中文摘要：

目的探讨地塞米松（dexamethasone，DEX）对小鼠肾缺血再灌注损伤的作用及其机制。方法建立小鼠肾缺血再灌注损伤模型。18只雄性C57BL／6小鼠随机分为3个组（n=6），分别为假手术组（Sham）、肾缺血再灌注损伤模型组（IRI）和DEX预处理组。Sham和IRI组缺血前60min予生理盐水（腹腔注射），DEX组缺血前60min给予DEX（4mg／kg），IRI组和DEX组血管夹夹闭左侧肾蒂，置于32℃温箱后1h松开血管夹，去除右肾。Sham组操作同上，但不夹闭左侧肾蒂，再灌注24h后处死小鼠，收集血清和肾脏标本。PAS染色后观察肾脏病理形态学变化，PCR检测白细胞介素6（interleukin6，IL-6）、干扰素γ（interferonγ，IFN-γ）和肿瘤坏死因子（tumornecrosisfactorOt，TNF-a）Westernblotting检测pAkt和总的Akt。结果与Sham组相比，IRI组血清肌酐和血尿素氮明显升高。病理检查可见肾脏内肾小管上皮细胞明显肿胀坏死、蛋白管型形成明显，还可观察到炎症细胞浸润明显增加。PCR显示IL-6、IFN-γ和TNF-a mRNA水平明显上调，Westernblotting显示p-Akt蛋白表达量明显增加，但Akt蛋白表达量无明显差异。与IRI组相比，DEX治疗组血清肌酐、血尿素氮明显下降，肾小管上皮细胞肿胀坏死减轻、炎症细胞浸润减少，IL-6、IFN-γ和TNF-a表达降低，p-Akt表达减少，但Akt蛋白表达量无明显差异。结论DEX预处理可通过抑制Akt信号通路激活，从而抑制炎症反应，从而减轻肾缺血再灌注损伤。

英文摘要：

Objective To investigate potential protective effect of glucocorticoid receptor（GR） agonist dexamethasone on renal ischemia reperfusion injury （IRI） and the possible mechanism. Methods Eighteen male C57BL/6 mice were randomly divided into three groups., sham group（sham）, renal IRI group（IRI）, and dexamethasone pretreatment group（DEX）. The mice in IRI group and sham group were given saline 1 h before ischemia（4 mg/kg）, and those in DEX group given dexamethasone （4 mg/kg）1 h before ischemia. The mice in IRI and DEX groups were kept in 320 infant incubators for 1 h after clamping their left renal pedicles,and then the right kidneys were removed. The mice in sham group underwent the same process,except for clamping the left renal pedicles. These mice were sacri- ficed after 24 h of reperfusion. Blood samples were collected and the levels of serum creatinine（Cr） and blood urea nitrogen（BUN） were measured. The pathology of renal tissues was observed according to PAS staining, and the mRNA levels of IL-6, IFN-γ and TNF-a were detected by PCR. The protein lev- els of p-Akt and Akt were examined by Western blotting. Results As compared with the sham group, the levels of serum Cr and BUN in IRI group were significantly increased. Moreover, renal tubular nec- rosis,proteincast,inflammatory cell infiltration, the mRNA levels of IL-6, IFN-γ and TNF-a, and the protein expression level of p-Akt were significantly increased, but the protein expression levels of Akt had no significant difference. As compared with the IRI group, the levels of serum Cr and BUN in DEX group were significantly reduced. Moreover, renal tubular necrosis, proteincast, inflammatory cell infil- tration, the mRNA levels of IL6, IFN-γ and TNF-a, and the protein expression level of p-Akt were significantly decreased, but the protein expression level of Akt had no significant difference. Conclusions GR agonist dexamethasone reduces renal IRI by attenuating inflammation though inhibi- ting Akt signal pathway activation.