中文摘要：

目的 研究糖皮质激素受体（GR）激动药地塞米松（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组（n＝ 6）,分别为假手术（SHAM）组、肾缺血-再灌注损伤模型（IRI）组、地塞米松预处理（DEX）组.SHAM组和IRI组缺血前1 h给予0.9%氯化钠溶液（4 mg·kg-1,腹腔注射）,DEX组缺血前1 h给予地塞米松（4 mg·kg-1,腹腔注射）,IRI组和DEX组血管夹夹闭左肾动脉,置于32 ℃温箱后1 h松开血管夹,去除右肾.SHAM组操作同上,但不夹闭左肾动脉.再灌注24 h后处死小鼠,收集血清和肾脏标本.测定血尿素氮（BUN）和血清肌酐（Cr）,PAS染色后显微镜下观察肾脏形态学变化,PCR检测单核细胞趋化蛋白（MCP-1）和干扰素（IFN-γ）.结果 与SHAM组相比,IRI组血清肌酐,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MCP-1,IFN-γ明显上调.与IRI组相比,DEX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,MCP-1、IFN-γ表达降低.结论 GR激动药DEX可通过抑制炎症反应减轻肾缺血-再灌注损伤.

英文摘要：

Objective To investigate potential protection and mechanism of glucocorticoid receptor （GR） agonist dexamethasone on renal ischemia-reperfusion injury. Methods Eighteen male C57BL/6 mice were randomly divided into three groups：SHAM group（ SHAM）, kidney i schemia reperfusion injury group（ IRI）, and dexamethasone pretreatment group（DEX）. The mice in IRI group and SHAM group received saline 1 h before ischemia（4 mg· kg-1 , ip）, But the mice in DEX group received dexamethasone（4 mg ·kg-1, IP） 1 h before ischemia. The mice in the IRI and DEX groups were kept in 32 ℃ infant incubator for 1 h after clamping their renal pedicles, and then the right kidneys were removed. The mice in SHAM group underwent the same process, except for clamping the renal pedicles. These mice were sacrificed after 24 h of reperfusion. Blood samples were collected and the levels of serum creatinine （Cr） and urea nitrogen （ BUN ） were measured. The pathology of renal tissues was observed according to PAS staining, and the mRNA levels of MCP-land IFN-γ were measured by PCR. Results Compared with the SHAM group, the levels of Cr and BUN in IRI group were significantly higher. Moreover, renal tubular necrosis, proteincast, inflammatory cell infiltration, and the mRNA level of MCP-1 and IFN-γ, were all higher in IRI group than in the SHAM group. Conclusion GR agonist dexamethasone reduces renal ischemia-reperfusion injury by inhibiting inflammation.