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

机译:木犀草素对脂多糖诱导的小鼠急性肾损伤的保护作用

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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.
机译:背景技术败血症可在细菌感染的患者中引起严重的急性肾损伤,特别是在重症监护患者中。木犀草素,一种具有生物活性的类黄酮,具有肾脏保护和抗炎作用。本研究旨在探讨木犀草素在减轻脂多糖(LPS)致肾损伤中的作用及其潜在机制。材料与方法ICR小鼠经LPS(25 mg / kg)处理或不接受木犀草素预处理(40 mg / kg,三天)。检查这些小鼠的肾功能,组织学变化,氧化应激程度和肾小管凋亡。评估了木犀草素对LPS诱导的肾肿瘤坏死因子-α(TNF-α),NF-κB,MCP-1,ICAM-1和裂解的caspase-3表达的影响。结果脂多糖导致小鼠快速肾脏损伤,血尿素氮(BUN)和血清肌酐(Scr)水平升高,肾小管坏死和氧化应激增加,而木犀草素预处理可减轻这种肾脏损伤并改善肾功能显着。 LPS处理可增加TNF-α,NF-κB,IL-1β,裂解的caspase-3,MCP-1和ICAM-1表达,而木犀草素预处理可逆转这些干扰的表达。结论这些结果表明木犀草素可通过改善肾脏的氧化状态,减少NF-κB的活化以及炎性和凋亡因子,进而干扰凋亡相关蛋白的表达来改善脂多糖介导的肾毒性。

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