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exhaustive swimming exercise related kidney injury in rats - protective effects of acetylbritannilactone.

Exhaustive swimming exercise related kidney injury in rats - protective effects of acetylbritannilactone.

机构信息

Department of Nephrology, Bethune International Peace Hospital of People's Liberation Army (PLA), Shijiazhuang, China.

出版信息

Int J Sports Med. 2012 Jan;33(1):1-7. doi: 10.1055/s-0031-1284397. Epub 2011 Nov 21.

Abstract

The aim of this study was to investigate the protective effects of acetylbritannilactone (ABL) on renal injury induced by acute exhaustive exercise in the rat. The exhaustive exercise induced kidney injury in rats was established by exhaustive swimming (ES). ABL (26 mg/kg) or polyglycol (control) were administrated orally by gastric gavage 24 h before training. Renal function, biochemical index, renal histopathological change, oxidative stress indices, renal cell apoptosis and inflammatory molecules were checked after ES, for 6 h and 24 h. It was found that immediately after exhaustive swimming, the serum urea and creatinine were significantly higher in ES rats, and the same for serum creatine kinase. All the values were reduced in the ES rats treated with ABL. The increase of superoxide dismutase activity and decrease of malondialdehyde content in the kidney were found in rats with ABL treatment. Tubular cell apoptosis at different time points after ES were significantly reduced by the ABL treatment. The increased expression of TNF-α and NF-κB induced by ES was also significantly decreased by ABL treatment. Our results suggest that ABL protects rats from overtraining-induced kidney injury by inhibiting renal cell apoptosis and suppressing oxidative-stress generation and inhibiting inflammation.

摘要

本研究旨在探讨乙酰基二氢对叶豆酮(ABL)对大鼠急性力竭运动诱导的肾损伤的保护作用。通过力竭游泳(ES)建立大鼠力竭运动诱导的肾损伤模型。ABL(26mg/kg)或聚乙二醇(对照)在训练前 24 小时通过灌胃口服给药。ES 后 6 小时和 24 小时检查肾功能、生化指标、肾组织病理学变化、氧化应激指标、肾细胞凋亡和炎症分子。结果发现,力竭游泳后,ES 大鼠血清尿素和肌酐明显升高,血清肌酸激酶也升高,而 ABL 治疗的 ES 大鼠则降低。ABL 治疗可增加肾脏中超氧化物歧化酶的活性,降低丙二醛的含量。ABL 治疗可显著减少 ES 后不同时间点肾小管细胞的凋亡。ABL 治疗还可显著降低 ES 诱导的 TNF-α和 NF-κB 的表达增加。我们的结果表明,ABL 通过抑制肾细胞凋亡、抑制氧化应激的产生和抑制炎症来保护大鼠免受过度训练引起的肾损伤。

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