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Activated protein C protects myocardium via activation of anti-apoptotic pathways of survival in ischemia-reperfused rat heart.

Ding JW, Tong XH, Yang J, Liu ZQ, Zhang Y, Yang J, Li S, Li L - J. Korean Med. Sci. (2010)

Bottom Line: However, the protection mechanism of APC is not fully understood.APC reduced the expression of pro-apoptotic genes, Bax and cytochrome c.These findings suggest that APC produces cardioprotective effect by preserving the expression of proteins and genes involved in anti-apoptotic pathways, regardless of the timing of administration.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, the First College of Clinical Medical Science, China Three Gorges University, Yichang, Hubei, China.

ABSTRACT
Activated protein C (APC) is known to be beneficial on ischemia reperfusion injury in myocardium. However, the protection mechanism of APC is not fully understood. The purpose of this study was to investigate the effects and possible mechanisms of APC on myocardial ischemic damage. Artificially ventilated anaesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 hr of reperfusion. Rats were randomly divided into four groups; Sham, I/R, APC preconditioning and postconditioning group. Myocardial infarct size, apoptosis index, the phosphorylation of ERK1/2, Bcl-2, Bax and cytochrome c genes and proteins were assessed. In APC-administrated rat hearts, regardless of the timing of administration, infarct size was consistently reduced compared to ischemia/reperfusion (I/R) rats. APC improved the expression of ERK1/2 and anti-apoptotic protein Bcl-2 which were significantly reduced in the I/R rats. APC reduced the expression of pro-apoptotic genes, Bax and cytochrome c. These findings suggest that APC produces cardioprotective effect by preserving the expression of proteins and genes involved in anti-apoptotic pathways, regardless of the timing of administration.

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Related in: MedlinePlus

Effect of APC treatment on p-ERK protein in rat heart after 30 min ischemia and 2 h reperfusion. The phosphorylation was quantified by densitometry using image analysis program. Mean±SE, n=6.*P<0.01 vs sham; †P<0.01 vs I/R.
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Figure 3: Effect of APC treatment on p-ERK protein in rat heart after 30 min ischemia and 2 h reperfusion. The phosphorylation was quantified by densitometry using image analysis program. Mean±SE, n=6.*P<0.01 vs sham; †P<0.01 vs I/R.

Mentions: Western blot analysis of ERK1/2 is shown in Fig. 3. I/R injury obviously increased P-ERK1/2 expression (3.4±0.21; respectively) compared to the sham as measured densitometrically (fold relative to sham). In contrast to the I/R group, APC treatment significantly increased P-ERK1/2 expression (7.45±0.34 vs 3.4±0.21, P<0.01 and 6.98±0.31 vs 3.4±0.21, P<0.01). Phosphorylations of ERK1/2 were similar between the APC-administrated groups (Fig. 3).


Activated protein C protects myocardium via activation of anti-apoptotic pathways of survival in ischemia-reperfused rat heart.

Ding JW, Tong XH, Yang J, Liu ZQ, Zhang Y, Yang J, Li S, Li L - J. Korean Med. Sci. (2010)

Effect of APC treatment on p-ERK protein in rat heart after 30 min ischemia and 2 h reperfusion. The phosphorylation was quantified by densitometry using image analysis program. Mean±SE, n=6.*P<0.01 vs sham; †P<0.01 vs I/R.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2966998&req=5

Figure 3: Effect of APC treatment on p-ERK protein in rat heart after 30 min ischemia and 2 h reperfusion. The phosphorylation was quantified by densitometry using image analysis program. Mean±SE, n=6.*P<0.01 vs sham; †P<0.01 vs I/R.
Mentions: Western blot analysis of ERK1/2 is shown in Fig. 3. I/R injury obviously increased P-ERK1/2 expression (3.4±0.21; respectively) compared to the sham as measured densitometrically (fold relative to sham). In contrast to the I/R group, APC treatment significantly increased P-ERK1/2 expression (7.45±0.34 vs 3.4±0.21, P<0.01 and 6.98±0.31 vs 3.4±0.21, P<0.01). Phosphorylations of ERK1/2 were similar between the APC-administrated groups (Fig. 3).

Bottom Line: However, the protection mechanism of APC is not fully understood.APC reduced the expression of pro-apoptotic genes, Bax and cytochrome c.These findings suggest that APC produces cardioprotective effect by preserving the expression of proteins and genes involved in anti-apoptotic pathways, regardless of the timing of administration.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, the First College of Clinical Medical Science, China Three Gorges University, Yichang, Hubei, China.

ABSTRACT
Activated protein C (APC) is known to be beneficial on ischemia reperfusion injury in myocardium. However, the protection mechanism of APC is not fully understood. The purpose of this study was to investigate the effects and possible mechanisms of APC on myocardial ischemic damage. Artificially ventilated anaesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 hr of reperfusion. Rats were randomly divided into four groups; Sham, I/R, APC preconditioning and postconditioning group. Myocardial infarct size, apoptosis index, the phosphorylation of ERK1/2, Bcl-2, Bax and cytochrome c genes and proteins were assessed. In APC-administrated rat hearts, regardless of the timing of administration, infarct size was consistently reduced compared to ischemia/reperfusion (I/R) rats. APC improved the expression of ERK1/2 and anti-apoptotic protein Bcl-2 which were significantly reduced in the I/R rats. APC reduced the expression of pro-apoptotic genes, Bax and cytochrome c. These findings suggest that APC produces cardioprotective effect by preserving the expression of proteins and genes involved in anti-apoptotic pathways, regardless of the timing of administration.

Show MeSH
Related in: MedlinePlus