Zhang Jiong, Yao Ying, Xiao Fang, Lan Xiaoqin, Yu Chong, Zhang Ying, Jiang Cao, Yang Juan, Pei Guangchang, Li Yueqiang, Rong Song, Hu Shuang, Li Junhua, Xu Gang
Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, People's Republic of China.
Int J Clin Exp Pathol. 2013 Oct 15;6(11):2366-75. eCollection 2013.
Dexamethasone (DEX), a ligand for glucocorticoid receptor (GR), has long been used in the clinical practice due to its anti-inflammatory and immunosuppressive properties. Given that ischemia/reperfusion (IR)-induced renal injury is featured by the excessive immune response; the current study is therefore designed to address the impact of dexamethasone on IR-induced renal injury, a common disorder in the clinical settings. Precondition of mice with 4 mg/kg of dexamethasone significantly attenuated IR-induced injury as manifested by the improved renal function along with ameliorated pathological changes and suppressed inflammatory infiltration. Mechanistic studies revealed that dexamethasone promotes GR activation, and by which it attenuates the signals for PI3K/AKT activation. Attenuated PI3K/AKT signaling thus suppresses inflammatory response which then protects kidneys from IR-induced injury. All together, our data support that dexamethasone could be a good alternative therapy for prevention and treatment of IR-induced renal injury in the clinical practice.
地塞米松（DEX）是糖皮质激素受体（GR）的配体，由于其抗炎和免疫抑制特性，长期以来一直用于临床实践。鉴于缺血/再灌注（IR）诱导的肾损伤以过度免疫反应为特征；因此，本研究旨在探讨地塞米松对IR诱导的肾损伤的影响，这是临床环境中一种常见的病症。用4mg/kg地塞米松预处理小鼠可显著减轻IR诱导的损伤，表现为肾功能改善、病理变化减轻和炎症浸润受到抑制。机制研究表明，地塞米松促进GR激活，并由此减弱PI3K/AKT激活信号。减弱的PI3K/AKT信号传导因此抑制炎症反应，从而保护肾脏免受IR诱导的损伤。总之，我们的数据支持地塞米松可能是临床实践中预防和治疗IR诱导的肾损伤的一种良好替代疗法。
