title: Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice.
abstract: BACKGROUND Sepsis can cause serious acute kidney injury in bacterium-infected patients, especially in intensive care patients. Luteolin, a bioactive flavonoid, has renal protection and anti-inflammatory effects. This study aimed to investigate the effect and underlying mechanism of luteolin in attenuating lipopolysaccharide (LPS)-induced renal injury. MATERIAL AND METHODS ICR mice were treated with LPS (25 mg/kg) with or without luteolin pre-treatment (40 mg/kg for three days). The renal function, histological changes, degree of oxidative stress, and tubular apoptosis in these mice were examined. The effects of luteolin on LPS-induced expression of renal tumor necrosis factor-α (TNF-α), NF-κB, MCP-1, ICAM-1, and cleaved caspase-3 were evaluated. RESULTS LPS resulted in rapid renal damage of mice, increased level of blood urea nitrogen (BUN), and serum creatinine (Scr), tubular necrosis, and increased oxidative stress, whereas luteolin pre-treatment could attenuate this renal damage and improve the renal functions significantly. Treatment with LPS increased TNF-α, NF-κB, IL-1β, cleaved caspase-3, MCP-1, and ICAM-1 expression, while these disturbed expressions were reversed by luteolin pre-treatment. CONCLUSIONS These results indicate that luteolin ameliorates LPS-mediated nephrotoxicity via improving renal oxidant status, decreasing NF-κB activation and inflammatory and apoptosis factors, and then disturbing the expression of apoptosis-related proteins.
authors.affiliation: Department of Intensive Care Unit, Tianjin Union Medicine Center, Tianjin, China (mainland).
authors.forename: Shao-Bin
authors.initials: SB
authors.lastname: Xin
authors.affiliation: Department of Oncology, Tianjin Union Medicine Center, Tianjin, China (mainland).
authors.forename: Hao
authors.initials: H
authors.lastname: Yan
authors.affiliation: Department of Integrated Chinese and Western Medicine, Tianjin Anding Hosptial, Tianjin, China (mainland).
authors.forename: Jing
authors.initials: J
authors.lastname: Ma
authors.affiliation: Department of Intensive Care Unit, Tianjin Union Medicine Center, Tianjin, China (mainland).
authors.forename: Qiang
authors.initials: Q
authors.lastname: Sun
authors.affiliation: Department of Intensive Care Unit, Tianjin Union Medicine Center, Tianjin, China (mainland).
authors.forename: Li
authors.initials: L
authors.lastname: Shen
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001806:Blood Urea Nitrogen; D053148:Caspase 3 / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D053938:DNA Fragmentation / Q000187:drug effects; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D007677:Kidney Function Tests; D008070:Lipopolysaccharides; D047311:Luteolin / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008813:Mice, Inbred ICR; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D020011:Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D053148:Caspase 3; D047311:Luteolin