Summary
To observe the effect of ginsenoside Re on cardiomyocyte apoptosis and Bcl-2/Bax gene expression after ischemia (30 min) and reperfusion (6 h) in rats and to elucidate the possible mechanisms of ginsenoside Re on inhibition of cardiomyocyte apoptosis, the ischemia/reperfusion heart model was established by ligating the left anterior descending branch of coronary artery in Wistar rats. The apoptotic cardiomyocytes were confirmed by transmission electron microscopy and counted byin situ nick end labeling (TUNEL) method and light microscopy. The mRNA and protein expression of Bcl-2 and Bax genes were studied byin situ hybridization and immunohistochemical staining. Mean optical density (OD) value of the positive fields of mRNA and protein expression was quantitatively examined by image analysis system. The results were as follows: (1) The apoptotic cardiomyocytes were found in ischemic fields in the ischemia/reperfusion group and weren’t observed in the sham-operation group by transmission electron microscopy; (2) The numbers of the apoptotic cells were 134.45±45.61/field in the ischemia/reperfusion group, and 90.66±19.22/field in the ginsenoside Re-treated group. The differences was significant between two groups (P<0.01); (3) Gene expression of Bcl-2 and Bax were increased significantly in the ischemia/reperfusion group and ginsenoside Re-treated group when compared with the sham-operation group. There was no significant difference in the gene expression of Bcl-2 between the ginsenoside Re-treated group and ischemia/reperfusion group (P>0.05), but gene expression of Bax was decreased significantly in the ginsenoside Re-treated group as compared with the ischemia/reperfusion group (P<0.01). The ratio of Bcl-2/Bax was increased significantly in the ginsenoside Re-treated group when compared with the ischemia/reperfusion group and sham-operation group. These findings suggest that myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and ginsenoside Re can significantly inhibit cardiomyocyte apoptosis induced by ischemia-reperfusion in rats. It is concluded that ginsenoside Re inhibits cardiomyocyte apoptosis by inhibiting expression of pro-apoptotic Bax gene and raising the ratio of Bcl-2/Bax.
Similar content being viewed by others
References
Gottlieb R A, Engler R L. Apoptosis in myocardial ischemia-reperfusion. Ann N Y Acad Sci, 1999,874:412
Maffei-Facino R, Carini M, Aldini Get al. Panax ginseng administration in the rat prevents myocardial ischemia-reperfusion damage induced by hyperbaric oxygen: evidence for an antioxidant intervention. Planta Med, 1999, 65(7):614
2000, 7(4): 256
1994, 74(10): 626
2000, 9(3): 261
Strasser A, Harris AW, Jacks Tet al. DNA damage can induce apoptosis in proliferating lymphoid cells via p53-independent mechanisms inhibitable by Bcl-2. Cell, 1994,79(2):329
Yin X M, Oltvai Z N, Korsmeyer S J. BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax. Nature, 1994,369(6478):321
Oltvai Z N, Milliman C L, Korsmeyer S J. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell, 1993,74(4):609
Yang E, Zha J, Jockel Jet al. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell, 1995,80(2):285
Green D R, Reed J C. Mitochondria and apoptosis. Science, 1998,281(5381):1309
Cook S A, Pool-Wilson P A. Cardiac myocyte apoptosis. Eur Heart J, 1999,20:1619
White E. Life, death, and the pursuit of apoptosis. Genes Dev, 1996,10:1
Jayanthi S, Deng X, Bordelon Met al. Methamphetamine causes differential regulation of pro-death and anti-death Bcl-2 genes in the mouse neocortex. FASEB J, 2001,15(10):1745
Author information
Authors and Affiliations
Additional information
This project was supported by a grant from the Natural Sciences Foundation of Hubei Province (No. 2000J050).
Rights and permissions
About this article
Cite this article
Liu, Z., Li, Z. & Liu, X. Effect of ginsenoside Re on cardiomyocyte apoptosis and expression of Bcl-2/Bax gene after ischemia and reperfusion in rats. Current Medical Science 22, 305–309 (2002). https://doi.org/10.1007/BF02896771
Received:
Published:
Issue Date:
DOI: https://doi.org/10.1007/BF02896771