Inhibitory effects of cudratricusxanthone O on particulate matter-induced pulmonary injury

• Published in: International journal of environmental health research 2021-04, Vol.31 (3), p.271-284
• Main Authors: Lee, Wonhwa, Ku, Sae-Kwang, Kim, Tae In, Kim, Eun-Nam, Park, Eui Kyun, Jeong, Gil-Saeng, Bae, Jong-Sup
• Format: Article
• Language: English
• Subjects: Air Pollutants - adverse effects; Air pollution; Akt; AKT protein; Alveoli; Animals; Bronchus; Cell activation; Cudratricusxanthone O; Cytokines; Endothelial cells; Endothelial Cells - drug effects; Histology; Inflammation; Injuries; Integrity; Kinases; Leukocyte migration; Leukocytes; Lung Injury - prevention & control; Lungs; Male; MAP kinase; Mice; Mice, Inbred BALB C; Moraceae - chemistry; Particulate emissions; Particulate matter; Particulate Matter - adverse effects; Permeability; Pneumonia - prevention & control; Pollutants; Protective Agents - pharmacology; Protein kinase; Proteins; Reactive oxygen species; vascular permeability; Xanthones - pharmacology
• ISSN: 0960-3123; 1369-1619
• DOI: 10.1080/09603123.2019.1652252

Particulate matter 2.5 (PM 2.5 ), aerodynamic diameter ≤ 2.5 μm, is the primary air pollutant that plays the key role for lung injury resulted from the loss of vascular barrier integrity. Cudratricusxanthone O (CTXO) is a novel xanthone compound isolated from the root of Cudrania tricuspidata Bureau. Here, we investigated the beneficial effects of CTXO against PM-induced lung endothelial cell (EC) barrier disruption and pulmonary inflammation. Permeability, leukocyte migration, activation of proinflammatory proteins, generation of reactive oxygen species (ROS), and histology were examined in PM 2.5 -treated ECs and mice. CTXO significantly scavenged PM 2.5 -induced ROS and inhibited the ROS-induced activation of p38 mitogen-activated protein kinase (MAPK). Concurrently, CTXO activated Akt, which helped maintain endothelial integrity. Furthermore, CTXO reduced vascular protein leakage, leukocyte infiltration, and proinflammatory cytokine release in the bronchoalveolar lavage fluid in PM-induced lung tissues. These results indicated that CTXO may exhibit protective effects against PM-induced inflammatory lung injury and vascular hyperpermeability.