Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice

被引:45
作者
Xin, Shao-bin [1 ]
Yan, Hao [2 ]
Ma, Jing [3 ]
Sun, Qiang [1 ]
Shen, Li [1 ]
机构
[1] Tianjin Union Med Ctr, Dept Intens Care Unit, Tianjin, Peoples R China
[2] Tianjin Union Med Ctr, Dept Oncol, Tianjin, Peoples R China
[3] Tianjin Anding Hosptial, Dept Integrated Chinese & Western Med, Tianjin, Peoples R China
来源
MEDICAL SCIENCE MONITOR | 2016年 / 22卷
关键词
Acute Kidney Injury; Inflammation; Lipopolysaccharides; Mice; Inbred C57BL; ACUTE KIDNEY INJURY; INFLAMMATORY RESPONSES; SIGNALING PATHWAY; OXIDATIVE STRESS; HEME OXYGENASE-1; REACTIVE OXYGEN; SEPTIC SHOCK; RAT MODEL; LPS; SEPSIS;
D O I
10.12659/MSM.898177
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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/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-alpha (TNF-alpha), NF-kappa B, 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-alpha, NF-kappa B, IL-1 beta, 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-kappa B activation and inflammatory and apoptosis factors, and then disturbing the expression of apoptosis-related proteins.
引用
收藏
页码:5173 / 5180
页数:8
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