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日本扁柏果皮提取物对氧化应激诱导的肺细胞凋亡死亡的体外和体内抑制作用

In Vitro and In Vivo Inhibitory Effect of Citrus Junos Tanaka Peel Extract against Oxidative Stress-Induced Apoptotic Death of Lung Cells.

作者信息

Kim Jin Woo, Jo Eun Hee, Moon Ji Eun, Cha Hanvit, Chang Moon Han, Cho Hyung Taek, Lee Min Kook, Jung Wan Sik, Lee Jin Hyup, Heo Wan, Kim Young Jun

机构信息

Department of Food and Biotechnology, Korea University, Sejong 8244, Korea.

Immunotech, Inc., Cheonan-si, Chungnam 31094, Korea.

出版信息

Antioxidants (Basel). 2020 Dec 4;9(12):1231. doi: 10.3390/antiox9121231.

DOI:10.3390/antiox9121231
PMID:33291640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7761914/
Abstract

Various stresses derived from both internal and external oxidative environments lead to the excessive production of reactive oxygen species (ROS) causing progressive intracellular oxidative damage and ultimately cell death. The objective of this study was to evaluate the protective effects of Tanaka peel extract (CE) against oxidative-stress induced the apoptosis of lung cells and the associated mechanisms of action using in vitro and in vivo models. The protective effect of CE was evaluated in vitro in NCI-H460 human lung cells exposed to pro-oxidant HO. The preventive effect of CE (200 mg/kg/day, 10 days) against pulmonary injuries following acrolein inhalation (10 ppm for 12 h) was investigated using an in vivo mouse model. Herein, we demonstrated the inhibitory effect of CE against the oxidative stress-induced apoptosis of lung cells under a highly oxidative environment. The function of CE is linked with its ability to suppress ROS-dependent, p53-mediated apoptotic signaling. Furthermore, we evaluated the protective role of CE against apoptotic pulmonary injuries associated with the inhalation of acrolein, a ubiquitous and highly oxidizing environmental respiratory pollutant, through the attenuation of oxidative stress. The results indicated that CE exhibits a protective effect against the oxidative stress-induced apoptosis of lung cells in both in vitro and in vivo models.

摘要

来自内部和外部氧化环境的各种应激会导致活性氧(ROS)过度产生,从而引起细胞内渐进性氧化损伤并最终导致细胞死亡。本研究的目的是使用体外和体内模型,评估田中果皮提取物(CE)对氧化应激诱导的肺细胞凋亡的保护作用及其相关作用机制。在体外,对暴露于促氧化剂HO的NCI-H460人肺细胞评估了CE的保护作用。使用体内小鼠模型研究了CE(200mg/kg/天,共10天)对丙烯醛吸入(10ppm,持续12小时)后肺损伤的预防作用。在此,我们证明了在高氧化环境下CE对氧化应激诱导的肺细胞凋亡具有抑制作用。CE的功能与其抑制ROS依赖性、p53介导的凋亡信号传导的能力有关。此外,我们通过减轻氧化应激,评估了CE对与吸入丙烯醛相关的凋亡性肺损伤的保护作用,丙烯醛是一种普遍存在且具有高度氧化性的环境呼吸污染物。结果表明,在体外和体内模型中,CE对氧化应激诱导的肺细胞凋亡均具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/becd0df1e388/antioxidants-09-01231-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/185f5af50288/antioxidants-09-01231-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/ce60d01f1546/antioxidants-09-01231-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/f31ac1e23833/antioxidants-09-01231-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/049dd32c7d79/antioxidants-09-01231-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/10bf3e1c3c3f/antioxidants-09-01231-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/becd0df1e388/antioxidants-09-01231-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/185f5af50288/antioxidants-09-01231-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/ce60d01f1546/antioxidants-09-01231-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/f31ac1e23833/antioxidants-09-01231-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/049dd32c7d79/antioxidants-09-01231-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/10bf3e1c3c3f/antioxidants-09-01231-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/624d/7761914/becd0df1e388/antioxidants-09-01231-g006.jpg

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