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目的探讨脂氧素A4受体激动剂BML-111对大鼠肾缺血-再灌注损伤的作用及其可能机制。方法 25只SD大鼠随机均分为五组:B组作为空白对照;A、C、D和E组建立肾缺血45min和再灌注模型,A、C、D和E组在肾缺血前分别腹腔注射生理盐液、脂氧素3mg/kg、锌原卟啉25mg/kg和脂氧素3mg/kg+锌原卟啉25mg/kg。测定血清肌酐(SCr)、血尿素氮(BUN)、丙二醛(MDA)和氨基葡萄糖苷酶(NAG)含量,免疫组化染色法检测血红素加氧酶1(HO-1)阳性表达,RT-PCR和Western blot分别检测HO-1蛋白和mRNA表达。结果 A、C、E组SCr、BUN、MDA、NAG水平以及HO-1表达均高于B组(P<0.01或P<0.05)。与A组相比,C组SCr、BUN、MDA和NAG水平降低(P<0.01),而HO-1表达增加(P<0.05)。与D组相比,E组SCr、BUN、MDA和NAG水平降低(P<0.05),而HO-1表达增加(P<0.05)。结论 BML-111能减轻大鼠肾缺血-再灌注损伤,保护肾功能,其机制可能与调节HO-1高表达、抑制氧自由基损伤有关。
Objective To investigate the effect of lipoxygenin A4 receptor agonist BML-111 on renal ischemia-reperfusion injury in rats and its possible mechanism. Methods Twenty-five Sprague-Dawley rats were randomly divided into five groups: Group B served as blank control; Group A, C, D and E established renal ischemia 45 min and reperfusion model, Group A, C, D and E before renal ischemia The rats were intraperitoneally injected with physiological saline, lipoxin 3mg / kg, zinc protoporphyrin 25mg / kg and lipoxin 3mg / kg + zinc protoporphyrin 25mg / kg. Serum creatinine (SCr), blood urea nitrogen (BUN), malondialdehyde (MDA) and glucosaminidase (NAG) were measured and the expression of heme oxygenase 1 (HO-1) The expression of HO-1 protein and mRNA were detected by RT-PCR and Western blot respectively. Results The levels of SCr, BUN, MDA, NAG and HO-1 in groups A, C and E were higher than those in group B (P <0.01 or P <0.05). Compared with group A, the levels of SCr, BUN, MDA and NAG in group C decreased (P <0.01), while the expression of HO-1 increased (P <0.05). Compared with group D, the levels of SCr, BUN, MDA and NAG in group E decreased (P <0.05), while the expression of HO-1 increased (P <0.05). Conclusion BML-111 can reduce renal ischemia-reperfusion injury and protect renal function in rats, and its mechanism may be related to the regulation of HO-1 overexpression and the inhibition of oxygen free radical injury.