Hepatoprotective effects of chlorogenic acid under hyperglycemic conditions

被引:7
作者
Farhood, Hattf Bazool [1 ,2 ]
Balas, Mihaela [2 ]
Gradinaru, Daniela [3 ]
Margina, Denisa [3 ]
Dinischiotu, Anca [2 ]
机构
[1] Univ Thi Qar, Coll Sci, Dept Chem, Thi Qar, Iraq
[2] Univ Bucharest, Dept Biochem & Mol Biol, Bucharest, Romania
[3] Carol Davila Univ Med & Pharm, Fac Pharm, Dept Biochem, Bucharest, Romania
来源
ROMANIAN BIOTECHNOLOGICAL LETTERS | 2019年 / 24卷 / 02期
关键词
Chlorogenic acid; hyperglycemia; hepatocytes; reactive oxygen species; OXIDATIVE STRESS; COFFEE CONSUMPTION; RISK-FACTORS; IN-VITRO; LIVER; SYNTHASE; MITOCHONDRIA; METABOLISM; ACTIVATION; PATHWAY;
D O I
10.25083/rbl/24.2/301.307
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Chlorogenic acids (CGAs) are a family of polyphenol compounds with antioxidant, anti-inflammatory and anticarcinogenic activities, that exerts hypoglycemic and hypolipidemic effects. In this study we focused on the investigation of the chlorogenic acid (3-O-Caffeoylquinic acid, CGA) effect on human hepatocytes cells under hyperglycemic (HG) condition. HepG2 (human liver carcinoma) cells grown in normoglycemic (NG, 5.5 mM glucose) and HG (25 mM and 35 mM glucose) culture media were pre- and post-treated with different doses of CGA (0 = control, 5, 10 and 50 mu M) for 24 and 48 h. The cellular metabolic activity and level of reactive oxygen species (ROS) were evaluated. Exposure to HG media caused an increase in cellular metabolic activity in a dose and time-dependent manner. In cells pre- or post-treated with CGA the cellular metabolic activity decreased in a CGA dose-dependent manner, reaching after 48 h a similar level with that of NG cells. Under HG condition, intracellular ROS were generated in higher amounts compared to NG ones. Both treatments reduced the excess of ROS produced in HG cells up to that of NG cells, revealing a pronounced antioxidant effect. Our findings demonstrate the potential of CGA to mitigate the damaging effects induced by HG conditions in both pre- and post- treatment of HepG2 cells.
引用
收藏
页码:301 / 307
页数:7
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