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目的:探讨银杏达莫注射液对肾缺血-再灌注损伤的保护作用及机制。方法:肾缺血1h再灌注1h建立大鼠肾缺血再灌注损伤模型,用银杏达莫注射液分别按剂量0.9、1.8、3.6mL/kg预处理7天。通过检测肾组织丙二醛含量、超氧化物歧化酶的活性及血肌酐、血尿素氮的含量。电镜下观察各组肾组织的形态学变化,West-ern印迹法观察p38 MAPK蛋白的活化情况。结果:缺血再灌注损伤后,肾组织出现明显病理改变,肾组织丙二醛含量升高,超氧化物歧化酶活性下降,血肌酐、尿素氮水平升高,肾组织p-p38MAPK蛋白水平显著上升。银杏达莫注射液预处理能降低血肌酐、尿素氮水平及肾组织丙二醛含量,增强超氧化物歧化酶活性和下调p-p38MAPK蛋白水平,与模型组比较有显著性差异(P<0.05和P<0.01)。电镜观察肾组织的病理改变也明显好转。银杏达莫注射液不同剂量组之间无明显差异。结论:银杏达莫注射液对肾缺血再灌注损伤有良好的保护作用,其机制可能是通过清除氧自由基、减轻脂质过氧化反应而下调p38MAPK蛋白的表达以减轻再灌注损伤程度,进而大鼠肾功能。
Objective: To investigate the protective effect of Yinxingdamo injection on renal ischemia-reperfusion injury and its mechanism. Methods: The model of renal ischemia-reperfusion injury was established in rats with renal ischemia 1h and reperfusion 1h. The rats were pre-treated with 0.9, 1.8 and 3.6 mL / kg of ginkgo-dipyridamole injection for 7 days respectively. By detecting the content of malondialdehyde in renal tissue, the activity of superoxide dismutase and the content of serum creatinine and blood urea nitrogen. The morphological changes of renal tissues were observed under electron microscope. The activation of p38 MAPK protein was observed by West-ern blotting. Results: After ischemia-reperfusion injury, the pathological changes of renal tissue were observed. The contents of malondialdehyde (MDA), superoxide dismutase (SOD), serum creatinine and urea nitrogen were increased in renal tissue, and the protein level of p-p38MAPK rise. Pretreatment with Ginkgo biloba injection could decrease serum creatinine, blood urea nitrogen, malondialdehyde (MDA) content, SOD activity and p-p38MAPK protein level in the model group (P <0.05) And P <0.01). Electron microscopy of renal tissue pathological changes also significantly improved. There was no significant difference between different dosage groups of Yinxingdamo injection. CONCLUSION: Ginkgo biloba injection has a good protective effect on renal ischemia-reperfusion injury. Its mechanism may be through the scavenging of oxygen free radicals, reducing lipid peroxidation and down-regulating the expression of p38MAPK protein to reduce the extent of reperfusion injury, thus Rat kidney function.