Kim Jeong-Won, Kim Jin-Hwa, Kim Chang-Yeop, Jeong Ji-Soo, Ko Je-Won, Kim Tae-Won
College of Veterinary Medicine (BK21 FOUR Program), Chungnam National University, 99 Daehak-ro, Daejeon, Republic of Korea.
J Ginseng Res. 2024 Mar;48(2):181-189. doi: 10.1016/j.jgr.2023.11.001. Epub 2023 Nov 7.
Cigarette smoke is generally accepted as a major contributor to chronic obstructive pulmonary disease (COPD), which is characterized by emphysematous lesions. In this study, we investigated the protective effects of Korean Red Ginseng (KRG) against cigarette smoke condensate (CSC)-induced emphysema.
Mice were instilled with 50 mg/kg of CSC intranasally once a week for 4 weeks, KRG was administered to the mice once daily for 4 weeks at doses of 100 or 300 mg/kg, and dexamethasone (DEX, positive control) was administered to the mice once daily for 2 weeks at 3 mg/kg.
KRG markedly decreased the macrophage population in bronchoalveolar lavage fluid and reduced emphysematous lesions in the lung tissues. KRG suppressed CSC-induced apoptosis as revealed by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling staining and Caspase 3 immunohistochemistry. Additionally, KRG effectively inhibited CSC-mediated activation of Bcl-2-associated X protein/Caspase 3 signaling, followed by the induction of cell survival signaling, including vascular endothelial growth factor/phosphoinositide 3-kinase/protein kinase B and . The DEX group also showed similar improved results and .
Taken together, KRG effectively inhibits macrophage-mediated emphysema induced by CSC exposure, possibly via the suppression of pro-apoptotic signaling, which results in cell survival pathway activation. These findings suggest that KRG has therapeutic potential for the prevention of emphysema in COPD patients.
香烟烟雾通常被认为是慢性阻塞性肺疾病(COPD)的主要促成因素,COPD以肺气肿病变为特征。在本研究中,我们调查了韩国红参(KRG)对香烟烟雾冷凝物(CSC)诱导的肺气肿的保护作用。
小鼠每周经鼻滴注50mg/kg的CSC,持续4周,KRG以100或300mg/kg的剂量每日给药小鼠1次,持续4周,地塞米松(DEX,阳性对照)以3mg/kg的剂量每日给药小鼠1次,持续2周。
KRG显著降低了支气管肺泡灌洗液中的巨噬细胞数量,并减少了肺组织中的肺气肿病变。末端脱氧核苷酸转移酶脱氧尿苷三磷酸缺口末端标记染色和半胱天冬酶3免疫组织化学显示,KRG抑制了CSC诱导的细胞凋亡。此外,KRG有效抑制了CSC介导的Bcl-2相关X蛋白/半胱天冬酶3信号通路的激活,随后诱导了包括血管内皮生长因子/磷脂酰肌醇3激酶/蛋白激酶B等细胞存活信号通路。DEX组也显示出类似的改善结果。
综上所述,KRG可能通过抑制促凋亡信号通路,激活细胞存活途径,有效抑制CSC暴露诱导的巨噬细胞介导的肺气肿。这些发现表明,KRG在预防COPD患者肺气肿方面具有治疗潜力。