摘要
目的探讨血红素氧合酶-1(Heme oxygenase-1,HO-1)在低氧预适应时对大鼠肾缺血-再灌注损伤的保护机制。方法建立大鼠的肾缺血-再灌注损伤动物模型,观察大鼠再灌注后肾脏免疫组织化学变化;检测HO-1基因在大鼠肾脏的表达情况。并就上述结果行相关分析。结果与正常对照组相比,Co PP组HO-1mRNA表达量最高,其余依次降低为实验对照组、低氧+Zn PP组、低氧组,差异有显著性(P<0.01)。Co PP组SOD活性最高,其余依次为低氧组、Zn PP组,差异有显著性(P<0.05)。Co PP组MDA含量最低,其余依次升高为低氧组、低氧+Zn PP组、Zn PP组,差异有显著性(P<0.05)。结论经钴原卟啉(Co PP)处理和低氧预适应使HO-1表达增强,肾脏缺血-再灌注时的细胞损伤减轻,其机制可能与降低氧自由基损伤相关。
Objective To investigate the protective effects of heme oxygenase - 1 （ HO - 1 ） in Renal ischemia/ repeffusion injury on rats under hypoxia and explore the possible mechanism. Methods Rat renal ischemia/repeffusion injury model was established. The expression of HO - 1 mRNA was detected by RT - PCR. The vitality of SOD and the quantity of MDA were detected in rat renal isehemia/repeffusion injury models treated with HO - 1 inducer cobalt protoporphyrin （ CoPP）, zinc protoporphyrin （ ZnPP, HO - 1 inhibitor） and hypoxic preconditioning. Results HO - 1 mRNA level expression results showed that：compared with normal control group, the CoPP group expression was the highest, the other groups such as control group, hypoxia ＋ ZnPP group, hypoxia group, also showed significant difference（P 〈 0.01 ）. SOD activity in CoPP group was the highest,followed with low oxygen and ZnPP group, respectively, showed significant difference （ P 〈 0.05 ）. MDA content in CoPP group was the lowest, while the hypoxia, hypoxia ＋ ZnPP group and ZnPP group showed significant difference （ P 〈 0.05 ） as well. Conclusion The up regulation of HO - 1 expression induced by CoPP and hypoxic preconditioning can reduce the degree of damage of the tubular epithelial cells and subsequently alleviate the renal ischemia reperfusion injury. One of its main mechanisms may be related with anti oxygen free radicals.
出处
《青海医学院学报》
CAS
2015年第3期158-162,共5页
Journal of Qinghai Medical College
基金
青海大学中青年科研基金项目(项目编号:2011-QYY-6)
