Lycopene protects against hypoxia reoxygenation-injury by preventing calpain activation
10.3760/cma.j.issn.0253-3758.2013.08.006
- VernacularTitle:番茄红素通过抑制细胞钙蛋白酶活化减轻心肌细胞缺氧复氧损伤
- Author:
Rong-Chuan YUE
1
;
Hou-Xiang HU
;
Tao LUO
;
Ke LI
;
Shuang ZHANG
;
Lei XU
Author Information
1. 川北医学院附属医院心内科
- Keywords:
Myocardial reperfusion injury;
Calpain;
Lycopene
- From:
Chinese Journal of Cardiology
2013;41(8):654-658
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the possible mechanism of lycopene on protecting against hypoxia/reoxygenation (H/R)-injury.Methods Primary cultured cardiomyocytes,isolated from neonatal mouse,were divided into three groups randomly:control group(C) ; H/R group(4 h H followed by 8 h R) ;lycopene + H/R group(L + H/R),in which the cardiomyocytes were pretreated with lycopene for 4 h before H/R.The survival of cardiomyocytes was counted.Apoptotic cells were detected by TUNEL assays.The release of cytochrome c from mitochondrial matrix into the cytosol,the activity of caspase-3,intracellular ROS levels and the activity of calpain were also determined in these groups respectively at the same time.Results The pretreatment of cardiomyocytes with lycopene significantly improved the survival of cardiomyocytes [C:(89.84 ± 5.15) ％,H/R:(63.59 ± 5.11) ％,L + H/R:(79.25 ± 1.48) ％,P ＜0.05] and reduced the extent of apoptosis [C:(10.37 ± 1.25) ％,H/R:(32.03 ± 4.79) ％,L + H/R:(22.57 ± 3.22) ％,P ＜ 0.05],significantly reduced caspase-3 activation [C:(2.61 ± 0.19),H/R:(5.82±0.92),L + H/R:(3.74 ±0.64) pNA pmol/μg protein,P ＜0.05].To further study the mechanism underlying the benefits of lycopene,interactions between lycopene and calpain activation were examined.Lycopene pretreatment of cardiomyocytes suppressed the activation of calpain (C:272.33 ±300.46,H/R:1156.00 ± 212.02,L + H/R:607.33 ± 166.23,P ＜ 0.05) by reducing the H/R induced increased intracellular ROS levels [C:100％,H/R:(239.79 ± 27.27)％,L + H/R:(188.19 ±17.63) ％,P ＜ 0.05].Conclusion Lycopene may protect against hypoxia/reoxygenation-induced injury by preventing calpain activation.
