title: Sinomenine protects mice against ischemia reperfusion induced renal injury by attenuating inflammatory response and tubular cell apoptosis.
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.
authors.affiliation: Changhai Hospital, Second Military Medical University Shanghai 200003, China.
authors.forename: Zhiqing
authors.initials: Z
authors.lastname: Zhao
authors.forename: Rui
authors.initials: R
authors.lastname: Guan
authors.forename: Shaohua
authors.initials: S
authors.lastname: Song
authors.forename: Mingjian
authors.initials: M
authors.lastname: Zhang
authors.forename: Fang
authors.initials: F
authors.lastname: Liu
authors.forename: Meng
authors.initials: M
authors.lastname: Guo
authors.forename: Wenyuan
authors.initials: W
authors.lastname: Guo
authors.forename: Qilin
authors.initials: Q
authors.lastname: Yu
authors.forename: Luding
authors.initials: L
authors.lastname: Zhang
authors.forename: Quanxing
authors.initials: Q
authors.lastname: Wang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D015415:Biomarkers / Q000097:blood; D001806:Blood Urea Nitrogen; D054357:Chemokine CXCL10 / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D019610:Cytoprotection; D004195:Disease Models, Animal; D018836:Inflammation Mediators / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007684:Kidney Tubules / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009019:Morphinans / Q000494:pharmacology*; D016328:NF-kappa B / Q000378:metabolism; D009393:Nephritis / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D015427:Reperfusion Injury / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D054357:Chemokine CXCL10; C485433:Cxcl10 protein, mouse; C090509:Icam1 protein, mouse; D018836:Inflammation Mediators; D015850:Interleukin-6; D009019:Morphinans; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; C009271:sinomenine; D003404:Creatinine
keywords: Sinomenine; apoptosis; inflammation; reperfusion injury
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