A Novel Compound, "FA-1" Isolated from Prunus mume, Protects Human Bronchial Epithelial Cells and Keratinocytes from Cigarette Smoke Extract-Induced Damage.

A Novel Compound, "FA-1" Isolated from Prunus mume, Protects Human Bronchial Epithelial Cells and Keratinocytes from Cigarette Smoke Extract-Induced Damage.
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从梅花中分离出的一种新型化合物“FA-1”可保护人支气管上皮细胞和角质形成细胞免受香烟烟雾提取物引起的损伤。

DOI:
10.1038/s41598-018-29701-2
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发表时间:
2018-07-31
期刊:
影响因子:
4.6
通讯作者:
Nyunoya T
Nyunoya T
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Jang AJ;Lee JH;Yotsu-Yamashita M;Park J;Kye S;Benza RL;Passineau MJ;Jeon YJ;Nyunoya T

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日本杏提取物(JAE)具有抗氧化剂和抗炎剂的生物学特性。我们推测JAE可能对香烟烟雾(CS)诱导的DNA损伤和细胞毒性产生治疗作用。在这项研究中,我们发现浓缩的JAE可以防止香烟烟雾提取物(CSE)诱导的细胞毒性和DNA损伤,并伴有醛脱氢酶(ALDH)2,3A 1和沃纳综合征蛋白(WRN)在永生化人支气管上皮细胞(HBEC 2)和正常人表皮角质形成细胞(NHEK)中的水平增加。使用离心分配色谱(CPC)方法,我们鉴定了一种未描述的化合物,5-羟甲基-2-糠醛双(5-甲酰基糠基)缩醛(我们命名为FA-1),负责对CSE的保护作用。这种化学结构迄今为止还没有从天然来源报道。在HBEC 2和NHEK细胞中均观察到分离的FA-1对CSE的保护作用。本文所述的研究表明,从JAE分离的FA-1通过增加ALDH和DNA修复的多种同工酶和减少氧化应激来保护免受CSE诱导的DNA损伤和细胞凋亡。
Extract of the Japanese apricot (JAE) has biological properties as an antioxidant and anti-inflammatory agent. We hypothesized that JAE might exert therapeutic effects on cigarette smoke (CS)-induced DNA damage and cytotoxicity. In this study, we found that concentrated JAE protects against cigarette smoke extract (CSE)-induced cytotoxicity and DNA damage accompanied by increased levels of aldehyde dehydrogenase (ALDH)2, 3A1, and Werner’s syndrome protein (WRN) in immortalized human bronchial epithelial cells (HBEC2) and normal human epidermal keratinocytes (NHEK). Using the centrifugal partition chromatography (CPC) method, we identified an undescribed compound, 5-hydroxymethyl-2-furaldehyde bis(5-formylfurfuryl) acetal (which we named FA-1), responsible for the protective effects against CSE. This chemical structure has not been reported from a natural source to date. Protective effects of isolated FA-1 against CSE were observed in both HBEC2 and NHEK cells. The studies described herein suggest that FA-1 isolated from JAE protects against CSE-induced DNA damage and apoptosis by augmenting multiple isozymes of ALDH and DNA repair and reducing oxidative stress.
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