大车前苷通过Akt/Nrf2/HO-1信号通路减轻辐射致大鼠肾损伤的研究

Plantamajoside alleviated radiation-induced kidney injury through the Akt/Nrf2/HO-1 signaling pathway

目的 探讨大车前苷能够对辐射致肾损伤的保护作用及其可能机制。方法 30只健康雄性SD大鼠随机分为正常对照组、辐射损伤模型组和大车前苷0.8g/kg组,每组10只。通过血清肌酐(Cr)和尿酸(BUA)含量测定及病理染色评价肾脏损伤;TUNEL染色检测肾脏凋亡;ELISA方法检测血清丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的表达;Western blot方法检测肾组织Akt、Nrf2和HO-1蛋白的表达。结果 与正常对照相比,模型组大鼠血清中Cr和BUA含量与明显升高,可见肾小球萎缩和肾小管扩张,组织细胞发生氧化应激损伤;氧化应激相关蛋白MDA表达升高,SOD和GSH表达降低;Akt、Nrf2和HO-1通路蛋白表达降低。与模型组相比,大车前苷干预能够降低血清Cr和BUA含量,减轻肾脏组织氧化应激损伤,下调MDA表达,上调SOD和GSH表达,增加Akt、Nrf2和HO-1通路蛋白表达。结论 大车前苷可能通过激活Akt/Nrf2/HO-1信号通路减轻氧化应激损伤对辐射致肾损伤起保护作用。

Objective To investigate the role and mechanism of plantamajoside on radiation induced kidney injury in rats.Methods Thirty healthy male SD rats were randomly divided into normal control group,the radiation induced kidney injury group and O0.8g/kg plantamajoside group,with 10 rats in each group.Serum creatinine(Cr)and uric acid(BUA)were measured and pathological staining was used to evaluate renal injury.TUNEL staining was used to detect apoptosis of cells in renal tissue of rats.ELISA was used to detect the contents of malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione(CSH)in serum.Western blot was used to detecte the expressions of Akt,Nrf2 and HO-1 in renal tissue.Results Compared with the normal control group,the content of Cr and BUA in serum of the model group was significantly increased,and the glomerular atrophy and renal tubule dilation were observed,and the cells of renal tissue were damaged by oxidative stress.The expression of MDA was increased,and the expressions of SOD and GSH were decreased.The expressions of Akt,Nrf2 and HO-1 pathway proteins were decreased.Compared with the model group,Plantamajoside intervention could decrease contents of Cr and BUA in serum,alleviate oxidative stress damage in kidney tissue,downregulate the expression of MDA,up-regulate the expressions of SOD and GSH,and increase the expressions of Akt,Nrf2 and HO-1.Conclusion Plantamajoside may play a protective role in radiation-induced kidney injury by reducing oxidative stress by activating Akt/Nrf2/HO-1 signaling pathway.