百里醌预处理对大鼠肾缺血再灌注损伤的影响

发布时间：2018-03-13 18:09

本文选题：百里醌　切入点：肾缺血再灌注损伤　出处：《中国现代医学杂志》2017年13期 　论文类型：期刊论文

【摘要】：目的探讨百里醌对大鼠肾缺血再灌注损伤的影响及机制。方法随机将60只雄性SD大鼠分成假手术组(Sham组)、肾缺血再灌注损伤组(IRI组)和百里醌不同浓度预处理组(Thy组)。IRI组和Thy组用无创血管夹夹闭左侧肾蒂复制IRI模型,Sham组操作同上,但不夹闭左侧肾蒂。Thy组在缺血前45 min给予百里醌5、10、20和40 mg/kg腹腔注射。Sham组和IRI组在同一时间给予等体积生理盐水腹腔注射。再灌注24 h后处死小鼠,收集血清和肾脏标本。PAS染色检测肾脏病理改变,ELISA检测尿素氮(BUN)、肌酐(Cr)、丙二醛(MDA)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)的表达、白细胞介素8(IL-8)、干扰素(IFN-γ)和肿瘤坏死因子(TNF-α)的表达,Western blot检测JAK2、STAT3、P-JAK2、P-STAT3、P53和P21蛋白表达,逆转录聚合酶链反应(RT-PCR)检测IL-8、IFN-γ和TNF-α的信使RNA水平(m RNA)。结果缺血再灌注损伤增加BUN、Cr、P-JAK2、P-STAT3、P53、P21、MDA、IL-8、IFN-γ和TNF-α的表达以及肾组织病理改变,同时减少CAT、GPX与SOD表达。而百里醌治疗,可减少BUN、Cr、P-JAK2、P-STAT3、P53、P21、MDA、IL-8、IFN-γ和TNF-α表达以及肾组织病理改变,增加CAT、GPX与SOD表达,3组之间JAK2和STAT3表达无差异。结论百里醌预处理可减轻肾缺血再灌注损伤,其作用机制部分是通过抑制JAK2/STAT3/P53信号通路介导的炎症和氧化应激。
[Abstract]:Objective to investigate the effect and mechanism of thyriquinone on renal ischemia-reperfusion injury in rats. Methods Sixty male SD rats were randomly divided into sham-operated group (Sham group), renal ischemia-reperfusion injury group (IRI group) and baroquinone preconditioning group (with different concentrations). The IRI model was induced by non-invasive occlusion of the left renal pedicle in the Thy group, the IRI group and the Thy group, and the same operation was performed in the sham group. However, the left renal pedicle. Thy group was given intraperitoneal injection of thyriquinone 510 10 20 and 40 mg/kg at the same time at the same time in the left renal pedicle group. The mice were sacrificed after 24 h reperfusion. Serum and kidney samples were collected by pas staining to detect renal pathological changes. Elisa was used to detect the expression of urea nitrogen bun, creatinine, malondialdehyde (MDAA), catalase (catalase), glutathione peroxidase (Glutathione peroxidase) and superoxide dismutase (SOD). The expression of IL-8, IFN- 纬 and TNF- 伪 was detected by Western blot. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the messenger RNA level of IL-8, IFN- 纬 and TNF- 伪. Results the expression of IL-8 IFN- 纬 and TNF- 伪 and the expression of IL-8 IFN- 纬 and TNF- 伪 in renal tissue were increased after ischemia-reperfusion injury. It can reduce the expression of IL-8 IFN- 纬 and TNF- 伪 in renal tissue and increase the expression of JAK2 and STAT3 in the three groups. Conclusion the pretreatment of thymidine can reduce renal ischemia-reperfusion injury. Its mechanism is partly through inhibition of JAK2/STAT3/P53 signaling pathway mediated inflammation and oxidative stress.
【作者单位】：华中科技大学同济医学院附属普爱医院肾内科;
【分类号】：R692.5

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