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D-galactose induced inflammation lipid peroxidation and platelet activation in rats

机译:D-半乳糖诱导的大鼠炎症脂质过氧化和血小板活化

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Background: To investigate events possibly related to the development of d-galactose induced senescence, we examined whether 8-iso PGF2α formation, a marker of in vivo lipid peroxidation is altered and whether its biosynthesis is associated with 11-dehydro-TXB2 excretion rate, as a marker of in vivo platelet activation. In this setting, we also investigated the relationship between proinflammatory mediators (IL-6 and TNF-α from one, and lipid peroxidation and platelet activation, from another aspect. Methods and results: Forty animals were divided, depending on treatment with d-galactose into: placebo and d-galactose treated rats. 8-iso-PGF2α, IL-6 and TNF-α were measured in plasma, while 11-dehydro-TXB2 was determined in the urine after a six week treatment with d-galactose. Compared to placebo, d-galactose treated animals showed significantly higher levels of all measured parameters. Conclusions: d-galactose induced changes in the rate of F2-isoprostane formation are associated with the changes in the excretion rate of 11-dehydro-TXB2.
机译:背景:为调查可能与d-半乳糖诱导的衰老发展有关的事件,我们检查了8-isoPGF2α的形成,体内脂质过氧化的标志物是否发生了改变,以及其生物合成是否与11-脱氢-TXB2的排泄率有关,作为体内血小板活化的标志。在这种情况下,我们还从另一个方面研究了促炎介质(IL-6和TNF-α与脂质过氧化和血小板活化之间的关系)方法和结果:分为40只动物,具体取决于d-半乳糖的治疗分别于安慰剂和d-半乳糖治疗的大鼠中测定血浆中的8-iso-PGF2α,IL-6和TNF-α,而在d-半乳糖治疗6周后尿中测定的11-dehydro-TXB2。对安慰剂而言,经d-半乳糖处理的动物的所有测得参数水平均显着较高结论:d-半乳糖诱导的F2-异前列腺素形成速率的变化与11-脱氢-TXB2排泄率的变化有关。

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