摘要
目的研究受体高压氧预处理在大鼠同系异体肾移植模型中对移植肾的影响及其机制。方法 40只雄性SD大鼠随机分为3组:(1)对照组(Sham组);(2)肾移植组(KTx组);(3)高压氧预处理组(HBO+KTx组)。高压氧预处理24 h后行肾移植手术。每组大鼠术后24 h后处死,检测血清肌酐(Scr)、尿素氮(BUN),移植肾组织中超氧化物歧化酶(SOD)、丙二醛(MDA)及血红素加氧酶-1(HO-1),肾组织固定后行病理检查。结果与KTx组相比,HBO+KTx组中血清Scr、BUN明显降低;肾组织MDA水平明显下降,SOD活性显著提高。经高压氧预处理后,HBO+KTx组中肾小管坏死的比例明显减少。HBO+KTx组中的HO-1含量明显高于KTx组。结论高压氧预处理能够减轻移植肾组织脂质过氧化、增强抗氧化酶活性,并且提高HO-1含量,进而起到肾保护作用。
Objective To investigate the effect of hyperbaric oxygen preconditioning on syngeneic kidneytransplantation in rats and to explore the potential mechanism. Methods Forty male SD rats were randomly divid-ed into control group(Sham group),kidney transplantation group(KTx group)and hyperbaric oxygen precondi-tioning group(HBO + KTx group). Kidney transplantation was performed 24 h after hyperbaric preconditioning.Rats were sacrificed 24 h after the transplantation. Serum creatinine(Scr)and blood urea nitrogen(BUN)were de-tected. The level of superoxide dismutase(SOD),malondialdehyde(MDA)and heme oxygenase-1(HO-1)in thegraft was examined. Kidney pathological examination was performed after renal tissue fixed. Results Comparedwith the KTx group,HBO + KTx group showed lower Scr and BUN level. The MDA level was decreased and theSOD activity was increased significantly after hyperbaric oxygen preconditioning in HBO + KTx group. Renal tubu-lar necrosis was significantly reduced in HBO + KTx group. HO-1 level in HBO + KTx group was significantly high-er than that of KTx group. Conclusion Hyperbaric oxygen preconditioning can reduce lipid peroxidation,en-hance antioxidant enzyme activity and improve the level of HO-1 in graft tissue,thus attenuating kidney injury.
作者
陈晓翔
张辉
杨璐
熊玮
黄雄庆
CHEN Xia- oxiang;ZHANG Hui;YANG Lu;XIONG Wei;HUANG Xiongqing.(Department of Anesthesiology, the First Affiliat- ed Hospital of Sun Yat-sen University, Guangzhou 510080, China)
出处
《实用医学杂志》
CAS
北大核心
2018年第8期1258-1261,共4页
The Journal of Practical Medicine
基金
国家自然科学基金资助项目(编号:81670592)
关键词
肾移植
高压氧预处理
血红素加氧酶-1
kidney transplantation
hyperbaric oxygen preconditioning
heme oxygenase-1