CCL-2, and CXCL1 as the potential key factors involved in COPD suppression.