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D-半乳糖诱导大鼠发生炎症、脂质过氧化和血小板活化。

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

作者信息

Hadzi-Petrushev Nikola, Stojkovski Velimir, Mitrov Dine, Mladenov Mitko

机构信息

Faculty of Natural Sciences and Mathematics, Institute of Biology, "Ss. Cyril and Methodius" University, P.O. Box 162, 1000 Skopje, Macedonia.

Faculty of Veterinary Medicine, "Ss. Cyril and Methodius" University, 1000 Skopje, Macedonia.

出版信息

Cytokine. 2014 Sep;69(1):150-3. doi: 10.1016/j.cyto.2014.05.006. Epub 2014 Jun 6.

DOI:10.1016/j.cyto.2014.05.006
PMID:24907931
Abstract

BACKGROUND

To investigate events possibly related to the development of D-galactose induced senescence, we examined whether 8-iso PGF(2α) formation, a marker of in vivo lipid peroxidation is altered and whether its biosynthesis is associated with 11-dehydro-TXB(2) 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-PGF(2α), IL-6 and TNF-α were measured in plasma, while 11-dehydro-TXB(2) 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 F(2)-isoprostane formation are associated with the changes in the excretion rate of 11-dehydro-TXB(2).

摘要

背景

为了研究可能与D-半乳糖诱导衰老发展相关的事件,我们检测了体内脂质过氧化标志物8-异前列腺素F2α(8-iso PGF(2α))的生成是否改变,以及其生物合成是否与体内血小板活化标志物11-脱氢血栓素B2(11-dehydro-TXB(2))的排泄率相关。在此背景下,我们还研究了促炎介质(一方面的白细胞介素-6和肿瘤坏死因子-α)与另一方面的脂质过氧化和血小板活化之间的关系。

方法与结果

根据是否用D-半乳糖处理,将40只动物分为:安慰剂组和D-半乳糖处理组大鼠。在用D-半乳糖处理六周后,检测血浆中的8-异前列腺素F2α、白细胞介素-6和肿瘤坏死因子-α,同时测定尿液中的11-脱氢血栓素B2。与安慰剂组相比,D-半乳糖处理组动物的所有检测参数水平均显著更高。

结论

D-半乳糖诱导的F2-异前列腺素生成速率变化与11-脱氢血栓素B2排泄率变化相关。

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