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Published on: May 4, 2015
Interleukin-6/soluble interleukin-6 receptor complex reduces infarct size via inhibiting myocardial apoptosis
Kenichi Matsushita1, Shiro Iwanaga, Takahiro Oda
1Cardiopulmonary Division, Department of Medicine, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
Insights
Interleukin-6 (IL-6) complexed with soluble IL-6 receptor (sIL-6R) inhibits cardiomyocyte apoptosis and reduces infarct size in reperfused myocardial infarction. This finding suggests a potential therapeutic strategy for limiting reperfusion injury.
Area of Science:
- Cardiovascular Research
- Cellular Biology
- Immunology
Background:
- Myocardial infarction leads to reperfusion injury, characterized by cardiomyocyte apoptosis.
- Interleukin-6 (IL-6) is a cytokine known to inhibit apoptosis in other cell types via the IL-6 receptor (IL-6R).
Purpose of the Study:
- To investigate whether the IL-6/soluble IL-6R complex can inhibit myocardial apoptosis and reduce infarct size in acute myocardial infarction with reperfusion.
- To evaluate the therapeutic potential of the IL-6/sIL-6R complex in limiting reperfusion injury.
Main Methods:
- Rats underwent coronary artery occlusion followed by reperfusion.
- Groups received either IL-6/sIL-6R complex, IL-6 alone, sIL-6R alone, or vehicle control.
- Cardiomyocyte apoptosis was assessed using DNA gel electrophoresis and TUNEL staining; infarct size was quantified via tetrazolium chloride staining.
Main Results:
- The IL-6/sIL-6R complex significantly inhibited cardiomyocyte apoptosis in the reperfused myocardium.
- The infarct area was markedly reduced in the complex group (23.8%) compared to vehicle (37.9%), IL-6 (40.7%), or sIL-6R (37.5%) groups (P=0.0002).
- No significant reduction in apoptosis or infarct size was observed in groups receiving IL-6 or sIL-6R alone.
Conclusions:
- The IL-6/soluble IL-6 receptor complex effectively inhibits cardiomyocyte apoptosis during reperfused acute myocardial infarction.
- This inhibition suggests a protective role against irreversible myocardial reperfusion injury.
Abstract:
Apoptosis of cardiomyocytes plays an important role in reperfusion injury following myocardial infarction. Conversely, interleukin-6 (IL-6)--a potent cytokine--inhibits myeloma cell apoptosis by activating GP130 through the IL-6 receptor (IL-6R). We hypothesized that the IL-6/soluble IL-6R complex can inhibit myocardial apoptosis, and limit infarct size in reperfused acute myocardial infarction. Anesthetized rats were randomly divided into five groups: sham, coronary occlusion and reperfusion rats administered IL-6/soluble IL-6R complex, IL-6 alone, soluble IL-6R (sIL-6R) alone, or a control vehicle. Rats were subjected to 30 min occlusion of the left coronary artery followed by 3 h reperfusion. After reperfusion, the hearts were excised. For detection and quantification of apoptosis, gel electrophoresis of extracted genomic DNA and TUNEL method of paraffin sections were performed. The percentage of the infarct area was measured using tetrazolium chloride staining. The cardiomyocyte apoptosis analysis revealed that apoptosis in the reperfused myocardium was inhibited only in the complex group. Furthermore, the percentage of the infarct area out of the area at risk was remarkably reduced in the complex group (23.8+/-1.8%), compared with that in the vehicle (37.9+/-3.7%), the IL-6 (40.7+/-1.0%), or the sIL-6R (37.5+/-2.4%) groups (P=0.0002). No significant differences were observed among the vehicle, IL-6, and sIL-6R groups. The IL-6/soluble IL-6 receptor complex inhibits cardiomyocyte apoptosis in reperfused acute myocardial infarction. It possibly reduces irreversible reperfusion injury.
