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白细胞介素-1家族在小鼠阿霉素心脏毒性模型中的表达 被引量:1

The expression of interleukin-1 family in mice with adriamycin-induced cardiotoxicity
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摘要 目的:探讨白细胞介素-1家族成员白细胞介素-1β(IL-1β),白细胞介素-1受体拮抗剂(IL-1Ra),白细胞介素-1(IL-1)受体I(IL-1RI)在小鼠急性阿霉素心脏毒性模型中的表达及其与心脏毒性的可能内在联系。方法:通过一次性腹腔注射阿霉素(15mg/kg),建立小鼠急性阿霉素心脏毒性模型。在给药前及给药后第3、7、14天分别取小鼠血清行ELISA法检测血清中IL-1β、IL-1Ra表达变化,并取小鼠心肌标本通过免疫组化、western blot法检测小鼠心肌组织中IL-1RI表达变化。同时,通过心肌组织病理学观察评价小鼠心肌损伤程度。结果:小鼠血清中IL-1β、IL-1Ra及心肌组织中IL-1RI均于阿霉素注射后表达升高,并于第7天达到最高。而心肌组织病理学观察显示小鼠在给药后第7天损伤明显。结论:IL-1家族在小鼠阿霉素心脏毒性模型中表达升高,提示其可能参与了阿霉素所致的小鼠心脏毒性损伤过程。 Objective:To study the expression of interleukin-1β(IL-1β), interleukin-1 receptor antagonist (IL-1Ra) and IL-1 receptor I (IL-1RI) in mice with acute adriamycin(ADR)-induced cardiotoxicity and try to find their potential correlations. Methods:Mouse models of acute cardiotoxicity was established by intraperitoneal injection of ADR (15 mg/kg). The expression of IL-1β and IL-1Ra in serum was detected by enzyme-linked immunosorbent assay (ELISA), while the expression of IL-1RI in cardiac tissues was detected by immunohistochemical staining and Western blot approaches. Cardiac tissue sections were used to evaluate the cardiac damage. Results:After ADR treatment, IL-1βand IL-1Ra concentrations in serum were highly induced and reached the maximum on day 7. IL-1RI protein in cardiac tissues was also expressed and reached the highest on day 7. Histopathological analysis of cardiac tissues showed obvious cardiac damage after 7 days of ADR treatment. Conclusion.. IL-1 family are highly induced and may be involved in the cardiotoxicity after ADR treatment.
出处 《国际心血管病杂志》 2010年第2期119-121,共3页 International Journal of Cardiovascular Disease
关键词 白细胞介素-1家族 阿霉素 心脏毒性 Interleukin-1 family Adriamycin Cardiotoxicity
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  • 1Young RC, Ozols RF, Myers CE. The anthracycline antineo plastic drugs[J]. N Engl J Med, 1981, 305(3) :139-153.
  • 2Doroshow JH. Effect of anthracycline antibiotics on oxygen radical formation in rat-heart[J]. Cancer Res, 1983, 43(2): 460-472.
  • 3Singal PK, Iliskovic N. Doxorubicin-induced cardiomyopathy [J].N EnglJ Med, 1998, 339(13): 900-905.
  • 4Dinarello CA. Interleukin-1[J]. Rev Infect Dis, 1984, 6(1) : 51-95.
  • 5Sims JE, Gayle MA, Slack JL, et al. Interleukin 1 signaling occurs exclusively via the type I receptor[J]. Proc Natl Acad Sei USA, 1993, 90(13): 6155-6159.
  • 6Arend WP. Interleukin-1 receptor antagonist: discovery, structure and properties[J]. Prog Growth Factor Res, 1990, 2 (4) : 193-205.
  • 7Bujak M, Frangogiannis NG. The role of IL-1 in the pathogenesis of heart disease[J]. Arch Immunol Ther Exp, 2009, 57(3): 165-176.
  • 8Arola OJ, Saraste A, Pulkki K, et al. Acute doxorubicin cardiotoxieity involves cardiomyocyte apoptosis[J]. Cancer Res, 2000, 60(7) : 1789-1792.
  • 9Hori M, Nishida K. Oxidative stress and left ventricular remodelling after myocardial infarction [J]. Cardiovasc Res, 2009, 81(3): 457-464.
  • 10FearonWF, Fearon DT. Inflammation and cardiovascular disease: role of the interleukin-1 receptor antagonist[J]. Circulation, 2008, 117(20): 2577- 2579.

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