International journal of clinical and experimental pathology · 2013
Sinomenine protects mice against ischemia reperfusion induced renal injury by attenuating inflammatory response and tubular cell apoptosis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zhao Zhiqing, Guan Rui, Song Shaohua, Zhang Mingjian, Liu Fang, Guo Meng, Guo Wenyuan, Yu Qilin, Zhang Luding, Wang Quanxing
Аннотация
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.
Предметные рубрики MeSH
AnimalsAnti-Inflammatory AgentsApoptosisBiomarkersBlood Urea NitrogenChemokine CXCL10CreatinineCytoprotectionDisease Models, AnimalInflammation MediatorsIntercellular Adhesion Molecule-1Interleukin-6Kidney TubulesMAP Kinase Signaling SystemMaleMiceMice, Inbred C57BLMorphinansNF-kappa BNephritisReperfusion InjuryTime FactorsTumor Necrosis Factor-alpha