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富含氯甾醇的[具体物质]部分通过抑制氧化应激和凋亡相关信号通路对颗粒物诱导的皮肤损伤具有[具体作用]。 (注:原文中against和via之前似乎缺失关键信息,翻译只能尽量根据现有内容完整表达)

Clionasterol-Rich Fraction of against Particulate Matter-Induced Skin Damage via Inhibition of Oxidative Stress and Apoptosis-Related Signaling Pathway.

作者信息

Liyanage N M, Nagahawatta D P, Jayawardena Thilina U, Jayawardhana H H A C K, Lee Hyo-Geun, Kim Young-Sang, Jeon You-Jin

机构信息

Department of Marine Life Sciences, Jeju National University, Jeju 63243, Korea.

Department of Chemistry, Biochemistry, and Physics, Université du Québec à Trois-Rivières, Trois-Rivières, QC G8Z 4M3, Canada.

出版信息

Antioxidants (Basel). 2022 Sep 28;11(10):1941. doi: 10.3390/antiox11101941.

DOI:10.3390/antiox11101941
PMID:36290664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9598668/
Abstract

The increasing airborne particulate matter (PM) consisting of environmental contaminants such as dust, aerosols, and fibers has become a global concern by causing oxidative stress that leads to apoptosis and skin damage. The current study evaluated the protective effect of (CR) against PM-induced skin damage using human keratinocytes and a zebrafish model. The clionasterol-rich hexane fraction (CRHF2) of CR exhibited superior protective activity through downregulating intracellular reactive oxygen species levels and mitochondrial ROS levels, as well as the PM-induced increase in apoptotic body formation and upregulation of apoptotic signaling pathway proteins, along with sub-G1 cell accumulation dose-dependently. Furthermore, in vivo results showed that CRHF2 potentially downregulates PM-induced cell death, ROS, and NO production in the zebrafish model. Hence, the results evidenced that the protective effect of CRHF2 is caused by inhibiting oxidative stress and mitochondrial-mediated apoptosis in cells. Therefore, has the potential to be used in the development of pharmaceuticals to attenuate PM-induced skin diseases.

摘要

由灰尘、气溶胶和纤维等环境污染物组成的空气中颗粒物(PM)不断增加,通过引起导致细胞凋亡和皮肤损伤的氧化应激,已成为全球关注的问题。当前研究使用人角质形成细胞和斑马鱼模型评估了(CR)对PM诱导的皮肤损伤的保护作用。CR中富含环桉醇的己烷馏分(CRHF2)通过下调细胞内活性氧水平和线粒体ROS水平,以及PM诱导的凋亡小体形成增加和凋亡信号通路蛋白的上调,以及亚G1期细胞积累,剂量依赖性地表现出卓越的保护活性。此外,体内结果表明,CRHF2在斑马鱼模型中可能下调PM诱导的细胞死亡、ROS和NO生成。因此,结果证明CRHF2的保护作用是通过抑制细胞中的氧化应激和线粒体介导的细胞凋亡引起的。因此,(CR)有潜力用于开发减轻PM诱导的皮肤疾病的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/3e46fa39d150/antioxidants-11-01941-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/d1c0fd5a651a/antioxidants-11-01941-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/4f2f6cbd3758/antioxidants-11-01941-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/85b33d0cdfe6/antioxidants-11-01941-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/c16126506d7e/antioxidants-11-01941-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/ad2a54eb4ce8/antioxidants-11-01941-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/f2d540c4bea4/antioxidants-11-01941-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/3e46fa39d150/antioxidants-11-01941-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/d1c0fd5a651a/antioxidants-11-01941-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/4f2f6cbd3758/antioxidants-11-01941-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/85b33d0cdfe6/antioxidants-11-01941-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/c16126506d7e/antioxidants-11-01941-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/ad2a54eb4ce8/antioxidants-11-01941-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/f2d540c4bea4/antioxidants-11-01941-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a11d/9598668/3e46fa39d150/antioxidants-11-01941-g007.jpg

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