Summary
In order to study the effects of losartan on cardiomyocyte apoptosis following ischemia (0.5 h) and reperfusion (48 h) in vivo and bcl-2 and bax gene expression, TUNEL staining method, immunohistochemistry and in situ hybridization histochemistry (ISHH) were used to monitor the apoptotic cells, mRNA and protein of gene expression, respectively. Image processing system was used to quantitively dispose the positive metric substance of both immunohistochemistry and ISHH through the average optical density (OD) value. The number of the apoptotic cells were 38 ±9 (control group), 0–1 (sham operation group) and 9±4 (losartan-treated group) in each visual field respectively with the difference among the groups being significant (P < 0.001). OD values of bcl-2 (ISHH) were 0.07425 ± 0. 02029 (control group), 0. 05961 ± 0.009932 (sham operation group) and 0.07619±0. 01445 (losartan-treated group) respectively, while OD values of bcl-2 (immunohistochemistry) were 0.1374 ± 0.01367 (control group), 0. 08510±0. 01862 (sham operation group) and 0.1252±0.02064 (losartan-treated group), bcl-2 gene expression was increased significantly in the control group and losartan-treated group as compared with sham operation group (P < 0.05). OD value of bax (immunohistochemistry) was 09727±0.02230 (control group), 0.06182 ± 0.01430 (sham operation group) and 0.06213 ± 0.01420 (losartan-treated group). bax gene expression was decreased very significantly in losartan-treated group and sham operation group as compared with control group (P < 0.001). Bcl-2/ bax ratio was 1.413 (control group), 1.376 (sham operation group) and 2.016 (losartan-treated group) respectively. The results indicated that losartan might inhibit cardiomyocyte apoptosis following ischemia and reperfusion. The mechanism might be that bax gene expression was inhibited to increase bcl-2/bax ratio.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Di Pasquale P, Cannizzaro S, Longo A Met al. Captopril plus losartan in early post-infarction. Neurohormonal effects: a pilot atudy. G Ital Cardiol, 1997, 27 (12): 1256
Di Pasquale P, Bucca V, Scalzo Set al. Safety, tolerability, and neurohormonal changes of the combination captopril plus losartan in the early postinfarction aeriod: a pilot study. Cardiovasc’ Drugs Ther, 1998, 12 (2): 211
Unger T, Chung O, Csikos Tet al. Angiotensin receptors. J Hypertens Suppl, 1996, 14(5): S95
Fliss H, Gaottinger D. Apoptosis in ischemic and reperfusion rat myocardium. Circ Res, 1996, 79(5): 949
Saraste A, Pulkki K, Kallajoki Met al. Apoptosis in human acute myocardial infarction. Circulation, 1997, 95(2): 320
Takemura G, Ohno M, Hayakawa Yet al. Role of apoptosis in the disappearance of infiltrated and proliferated interstitial cells after myocardial infarction. Circ Res, 1998, 82(11): 1130
Freude B, Masters T N, Kostin Set al. Cardiomyocyte apoptosis in acute and chronic conditions. Basic Res Cardiol, 1998, 93(2): 85
Chakrabarti S, Hoque A N, Karmazyn M. A rapid ischemia-induced apoptosis in isolated rat hearts and its attenuation by the sodium-hydrogen exchange inhibitor HOE 642 (Cariporide). J Mol Cell Cardiol, 1997, 29 (11): 3169
Misao J, Hayakawa Y, Ohno Met al. Expression of Bcl-2 protein, an inhibitor of apoptosis, and Bax, an accelerator of apoptosis, in ventricular myocytes of human hearts with myocardial infarction. Circulation, 1996, 94(7): 1506
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Dongqing, Z., Liming, Y., Zhengxiang, L. et al. Study on the effects of losartan on cardiomyocyte apoptosis and gene expression after ischemia and reperfusion in vivo in rats. Current Medical Science 20, 49–52 (2000). https://doi.org/10.1007/BF02887675
Received:
Published:
Issue Date:
DOI: https://doi.org/10.1007/BF02887675