实验性糖尿病期间内皮型一氧化氮合酶内源性调节因子对一氧化氮稳态和血清脂蛋白的影响。

Effects of endogenous regulators of endothelial NO synthase on nitric oxide homeostasis and blood serum lipoproteins during experimental diabetes mellitus.

作者信息

Dzugkoev S G, Metel'skaya V A, Dzugkoeva F S

机构信息

Institute of Biomedical Studies, Vladikavkaz Research Center, Russian Academy of Sciences and Government of the Republic of North Ossetia-Alania, Vladikavkaz; National Research Center of Preventive Medicine, Ministry of Health and Social Development of the Russian Federation, Moscow, Russia.

出版信息

Bull Exp Biol Med. 2013 Dec;156(2):205-8. doi: 10.1007/s10517-013-2311-1.

DOI:10.1007/s10517-013-2311-1

PMID:24319749

Abstract

Experimental diabetes mellitus was associated with the development of oxidative stress and a decrease in blood concentration of total nitric oxide (NO) metabolites. Administration of L-arginine induced positive changes in the LPO-antioxidant enzyme system and elevated NO concentration in blood serum, whereas L-NAME, inhibitor of eNOS (NOS-III) increased LPO intensity via SOD inhibition and reduced NO content. Combined administration of Q10 and L-arginine led the suppression of oxidative stress and significant increase in NO level. Combined treatment with Q10 and L-NAME partly abolished the effects of the inhibitor on the parameters of the LPO-antioxidant enzyme system and NO concentration. In all variants of the study, Q10 stimulated eNOS expression and increases NO bioavailability by reducing the levels of total cholesterol and LDL and increasing HDL content in blood serum.

摘要

实验性糖尿病与氧化应激的发展以及血液中总一氧化氮（NO）代谢产物浓度的降低有关。给予L-精氨酸可使脂质过氧化（LPO）-抗氧化酶系统产生积极变化，并提高血清中NO浓度，而内皮型一氧化氮合酶（eNOS，即NOS-III）抑制剂L-NAME通过抑制超氧化物歧化酶（SOD）增加LPO强度并降低NO含量。联合给予辅酶Q10（Q10）和L-精氨酸可抑制氧化应激并使NO水平显著升高。Q10与L-NAME联合治疗部分消除了该抑制剂对LPO-抗氧化酶系统参数和NO浓度的影响。在该研究的所有变体中，Q10通过降低血清中总胆固醇和低密度脂蛋白（LDL）水平并增加高密度脂蛋白（HDL）含量来刺激eNOS表达并提高NO生物利用度。