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脂多糖和n-3多不饱和脂肪酸给药对自发性高血压大鼠主动脉功能的影响。

Consequences of lipopolysaccharide and n-3 polyunsaturated fatty acid administration on aortic function of spontaneously hypertensive rats.

作者信息

Kaprinay Barbara, Sotnikova Ruzena, Frimmel Karel, Krizak Jakub, Bernatova Iveta, Navarova Jana, Okruhlicova Ludmila

机构信息

Institute of Experimental Pharmacology and Toxicology, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.

出版信息

Gen Physiol Biophys. 2017 Jul;36(3):353-359. doi: 10.4149/gpb_2016054.

Abstract

The aim of the work was to study the delayed effect of lipopolysaccharide (LPS) administration on endothelial function of the aorta of rats with genetic hypertension. Further, the possibility to ameliorate LPS-induced changes by n-3 polyunsaturated fatty acids (n-3 PUFA) was tested. Rats received a bolus of 1 mg/kg LPS i.p.; n-3 PUFA were administered in the dose of 30 mg/kg daily for 10 days p.o.. Ten days after receiving of LPS, the body weight gain of rats was statistically lower compared to control rats (p < 0.05). n-3 PUFA administration to LPS rats had no effect on this parameter. The TBARS and NAGA concentrations in plasma were significantly increased in the LPS group (p < 0.05) and n-3 PUFA administration returned them to control values. In functional studies, phenylephrine (PE, 1 µmol/l) evoked contraction of aortas which was not statistically different among experimental groups. However, endothelium-dependent relaxation was depressed in the LPS group (p < 0.05) and n-3 PUFA slightly recovered it to control values. In conclusion, oxidative stress seems to be responsible for aortic endothelial dysfunction detected 10 days after administration of LPS to rats. n-3 PUFA slightly improved the function of the endothelium injured by LPS, probably thanks to their antioxidant properties. Prolonged administration of higher doses of n-3 PUFA should defend the vascular endothelium against detrimental effect of bacterial inflammation.

摘要

这项工作的目的是研究脂多糖(LPS)给药对遗传性高血压大鼠主动脉内皮功能的延迟影响。此外,还测试了n-3多不饱和脂肪酸(n-3 PUFA)改善LPS诱导变化的可能性。大鼠腹腔注射1 mg/kg LPS;n-3 PUFA以30 mg/kg的剂量口服给药,持续10天。接受LPS 10天后,与对照大鼠相比,大鼠的体重增加在统计学上较低(p < 0.05)。给LPS大鼠施用n-3 PUFA对该参数没有影响。LPS组血浆中TBARS和NAGA浓度显著升高(p < 0.05),施用n-3 PUFA后使其恢复到对照值。在功能研究中,去氧肾上腺素(PE,1 µmol/l)引起主动脉收缩,各实验组之间无统计学差异。然而,LPS组的内皮依赖性舒张受到抑制(p < 0.05),n-3 PUFA使其略有恢复至对照值。总之,氧化应激似乎是导致给大鼠施用LPS 10天后检测到的主动脉内皮功能障碍的原因。n-3 PUFA略微改善了受LPS损伤的内皮功能,这可能归功于它们的抗氧化特性。长期施用更高剂量的n-3 PUFA应能保护血管内皮免受细菌性炎症的有害影响。

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