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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한외과학회 Annals of Surgical Treatment and Research Annals of Surgical Treatment and Research Vol.88 No.3
- 발행연도
- 2015.2
- 수록면
- 152 - 159 (8page)
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초록· 키워드
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Purpose: Intimal hyperplasia (IH) is the main cause of restenosis or occlusion after vascular procedures. Imatinib mesylate and rapamycin are known to prevent IH. The purpose of this study was to evaluate the effect of these drugs on the regression of preformed IH in rat carotid injury model.
Methods: IH was established in rat carotid arteries using a balloon catheter. The drug effects were assessed in vitro on proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMC) in the neointima. And in vivo studies were carried out in 4 groups: imatinib, rapamycin, combined, and no medication. After 2-week oral medication, morphometric analysis evaluated the number and density of neointimal cells, intima-to-media (I/M) ratio and cross-sectional area. Cell proliferation, apoptosis, and collagen changes were also investigated by immunohistochemical staining (IHCS).
Results: Imatinib and rapamycin significantly inhibited VSMC proliferation and migration, and promoted apoptosis in vitro. In morphometric analysis, the number and density of neointimal cells decreased significantly in all medication groups compared with control group (P < 0.01). However, there was no significant difference in neointimal cross-sectional area and I/M ratio among groups. In IHCS, imatinib and rapamycin inhibited neointimal cell proliferation significantly. However, there was no significant change in cell apoptosis and collagen composition.
Conclusion: Combined treatment of with imatinib and rapamycin induced reduction of cell mass in preformed intimal hyperplasia, but failed to induce regression of intimal mass in this short-term medication study. Further studies will be needed with additional strategies of inducing lysis of the extracellular matrix.
Methods: IH was established in rat carotid arteries using a balloon catheter. The drug effects were assessed in vitro on proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMC) in the neointima. And in vivo studies were carried out in 4 groups: imatinib, rapamycin, combined, and no medication. After 2-week oral medication, morphometric analysis evaluated the number and density of neointimal cells, intima-to-media (I/M) ratio and cross-sectional area. Cell proliferation, apoptosis, and collagen changes were also investigated by immunohistochemical staining (IHCS).
Results: Imatinib and rapamycin significantly inhibited VSMC proliferation and migration, and promoted apoptosis in vitro. In morphometric analysis, the number and density of neointimal cells decreased significantly in all medication groups compared with control group (P < 0.01). However, there was no significant difference in neointimal cross-sectional area and I/M ratio among groups. In IHCS, imatinib and rapamycin inhibited neointimal cell proliferation significantly. However, there was no significant change in cell apoptosis and collagen composition.
Conclusion: Combined treatment of with imatinib and rapamycin induced reduction of cell mass in preformed intimal hyperplasia, but failed to induce regression of intimal mass in this short-term medication study. Further studies will be needed with additional strategies of inducing lysis of the extracellular matrix.
목차
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
참고문헌 (30)
참고문헌 신청
1. [학술지(정기간행물)] - Bauters C. / 1997 / The biology of restenosis / Prog Cardiovasc Dis 40 : 107 ~ 116
2. [학술지(정기간행물)] - Mitra AK. / 2006 / Cellular, molecular and immunological mechanisms in the pathophysiology of vein graft intimal hyperplasia / Immunol Cell Biol 84 : 115 ~ 124
3. [학술지(정기간행물)] - Moses JW. / 2003 / Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery / N Engl J Med 349 : 1315 ~ 1323
4. [학술지(정기간행물)] - Gregory CR. / 1993 / Its effect on cellular, growth factor, and cytokine response in injured vessels / Transplantation 55 : 1409 ~ 1418
5. [학술지(정기간행물)] - Buchdunger E. / 2000 / Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors / J Pharmacol Exp Ther 295 : 139 ~ 145
2. [학술지(정기간행물)] - Mitra AK. / 2006 / Cellular, molecular and immunological mechanisms in the pathophysiology of vein graft intimal hyperplasia / Immunol Cell Biol 84 : 115 ~ 124
3. [학술지(정기간행물)] - Moses JW. / 2003 / Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery / N Engl J Med 349 : 1315 ~ 1323
4. [학술지(정기간행물)] - Gregory CR. / 1993 / Its effect on cellular, growth factor, and cytokine response in injured vessels / Transplantation 55 : 1409 ~ 1418
5. [학술지(정기간행물)] - Buchdunger E. / 2000 / Abl protein-tyrosine kinase inhibitor STI571 inhibits in vitro signal transduction mediated by c-kit and platelet-derived growth factor receptors / J Pharmacol Exp Ther 295 : 139 ~ 145
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UCI(KEPA) : I410-ECN-0101-2016-514-001306601