摘要
目的探讨三叶苷(trilobatin,TLB)减轻下肢缺血再灌注(lower-limb ischemia reperfusion,LIR)所致的肾损伤及其机制。方法制备LIR模型,将C57BL6小鼠随机分为4组:对照组(不进行LIR模型制备)、损伤组(建立LIR模型)、预处理组(预先给予TLB,再建立LIR模型)、抑制剂组(预先给予SIRT3选择性抑制剂,再给予TLB,之后建立LIR模型)。LIR后,抽取外周血并分离肾组织,HE染色观察肾组织病理学改变及损伤评分,生化分析仪检测血清肌酐(Scr)、尿素氮(BUN)水平,DHE染色检测肾组织中活性氧(ROS)水平,相应试剂盒检测外周血丙二醛(MDA)、超氧化物歧化酶(SOD)含量,Western blot检测肾组织中沉默信息调节因子3(SIRT3)/超氧化物歧化酶2(SOD2)信号通路的蛋白表达情况。结果与对照组相比,损伤组肾组织病理学损伤评分增高,外周血中Scr、BUN和肾组织中ROS、MDA升高,肾组织中SOD降低,SIRT3、SOD2表达水平下调(P均<0.05);与损伤组比较,预处理组肾组织病理学损伤评分、Scr、BUN、ROS、MDA降低,SOD升高,SIRT3、SOD2表达水平上调(P均<0.05);与预处理组比较,抑制剂组肾组织病理学损伤评分、Scr、BUN、ROS、MDA升高,SOD下降,SIRT3、SOD2表达水平下调(P均<0.05)。结论三叶苷预处理可减轻下肢缺血再灌注的氧化应激反应,改善肾损伤,其机制可能与激活SIRT3/SOD2通路有关。
Objective To investigate whether trilobatin(TLB)can attenuate renal injury induced by lower limb ischemia-reperfusion(LIR)and its specific mechanism.Methods LIR model was prepared.C57BL6 mice were randomly divided into 4 groups:Control group(without LIR model preparation),injury group(establish LIR model),pretreatment group(give TLB in advance,and then establish LIR model),inhibitor group(SIRT3 selective inhibitor was given in advance,then TLB,and then LIR model was established).After LIR,peripheral blood was taken and renal tissue was separated.HE staining was used to observe the pathological changes and injury score of renal tissue.Biochemical analyzer was used to detect the levels of serum creatinine(Scr)and blood urea nitrogen(BUN),DHE staining was used to detect the levels of ROS in renal tissue,and corresponding kits were used to detect the contents of malondialdehyde(MDA)and superoxide dismutase(SOD)in peripheral blood.The protein expression abundance of silent information regulator 3(SIRT3)/superoxide dismutase 2(SOD2)signal pathway in renal tissue was detected by Western blot.Results Compared with the control group,the injury group showed higher renal histopathological injury scores,significantly higher Scr,BUN in peripheral blood and higher ROS,MDA in renal tissue,while SOD in renal tissue significantly decreased,SIRT3 and SOD2 expression levels were downregulated(P all<0.05).Compared with the injury group,the renal histopathological injury score,Scr,BUN,ROS and MDA decreased in the pretreatment group,whereas SOD increased,and the expression levels of SIRT3 and SOD2 were upregulated(P<0.05).Compared with the pretreatment group,the renal histopathological injury score,Scr,BUN and MDA significantly increased,SOD decreased,and the expression levels of SIRT3 and SOD2 were downregulated in the inhibitor group(P all<0.05).Conclusion Pretreatment of TLB can reduce the oxidative stress response induced by LIR and improve the renal injury induced by LIR in mice.Its mechanism may be related to the activation of S
作者
王磊
白艳辉
王鹏
李爱军
张冬芹
史坚
王秀丽
WANG Lei;BAI Yanhui;WANG Peng;LI Aijun;ZHANG Dongqin;SHI Jian;WANG Xiuli(Department of Anesthesiology,Third Hospital of Hebei Medical University,Shijiazhuang 050051,China;Department of anesthesiology,First Central Hospital of Baoding,Baoding 071000,China;Department of Geriatrics,First Central Hospital of Baoding,Baoding 071000,China;Cardiac surgery,First Central Hospital of Baoding,Baoding 071000,China)
出处
《宁夏医科大学学报》
2022年第10期989-994,共6页
Journal of Ningxia Medical University
基金
河北省医学科学研究课题计划(20220289)
保定市科技局基金项目(2141ZF092)。
