Chitooligosaccharides Protect Human Embryonic Hepatocytes Against Oxidative Stress Induced by Hydrogen Peroxide

被引:37
|
作者
Xu, Qingsong [1 ,2 ]
Ma, Pan [1 ,2 ]
Yu, Weiting [1 ]
Tan, Chengyu [3 ]
Liu, Hongtao [1 ,2 ]
Xiong, Chuannan [1 ,2 ]
Qiao, Ying [1 ,2 ]
Du, Yuguang [1 ]
机构
[1] Chinese Acad Sci, Dalian Inst Chem Phys, Dalian 116023, Peoples R China
[2] Chinese Acad Sci, Grad Univ, Beijing 100049, Peoples R China
[3] Dalian Fisheries Univ, Coll Marine Environm Engn, Dalian 116023, Peoples R China
关键词
Chitooligosaccharides; Human embryonic hepatocytes; Oxidative stress; Apoptosis; ANTIOXIDANT ACTIVITIES; IN-VITRO; CHITOSAN OLIGOSACCHARIDE; INDUCED APOPTOSIS; MOLECULAR-WEIGHT; MECHANISMS; PATHWAY; CELLS; MICE; OLIGOCHITOSAN;
D O I
10.1007/s10126-009-9222-1
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
Chitooligosaccharides (COS) has many biological activities, such as antitumor activity and hepatoprotective effect. Herein, we investigated the protective effect of COS against hydrogen peroxide (H(2)O(2))-induced oxidative stress on human embryonic hepatocytes (L02 cells) and its scavenging activity against the 1,1-diphenyl-2-picrylhydrazyl radical in vitro. The results showed that the lost cell viability induced by H(2)O(2) was markedly restored after 24 h pre-incubation with COS (0.1-0.4 mg/ml). This rescue effect could be related to the antioxidant property of COS, in which we showed that the radical scavenging activity of COS reached 80% at concentration of 2 mg/ml. In addition, COS could prevent cell apoptosis induced by H(2)O(2), as shown by the inhibition of the cleavage of poly (adenosine diphosphate-ribose) polymerase and increased expression of the anti-apoptotic protein Bcl-xL. Furthermore, we have utilized confocal laser microscopy to observe cellular uptake of COS, an important step for COS to exert its effects on target cells. Taken together, our findings suggested that COS could effectively protect L02 cells against oxidative stress, which might be useful in clinical setting during the treatment of oxidative stress-related liver damages.
引用
收藏
页码:292 / 298
页数:7
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