Methanolic extract of onion (Allium cepa) attenuates ischemia/hypoxia-induced apoptosis in cardiomyocytes via antioxidant effect
- 473 Downloads
Although there is growing awareness of the beneficial potential of onion intake to lower the risk of cardiovascular disease, there is little information about the effect of onion on ischemic heart injury, one of the most common cardiovascular diseases.
Aim of the study
This study investigates the effect of the methanol-soluble extract of onion on ischemic injury in heart-derived H9c2 cells in vitro and in rat hearts in vivo. The underlying mechanism is also investigated.
To evaluate the effect of onion on ischemia-induced cell death, LDH release and TUNEL-positivity were assessed in H9c2 cells, and the infarct size was measured in a myocardial infarct model. To investigate the mechanism of the cardioprotection by onion, the reactive oxygen species (ROS) level and the mitochondrial membrane potential (ΔΨm) were measured using an imaging technique; the caspase-3 activity was assayed, and Western blotting was performed to examine cytochrome c release in H9c2 cells.
The methanolic extract of onion had a preventive effect on ischemia/hypoxia-induced apoptotic death in H9c2 cells in vitro and in rat heart in vivo. The onion extract (0.05 g/ml) inhibited the elevation of the ROS, mitochondrial membrane depolarization, cytochrome c release and caspase-3 activation during hypoxia in H9c2 cells. In the in vivo rat myocardial infarction model, onion extract (10 g/kg) significantly reduced the infarct size, the apoptotic cell death of the heart and the plasma MDA level.
In conclusion, the results of this study suggest that the methanolic extract of onion attenuates ischemia/hypoxia-induced apoptosis in heart-derived H9c2 cells in vitro and in rat hearts in vivo, through, at least in part, an antioxidant effect.
KeywordsOnion extract Antioxidant Cardioprotection Ischemic injury Apoptosis
This study was supported by Technology Development Program for Agriculture and Forestry, Ministry for Agriculture, Forestry and Fisheries, and by “Specific Joint Agricultural Research-promoting Projects (20080401-033-302-001-02-00)”, RDA, Republic of Korea. This work was also supported by (2004) grant from “Department of Medical Sciences, The Graduate School, Ajou University”, and by a grant (CBM32-B3003-01-02-00) from the center for Biological Modulators of the 21st Century Frontier R&D Program of the Ministry of Science and Technology.
- 9.Center for Drug Evaluation and Research (2005) Pharmacology and toxicology, guidance for industry. Estimating the maximum safe dose in initial clinical trials for therapeutics in adult healthy volunteers, p 7. Available at http://www.fda.gov/cder/guidance/index.htm
- 10.Kim MJ, Moon CH, Kim MY, Lee S, Yi KY, Yoo SE, Lee SH, Baik EJ, Jung YS (2005) KR-32570, a novel Na+/H+ exchanger-1 inhibitor, attenuates hypoxia-induced cell death through inhibition of intracellular Ca2+ overload and mitochondrial death pathway in H9c2 cells. Eur J Pharmacol 525:1–7CrossRefGoogle Scholar
- 15.MacLellan WR, Schneider MD (1997) Death by design. Programmed cell death in cardiovascular biology and disease. Circ Res 81:137–144Google Scholar
- 16.McCord JM, Roy RS, Schaffer SW (1985) Free radicals and myocardial ischemia. The role of xanthine oxidase. Adv Myocardiol 5:183–189Google Scholar
- 17.Thompson-Gorman SL, Zweier JL (1990) Evaluation of the role of xanthine oxidase in myocardial reperfusion injury. J Biol Chem 265:6656–6663Google Scholar
- 25.Klanns-Dieter A (1983) Sulfur contends free radicals. In: Nygaard OF, Simic MG (eds) Radioprotectors and anticarcinogens. Academic Press, New York, pp 23–42Google Scholar