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青藤碱通过减轻炎症反应和肾小管细胞凋亡来保护小鼠免受缺血再灌注诱导的肾损伤。

Sinomenine protects mice against ischemia reperfusion induced renal injury by attenuating inflammatory response and tubular cell apoptosis.

作者信息

Zhao Zhiqing, Guan Rui, Song Shaohua, Zhang Mingjian, Liu Fang, Guo Meng, Guo Wenyuan, Yu Qilin, Zhang Luding, Wang Quanxing

机构信息

Changhai Hospital, Second Military Medical University Shanghai 200003, China.

出版信息

Int J Clin Exp Pathol. 2013 Aug 15;6(9):1702-12. eCollection 2013.

Abstract

Sinomenine (SIN) is a purified alkaloid from the Chinese herb Sinomenium acutum. Previous studies demonstrated that SIN possesses anti-inflammatory and anti-apoptotic properties. We thus in the present report conducted studies to examine its impact on ischemia reperfusion (IR) induced renal injury. Precondition of mice with 200 mg/kg of SIN provided significant protection for mice against IR-induced renal injury as manifested by the attenuated serum creatinine (Cre) and blood urea nitrogen (BUN) along with less severity for histological changes and tubular cell apoptosis. In line with these results, treatment of mice with SIN suppressed IR-induced inflammatory infiltration and the expression of chemokine CXCL-10, adhesion molecule ICAM-1, and cytokines TNF-а/IL-6. Mechanistic studies revealed that SIN inhibits NF-κB transcriptional activity to suppress IR-induced inflammatory response in the kidney, while it attenuates MAP kinase signaling to prevent tubular cells undergoing apoptosis after IR insult. Altogether, our data support that SIN could be a useful therapeutic agent for prevention and treatment of IR-induced renal injury in the clinical settings.

摘要

青藤碱(SIN)是从中药青风藤中提取的一种纯化生物碱。先前的研究表明,SIN具有抗炎和抗凋亡特性。因此,在本报告中,我们进行了研究以考察其对缺血再灌注(IR)诱导的肾损伤的影响。用200mg/kg的SIN对小鼠进行预处理,可显著保护小鼠免受IR诱导的肾损伤,表现为血清肌酐(Cre)和血尿素氮(BUN)降低,组织学变化和肾小管细胞凋亡的严重程度减轻。与这些结果一致,用SIN治疗小鼠可抑制IR诱导的炎症浸润以及趋化因子CXCL-10、黏附分子ICAM-1和细胞因子TNF-α/IL-6的表达。机制研究表明,SIN抑制NF-κB转录活性以抑制肾脏中IR诱导的炎症反应,同时减弱MAP激酶信号传导以防止IR损伤后肾小管细胞发生凋亡。总之,我们的数据支持SIN可能是临床环境中预防和治疗IR诱导的肾损伤的一种有用治疗药物。

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