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Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats.

Su Q, Li L, Liu YC, Zhou Y, Wen WM - World J Emerg Med (2013)

Bottom Line: Echocardiographic parameters displayed that the metoprolol group improved cardiac function significantly compared with the CME group (P<0.05).The myocardial apoptotic rate of the CME group as well as the contents of activated caspase-3 increased significantly (P<0.05), both of which were ameliorated significantly by metoprolol treatment (P<0.05).These results suggest that the inhibition of apoptosis can be a potential therapeutic strategy for the treatment of CME.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.

ABSTRACT

Background: Coronary microembolization (CME) is a serious complication following percutaneous coronary intervention (PCI) in patients with acute coronary syndromes. The use of metoprolol before PCI can significantly protect ischemic myocardium from myocardial damage, but the function of metoprolol in the treatment of CME is not entirely clear. This study was to explore the effect and significance of metoprolol on myocardial apoptosis and caspase-3 activation after CME in rats.

Methods: Thirty rats were randomly divided into three groups including sham-operation (control group), CME plus saline (CME group), CME plus metoprolol (metoprolol group), 10 rats for each group. The CME group was induced by injecting 3 000 polyethylene microspheres (42 μm) into the left ventricle during a 10-second occlusion of the ascending aorta; the control group was injected with physiological saline instead of microembolization ball; the metoprolol or saline group was given three intravenous bolus injections before CME. Echocardiography, TUNEL staining, and Western blotting were used to evaluate cardiac function, proportion of apoptotic cells and activation of caspase-3 respectively at 6 hours after operation.

Results: Echocardiographic parameters displayed that the metoprolol group improved cardiac function significantly compared with the CME group (P<0.05). The myocardial apoptotic rate of the CME group as well as the contents of activated caspase-3 increased significantly (P<0.05), both of which were ameliorated significantly by metoprolol treatment (P<0.05).

Conclusions: This study demonstrates that metoprolol can protect the myocardium during CME in rats by inhibiting apoptosis and improving cardiac function. These results suggest that the inhibition of apoptosis can be a potential therapeutic strategy for the treatment of CME.

No MeSH data available.


Related in: MedlinePlus

Effect of metoprolol on caspase-3 expression following CME. A: The relative expression levels of activated caspase-3 protein were determined by using western blot; the IA values were normalized to GAPDH expression levels. Lanes 1, 2, and 3 in the representative gel show caspase-3 expression in the control, CME (after 6 hours), and metoprolol groups, respectively. B: The data obtained (n=10) were expressed and compared between the groups as means ± SD values, herein presented graphically. Compared with the control group, *P<0.05; compared with the CME group, #P<0.05.
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Figure 5: Effect of metoprolol on caspase-3 expression following CME. A: The relative expression levels of activated caspase-3 protein were determined by using western blot; the IA values were normalized to GAPDH expression levels. Lanes 1, 2, and 3 in the representative gel show caspase-3 expression in the control, CME (after 6 hours), and metoprolol groups, respectively. B: The data obtained (n=10) were expressed and compared between the groups as means ± SD values, herein presented graphically. Compared with the control group, *P<0.05; compared with the CME group, #P<0.05.

Mentions: Since metoprolol treatment decreased apoptosis in CME rats. Western blot analysis was made of mitochondrial apoptotic pathway proteins, including activated caspase-3 (Figure 5). Compared with the control group, the CME group showed the significantly enhanced expression of activated caspase-3 in myocardial cells of rats (P<0.05). Compared with the CME group, the metoprolol group significantly decreased the contents of activated caspase-3 (P<0.05). Obviously, metoprolol treatment can reduce apoptosis in CME rats by inhibiting the expression of activated caspased-3.


Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats.

Su Q, Li L, Liu YC, Zhou Y, Wen WM - World J Emerg Med (2013)

Effect of metoprolol on caspase-3 expression following CME. A: The relative expression levels of activated caspase-3 protein were determined by using western blot; the IA values were normalized to GAPDH expression levels. Lanes 1, 2, and 3 in the representative gel show caspase-3 expression in the control, CME (after 6 hours), and metoprolol groups, respectively. B: The data obtained (n=10) were expressed and compared between the groups as means ± SD values, herein presented graphically. Compared with the control group, *P<0.05; compared with the CME group, #P<0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4129839&req=5

Figure 5: Effect of metoprolol on caspase-3 expression following CME. A: The relative expression levels of activated caspase-3 protein were determined by using western blot; the IA values were normalized to GAPDH expression levels. Lanes 1, 2, and 3 in the representative gel show caspase-3 expression in the control, CME (after 6 hours), and metoprolol groups, respectively. B: The data obtained (n=10) were expressed and compared between the groups as means ± SD values, herein presented graphically. Compared with the control group, *P<0.05; compared with the CME group, #P<0.05.
Mentions: Since metoprolol treatment decreased apoptosis in CME rats. Western blot analysis was made of mitochondrial apoptotic pathway proteins, including activated caspase-3 (Figure 5). Compared with the control group, the CME group showed the significantly enhanced expression of activated caspase-3 in myocardial cells of rats (P<0.05). Compared with the CME group, the metoprolol group significantly decreased the contents of activated caspase-3 (P<0.05). Obviously, metoprolol treatment can reduce apoptosis in CME rats by inhibiting the expression of activated caspased-3.

Bottom Line: Echocardiographic parameters displayed that the metoprolol group improved cardiac function significantly compared with the CME group (P<0.05).The myocardial apoptotic rate of the CME group as well as the contents of activated caspase-3 increased significantly (P<0.05), both of which were ameliorated significantly by metoprolol treatment (P<0.05).These results suggest that the inhibition of apoptosis can be a potential therapeutic strategy for the treatment of CME.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.

ABSTRACT

Background: Coronary microembolization (CME) is a serious complication following percutaneous coronary intervention (PCI) in patients with acute coronary syndromes. The use of metoprolol before PCI can significantly protect ischemic myocardium from myocardial damage, but the function of metoprolol in the treatment of CME is not entirely clear. This study was to explore the effect and significance of metoprolol on myocardial apoptosis and caspase-3 activation after CME in rats.

Methods: Thirty rats were randomly divided into three groups including sham-operation (control group), CME plus saline (CME group), CME plus metoprolol (metoprolol group), 10 rats for each group. The CME group was induced by injecting 3 000 polyethylene microspheres (42 μm) into the left ventricle during a 10-second occlusion of the ascending aorta; the control group was injected with physiological saline instead of microembolization ball; the metoprolol or saline group was given three intravenous bolus injections before CME. Echocardiography, TUNEL staining, and Western blotting were used to evaluate cardiac function, proportion of apoptotic cells and activation of caspase-3 respectively at 6 hours after operation.

Results: Echocardiographic parameters displayed that the metoprolol group improved cardiac function significantly compared with the CME group (P<0.05). The myocardial apoptotic rate of the CME group as well as the contents of activated caspase-3 increased significantly (P<0.05), both of which were ameliorated significantly by metoprolol treatment (P<0.05).

Conclusions: This study demonstrates that metoprolol can protect the myocardium during CME in rats by inhibiting apoptosis and improving cardiac function. These results suggest that the inhibition of apoptosis can be a potential therapeutic strategy for the treatment of CME.

No MeSH data available.


Related in: MedlinePlus