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补充 n-3 多不饱和脂肪酸可改善脂多糖诱导的大鼠炎症反应和肾脏 Na,K-ATP 酶的功能特性。

Supplementation with n-3 polyunsaturated fatty acids to lipopolysaccharide-induced rats improved inflammation and functional properties of renal Na,K-ATPase.

机构信息

Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic.

出版信息

Nutr Res. 2013 Sep;33(9):772-9. doi: 10.1016/j.nutres.2013.06.001. Epub 2013 Jul 26.

Abstract

Measurements of enzyme kinetics of renal Na, K-ATPase were used for characterization of ATP- and Na⁺-binding sites in rats that were subjected to 10 days of moderate inflammation that was induced by a single dose of Escherichia coli lipopolysaccharides (LPSs) at a dose of 1 mg kg⁻¹ body weight. We hypothesized that LPSs might initiate a malfunction of renal Na, K-ATPase, which is a key enzyme involved in regulation of sodium homeostasis in the organism. We also investigated the potential effect that fish oil (FO) has in the prevention of Na, K-ATPase alterations by administering FO daily at a dose of 30 mg kg⁻¹. Alone, LPS elevated the level of C-reactive protein by more than 500% and free radicals by 36% in plasma, as indicated by an increased level of malondialdehyde. The Na, K-ATPase was slightly altered in the vicinity of the ATP-binding site as suggested by the 9% increase of the concentration of ATP necessary for half-maximal activation of the enzyme, thus indicating a deteriorated binding of ATP as a consequence of inflammation. Daily supplementation of FO partly attenuated LPS-induced injury, as observed by a significant decrease in the plasma levels of C-reactive protein and free radicals, hence maintaining the activity of renal Na, K-ATPase to the level of healthy control animals. In conclusion, our findings showed that FO prevented an excessive malondialdehyde production in LPS-treated animals and stabilized renal Na, K-ATPase.

摘要

采用酶动力学方法测量肾钠钾 ATP 酶,以鉴定接受大肠杆菌脂多糖(LPS)单剂量(1mg/kg 体重)处理 10 天的大鼠中 ATP 和钠离子结合位点。我们假设 LPS 可能引发肾脏钠钾 ATP 酶的功能障碍,因为这种酶是调节机体钠稳态的关键酶。我们还研究了鱼油(FO)在预防钠钾 ATP 酶改变方面的潜在作用,方法是每天以 30mg/kg 的剂量给予 FO。单独给予 LPS 后,血浆中 C 反应蛋白的水平升高了 500%以上,自由基升高了 36%,这表明丙二醛水平升高。ATP 结合位点附近的钠钾 ATP 酶略有改变,这表明激活酶所需的 ATP 浓度增加了 9%,表明由于炎症导致 ATP 的结合恶化。FO 的每日补充部分减轻了 LPS 诱导的损伤,如血浆中 C 反应蛋白和自由基水平显著降低,从而使肾脏钠钾 ATP 酶的活性保持在健康对照组动物的水平。总之,我们的研究结果表明,FO 可防止 LPS 处理动物中丙二醛的过度产生,并稳定肾脏钠钾 ATP 酶。

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