目的 探讨丹红注射液对老龄家兔肾脏缺血再灌注损伤的保护作用及可能机制.方法阻断双侧肾动脉1h, 开放2 h造成家兔肾脏缺血再灌注损伤.选取造模成功的家兔分为4 组, 分别为假手术组 ( F组) 、缺血再灌注组 ( I组) 、丹红注射液10 ml/kg组 ( D1 组) 和20 ml/kg组 ( D2 组) .检测血清氧化应激指标丙二醛 (MDA)、超氧化物歧化酶 (SOD)、谷胱甘肽 (GSH)、谷胱甘肽过氧化物酶(GSH-Px) ; 肾脏功能指标肌酐 ( Cr) 及血尿素氮 ( BUN) ; 炎症因子白介素-1 ( IL-1) 和肿瘤坏死因子-α ( TNF-α) 含量水平.检测肾脏组织内皮素-1 ( ET-1) 水平.结果 与 I 组相比, D1 及 D2 组的血清氧化应激指标MDA明显降低 ( P <0.05) , 而 SOD、 GSH、 GSH -Px 明显增高 ( P <0.05) ; 肾功能指标Cr及BUN明显降低 ( P<0.05) ; D2 组的炎症因子IL-1 及TNF-α明显降低 ( P<0.05) ; D1 及D2 组肾组织ET-1 的含量明显降低 ( P<0.05) .结论 丹红注射液可以减轻家兔肾脏缺血再灌注损伤的氧化应激, 保护肾脏功能、可能与降低炎症因子及内皮素-1 的含量有关.
Objective To explore the protective effects and possible mechanisms of Danhong injection on renal ischemia-reperfusion injury in old rabbits. Methods Renal ischemia-reperfusion injury model was made by blocking bilateral renal arteries with arterial clips for 1 h and opening the clips to restore blood supply for 2 h in old rabbits. The rabbits were divided into 4 groups, sham group (group F), renal ischemia-reperfusion injury group ( group I), Danhong injection (10 ml/kg) group ( group D1), and Danhong injection (20 ml/kg) group ( group D2). Serum oxidative stress indicators including malondialdehyde ( MDA), su-peroxide dismutase (SOD), glutathione (GSH), glutathione peroxidase ( GSH-Px) were determined. Renal function indicators including creatinine (Cr) and urea nitrogen (BUN), inflammatory factors interleukin-1 ( IL-1) and tumor necrosis factor-α (TNF-α) were measured. Endothelin-1 (ET-1) level in the kidney was detected. Results Compared with group I, the levels of MDA were significantly decreased (P<0.05), but the levels of SOD, GSH and GSH-Px were significantly increased in group D1 and group D2 (P<0.05). The levels of Cr and BUN in group D1 and group D2 were significantly decreased (P<0.05). The lev-els of IL-1and TNF-α in group D2 were significantly decreased (P<0.05). The levels of ET-1 in group D1 and group D2 were significantly decreased (P<0.05). Conclusion Danhong injection may improve the renal function in rabbits with ischemia-reper-fusion injury. The mechanism underlying the protective effects involves the inhibition of oxidative stress which relates to the reduction of inflammatory factors and endothelin.