초록접수 현황
| 16F-240 | 구연 발표 |
The Effect of C-reactive Protein Deposition on Ischemia-Reperfusion Injury Model in Rat Myocardium
Se Jin Oh¹, Eun Na Kim², Chong Jai Kim², Jae-Sung Choi¹, Ki-Bong Kim³
¹Department of Thoracic and Cardiovascular Surgery, SMG-SNU Boramae Medical Center, Seoul National University College of Medicine, Seoul, Korea, ²Department of Pathology, Asan Medical Center, Asan Laboratory of Perinatal Science, Ulsan University College of Medicine, Seoul, Korea, ³Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
Background : The deposition of monomeric C-reactive protein (CRP) in myocardial infarct area and the complement systems aggravates the myocardial infarction. However, the effect of CRP on areas at risk (AAR) in ischemia-reperfusion injuries is unknown.
Methods : Myocardial ischemia-reperfusion injury model was produced by ligation of the left anterior descending coronary artery for 45 minutes followed by 45 minutes of reperfusion using female Sprague-Dawley rats (n = 17). Tissue from non-ischemic areas, areas at risk, and infarct areas determined by Evans blue and 2,3,5-triphenyltetrazolium chloride staining was obtained from the sham group (n = 3), the ischemia-reperfusion injury without CRP injection group (I/R only group, n = 5), and the ischemia-reperfusion injury with CRP injection group (I/R + CRP group, n = 9). We assessed the effect of CRP intravenous infusions on infarct size, the third component of complement (C3) immunodeposition, mitochondrial structural remodeling, and apoptosis by immunohistochemistry, direct immunofluorescence, electron microscopy, and TUNEL assay, respectively. All images were analyzed using an automated morphology tool (InForm; PerkinElmer, Waltham, Massachusetts).
Results : The infarct was significantly larger in the I/R + CRP group than in the I/R only group. The anti-mCRP antibody confirmed that CRP deposition occurred in both the infarct and AAR of the I/R + CRP group. The myocardium did not exhibit CRP mRNA expression. CRP injection tended to increase IL-6 mRNA expression with marginal statistical significance. Injection activated C3 in the AAR and infarct of the I/R + CRP group. Apoptosis and mitochondrial destruction increased in the AAR of the I/R + CRP group.
Conclusion : These results strongly suggest the active participation of the deposition of CRP in the AAR in the progression of myocardial infarct following ischemia-reperfusion injury by complement activation and mitochondrial change.
Methods : Myocardial ischemia-reperfusion injury model was produced by ligation of the left anterior descending coronary artery for 45 minutes followed by 45 minutes of reperfusion using female Sprague-Dawley rats (n = 17). Tissue from non-ischemic areas, areas at risk, and infarct areas determined by Evans blue and 2,3,5-triphenyltetrazolium chloride staining was obtained from the sham group (n = 3), the ischemia-reperfusion injury without CRP injection group (I/R only group, n = 5), and the ischemia-reperfusion injury with CRP injection group (I/R + CRP group, n = 9). We assessed the effect of CRP intravenous infusions on infarct size, the third component of complement (C3) immunodeposition, mitochondrial structural remodeling, and apoptosis by immunohistochemistry, direct immunofluorescence, electron microscopy, and TUNEL assay, respectively. All images were analyzed using an automated morphology tool (InForm; PerkinElmer, Waltham, Massachusetts).
Results : The infarct was significantly larger in the I/R + CRP group than in the I/R only group. The anti-mCRP antibody confirmed that CRP deposition occurred in both the infarct and AAR of the I/R + CRP group. The myocardium did not exhibit CRP mRNA expression. CRP injection tended to increase IL-6 mRNA expression with marginal statistical significance. Injection activated C3 in the AAR and infarct of the I/R + CRP group. Apoptosis and mitochondrial destruction increased in the AAR of the I/R + CRP group.
Conclusion : These results strongly suggest the active participation of the deposition of CRP in the AAR in the progression of myocardial infarct following ischemia-reperfusion injury by complement activation and mitochondrial change.
첨부파일 : 추계초록접수.pptm
책임저자: Ki-Bong Kim
Department of Thoracic and Cardiovascular Surgery, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Korea
발표자: Se Jin Oh, E-mail : wpwnn@hanmail.net