Rutaecarpine alleviates renal ischemia reperfusion injury in rats by suppressing the JNK/p38 MAPK signaling pathway and interfering with the oxidative stress response.

Abstract	In the present study, the protective effect and the potential underlying mechanism of rutaecarpine (Ru) on renal ischemia reperfusion injury (IRI) in rats were investigated. A renal ischemia reperfusion mouse model was established. Ru at 30, 60 mg/kg administered intraperitoneally prior to reperfusion led to attenuated renal injury. The results demonstrated that Ru treatment significantly reduced the content of serum creatinine, urea nitrogen and neutrophil gelatinase‑associated lipocalin in rats with renal IRI. In addition, Ru treatment improved the degree of renal proximal tubular necrosis, decreased the content of inflammatory cytokines in reperfused renal tissue and increased serum superoxide dismutase levels to protect the kidney. The associated underlying mechanism may involve the inhibition of p38 kinase phosphorylation and c‑Jun N‑terminal kinase, anti‑lipid peroxidation, elimination of free radicals, and a reduction in the degree of apoptotic damage and oxidative stress injury induced by renal IRI. Therefore, Ru may be a suitable compound for the prevention and treatment of renal IRI.
Authors	Chunhua Wang, Zongyao Hao, Jun Zhou, Li Zhang, Yexiang Sun, Chaozhao Liang
Journal	Molecular medicine reports (Mol Med Rep) Vol. 16 Issue 1 Pg. 922-928 (Jul 2017) ISSN: 1791-3004 [Electronic] Greece
PMID	28560443 (Publication Type: Journal Article)
Chemical References	Biomarkers Cytokines Indole Alkaloids Inflammation Mediators Protective Agents Quinazolines Reactive Oxygen Species rutecarpine Superoxide Dismutase
Topics	Animals Biomarkers Biopsy Blood Urea Nitrogen Cytokines (metabolism) Disease Models, Animal Indole Alkaloids (pharmacology) Inflammation Mediators (metabolism) Kidney Diseases (drug therapy, metabolism, pathology) Kidney Function Tests MAP Kinase Signaling System (drug effects) Male Oxidative Stress (drug effects) Phosphorylation Protective Agents (pharmacology) Quinazolines (pharmacology) Rats Reactive Oxygen Species (metabolism) Reperfusion Injury (drug therapy, metabolism, pathology) Superoxide Dismutase (metabolism)

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