高丽红参通过抑制巨噬细胞驱动的细胞凋亡途径抑制香烟烟雾冷凝物诱发的肺气肿病变

IF 6.8 2区 医学 Q1 CHEMISTRY, MEDICINAL
Jeong-Won Kim, Jin-Hwa Kim, Chang-Yeop Kim, Ji-Soo Jeong, Je-Won Ko, Tae-Won Kim
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引用次数: 0

摘要

背景香烟烟雾被普遍认为是慢性阻塞性肺病(COPD)的主要致病因素,而慢性阻塞性肺病以肺气肿病变为特征。本研究探讨了高丽红参(KRG)对香烟烟雾冷凝物(CSC)诱导的肺气肿的保护作用。方法每周一次向小鼠体内灌注 50 毫克/千克的 CSC,连续灌注 4 周;每天给小鼠注射一次高丽红参,剂量为 100 或 300 毫克/千克,连续注射 4 周;每天给小鼠注射一次地塞米松(DEX,阳性对照),剂量为 3 毫克/千克,连续注射 2 周。结果 KRG能显著减少支气管肺泡灌洗液中的巨噬细胞数量,减轻肺组织中的气肿病变。末端脱氧核苷酸转移酶脱氧尿苷三磷酸缺口端标记染色和Caspase 3免疫组化显示,KRG抑制了CSC诱导的细胞凋亡。此外,KRG 还能有效抑制 CSC 介导的 Bcl-2-associated X 蛋白/Caspase 3 信号激活,继而在体内和体外诱导细胞存活信号,包括血管内皮生长因子/磷脂肌醇 3 激酶/蛋白激酶 B。结论综合来看,KRG 可有效抑制 CSC 暴露诱导的巨噬细胞介导的肺气肿,可能是通过抑制促凋亡信号传导,从而激活细胞存活通路。这些研究结果表明,KRG 具有预防慢性阻塞性肺病患者肺气肿的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Korean Red Ginseng suppresses emphysematous lesions induced by cigarette smoke condensate through inhibition of macrophage-driven apoptosis pathways

Korean Red Ginseng suppresses emphysematous lesions induced by cigarette smoke condensate through inhibition of macrophage-driven apoptosis pathways

Korean Red Ginseng suppresses emphysematous lesions induced by cigarette smoke condensate through inhibition of macrophage-driven apoptosis pathways

Background

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.

Methods

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.

Results

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 in vivo and in vitro. The DEX group also showed similar improved results in vivo and in vitro.

Conclusion

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.

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来源期刊
Journal of Ginseng Research
Journal of Ginseng Research CHEMISTRY, MEDICINAL-INTEGRATIVE & COMPLEMENTARY MEDICINE
CiteScore
11.40
自引率
9.50%
发文量
111
审稿时长
6-12 weeks
期刊介绍: Journal of Ginseng Research (JGR) is an official, open access journal of the Korean Society of Ginseng and is the only international journal publishing scholarly reports on ginseng research in the world. The journal is a bimonthly peer-reviewed publication featuring high-quality studies related to basic, pre-clinical, and clinical researches on ginseng to reflect recent progresses in ginseng research. JGR publishes papers, either experimental or theoretical, that advance our understanding of ginseng science, including plant sciences, biology, chemistry, pharmacology, toxicology, pharmacokinetics, veterinary medicine, biochemistry, manufacture, and clinical study of ginseng since 1976. It also includes the new paradigm of integrative research, covering alternative medicinal approaches. Article types considered for publication include review articles, original research articles, and brief reports. JGR helps researchers to understand mechanisms for traditional efficacy of ginseng and to put their clinical evidence together. It provides balanced information on basic science and clinical applications to researchers, manufacturers, practitioners, teachers, scholars, and medical doctors.
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