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泽兰黄酮对小鼠肾缺血再灌注损伤的保护作用。

Protective effect of eupatilin against renal ischemia-reperfusion injury in mice.

作者信息

Jeong E K, Jang H J, Kim S S, Oh M Y, Lee D H, Eom D W, Kang K S, Kwan H C, Ham J Y, Park C S, Jang D S, Han D J

机构信息

Department of Anesthesiology and Pain Medicine, Ulsan University College of Medicine, Gangneung Asan Hospital, Seoul, South Korea.

Department of Surgery, Ulsan University College of Medicine, Gangneung Asan Hospital, Seoul, South Korea.

出版信息

Transplant Proc. 2015 Apr;47(3):757-62. doi: 10.1016/j.transproceed.2014.12.044.

DOI:10.1016/j.transproceed.2014.12.044
PMID:25891726
Abstract

BACKGROUND

Eupatilin, a pharmacologically active flavone derived from Artemisia species, is known to have antioxidant and anti-inflammatory activities. Ischemia-reperfusion injury (IRI) is a major complication after renal transplantation, with inflammatory responses to IRI exacerbating the resultant renal injury. In the present study, we investigated whether eupatilin exhibits renoprotective activities against ischemia-reperfusion-induced acute kidney injury in mice.

MATERIALS AND METHODS

Renal IRI was induced in male C57BL/6 mice by bilateral renal pedicle occlusion for 30 minutes followed by reperfusion for 48 hours. Eupatilin (10 mg/kg body weight p.o.) was administered 4 days before IRI.

RESULTS

Treatment with eupatilin significantly decreased neutrophil gelatinase-associated lipocalin and kidney injury molecule-1 levels in urine, blood urea nitrogen level, and serum creatinine levels, as well as kidney tubular injury. Western blotting indicated that eupatilin significantly increased the levels of heat shock protein 70 and B-cell lymphoma protein, and it attenuated inducible nitric oxide synthase, Bcl-2-associated X protein, and caspase-3 levels 48 hours after IRI.

CONCLUSION

Our findings suggest that eupatilin is a promising therapeutic agent against acute ischemia-induced renal damage.

摘要

背景

灯盏乙素是一种从蒿属植物中提取的具有药理活性的黄酮,已知具有抗氧化和抗炎活性。缺血再灌注损伤(IRI)是肾移植后的主要并发症,对IRI的炎症反应会加重由此导致的肾损伤。在本研究中,我们调查了灯盏乙素对小鼠缺血再灌注诱导的急性肾损伤是否具有肾保护活性。

材料与方法

通过双侧肾蒂阻断30分钟,然后再灌注48小时,在雄性C57BL/6小鼠中诱导肾IRI。在IRI前4天给予灯盏乙素(10mg/kg体重,口服)。

结果

灯盏乙素治疗显著降低了尿液中中性粒细胞明胶酶相关脂质运载蛋白和肾损伤分子-1水平、血尿素氮水平和血清肌酐水平,以及肾小管损伤。蛋白质免疫印迹法表明,灯盏乙素显著提高了热休克蛋白70和B细胞淋巴瘤蛋白的水平,并在IRI后48小时降低了诱导型一氧化氮合酶、Bcl-2相关X蛋白和半胱天冬酶-3的水平。

结论

我们的研究结果表明,灯盏乙素是一种有前景的抗急性缺血性肾损伤的治疗药物。

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