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目的:成功建立肾脏缺血后再灌注损伤大鼠模型,研究缺血后处理对肾脏的保护作用。方法:夹闭大鼠左肾动静脉复制大鼠肾缺血再灌注损伤模型。雄性Wistar大鼠30只随机分成3组:缺血再灌注组(I/R,n=10),缺血后处理组(IPo,n=10),假手术组(S,n=10)。检测血肌酐浓度(Cr)、尿素氮(BUN),检测肾组织中超氧化物歧化酶(SOD)活性;取肾组织做HE染色,光镜下观察肾组织病理学变化。结果:S组血清肌酐水平为(63.83±17.26)μmol/L,血清尿素氮水平为(11.56±2.75)mmol/L。I/R组分别达到(175.94±64.53)μmol/L、(42.85±14.67)mmol/L,与S组相比差异有统计学意义(P<0.05),IPo组血清肌酐及尿素氮水平分别为(91.51±35.67)μmol/L、(15.91±4.12)mmol/L,与I/R组比较差异有统计学意义(P<0.05),而与S组比较差异无统计学意义(P>0.05);S组肾组织中SOD含量为(91.3±2.9)U/mgport,I/R组为(55.3±1.6)U/mg-port,与S组比较差异有统计学意义(P<0.05),IPo组SOD含量为(71.6±2.7)U/mgport,SOD活性较I/R组升高,差异有统计学意义(P<0.05);S组肾小球、肾小管未发现明显的形态学改变,I/R组病理形态与S组相比有显著差异,IPo组病理形态较I/R组明显减轻,统计学上有显著性差异。结论:缺血后处理对肾起保护作用,机制与增强了肾的抗氧化能力,减轻炎性细胞浸润有关。
OBJECTIVE: To establish a rat model of renal ischemia-reperfusion injury successfully and to study the protective effect of ischemic postconditioning on kidneys. Methods: Rat model of renal ischemia / reperfusion injury was induced by clipping the left renal artery and vein in rats. Thirty male Wistar rats were randomly divided into 3 groups: ischemia / reperfusion group (I / R, n = 10), ischemic postconditioning group (IPo, n = 10) and sham operation group (S, n = 10). Serum creatinine concentration (BUN) and serum creatinine (BUN) were measured to detect the activity of superoxide dismutase (SOD) in renal tissue. HE staining was used to observe the pathological changes of renal tissue. Results: Serum creatinine level in S group was (63.83 ± 17.26) μmol / L and serum urea nitrogen level was (11.56 ± 2.75) mmol / L. The levels of serum creatinine and urea nitrogen in IPo group were (175.94 ± 64.53) μmol / L and (42.85 ± 14.67) mmol / L, respectively, which were significantly different from those in S group (91.51 ± 35.67) μmol / L and (15.91 ± 4.12) mmol / L respectively, which were significantly different from those in I / R group (P <0.05) (91.3 ± 2.9) U / mgport in renal tissue and (55.3 ± 1.6) U / mg-port in I / R group, and there was significant difference between S group and S group (P <0.05) The SOD level was (71.6 ± 2.7) U / mgport and the activity of SOD was higher than that of the I / R group (P <0.05). No obvious morphological changes were found in the glomerular and tubular tubules in the S group, The pathological changes of I / R group were significantly different from those of S group. The pathological changes of IPo group were significantly reduced compared with I / R group, and there was a statistically significant difference. CONCLUSION: Ischemic postconditioning has a protective effect on the kidney, and its mechanism is related to enhancing renal antioxidant capacity and reducing inflammatory cell infiltration.