Protective Effects of Chestnut ( Castanea crenata ) Inner Shell Extract in Macrophage-Driven Emphysematous Lesion Induced by Cigarette Smoke Condensate

• Published in: Nutrients Vol. 15; no. 2; p. 253
• Main Authors: Jeong, Ji-Soo, Kim, Jeong-Won, Kim, Jin-Hwa, Kim, Chang-Yeop, Ko, Je-Won, Kim, Tae-Won
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 04.01.2023; MDPI
• Subjects: 1-Phosphatidylinositol 3-kinase; Acids; AKT protein; Animals; Bronchus; Castanea crenata; Chestnut; chestnut inner shell; Chronic obstructive pulmonary disease; Cigarette smoke; cigarette smoke condensate; Cigarette Smoking - adverse effects; Cigarettes; Condensates; Emphysema; Fibrosis; Kinases; Laboratories; Lavage; Lesions; Lung - pathology; Lung diseases; Lungs; Macrophages; Macrophages - metabolism; Matrix metalloproteinase; Mice; Molecular modelling; Nicotiana; Obstructive lung disease; Ostomy; Proteins; Pulmonary Disease, Chronic Obstructive - drug therapy; Pulmonary Disease, Chronic Obstructive - etiology; Pulmonary Disease, Chronic Obstructive - metabolism; Pulmonary Emphysema - chemically induced; Pulmonary Emphysema - drug therapy; Smoke; United States > US; South Korea; matrix metalloproteinase; cigarette smoke condensate; chestnut inner shell; emphysema
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu15020253

Chestnut ( ) inner shell extract (CIE), a curative herb in Korea, has diverse pharmacological effects against various diseases including pulmonary fibrosis, asthma, and chronic obstructive pulmonary disease (COPD). However, its molecular mechanisms of anti-emphysematous effects are still not fully elucidated. In the present study, we elucidate the efficacy of CIE against emphysematous lesion progression in a cigarette smoke condensate (CSC)-instilled mice and CSC-stimulated H292 cell line. The mice are administered CSC via intranasal instillation at 7-day intervals for 1 month after 1 week of pretreatment with CIE. CIE (100 or 300 mg/kg) is administered by oral gavage for 1 month. CIE decreased the macrophage count in bronchoalveolar lavage fluid and the severity of emphysematous lesions in lung tissue. Additionally, CIE suppressed the phosphatidylinositol 3-kinase/protein kinase B/nuclear factor kappa B signal pathway and thereby downregulated matrix metalloprotease-9 expression, which was confirmed in CSC-stimulated H292 cells. Thus, CIE effectively inhibited CSC-induced macrophage-driven emphysema progression in airways; this inhibition was associated with the suppression of protease-antiprotease imbalance. Our results propose that CIE has the potential for the alleviation of COPD.