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槲皮素联合适度运动训练对改善链脲佐菌素诱导的主动脉组织损伤的体内效应。

In Vivo Effects of Quercetin in Association with Moderate Exercise Training in Improving Streptozotocin-Induced Aortic Tissue Injuries.

作者信息

Chis Irina C, Coseriu Andrei, Simedrea Ramona, Oros Adrian, Nagy Andras L, Clichici Simona

机构信息

Department of Physiology, "Iuliu Hatieganu" University of Medicine and Pharmacy, Number 1-3, Clinicilor Street, RO-400023 Cluj-Napoca, Romania.

Department of Physiology, "Iuliu Haţieganu" University of Medicine and Pharmacy, Number 8, Victor Babes Street, RO-400012 Cluj-Napoca, Romania.

出版信息

Molecules. 2015 Dec 4;20(12):21770-86. doi: 10.3390/molecules201219802.

DOI:10.3390/molecules201219802
PMID:26690102
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6331973/
Abstract

BACKGROUND

Diabetes mellitus (DM) is a chronic endocrine-metabolic disorder associated with endothelial dysfunction. Hyperglycemia, dyslipidemia and abnormal nitric oxide-mediated vasodilatation are the major causal factors in the development of endothelial dysfunction in DM. The prevention of endothelial dysfunction may be a first target against the appearance of atherosclerosis and cardiovascular diseases. We have investigated the synergistic protective effects of quercetin administration and moderate exercise training on thoracic aorta injuries induced by diabetes.

METHODS

Diabetic rats that performed exercise training were subjected to a swimming training program (1 h/day, 5 days/week, 4 weeks). The diabetic rats received quercetin (30 mg/kg body weight/day) for 4 weeks. At the end of the study, the thoracic aorta was isolated and divided into two parts; one part was immersed in 10% formalin for histopathological evaluations and the other was frozen for the assessment of oxidative stress markers (malondialdehyde, MDA and protein carbonyls groups, PC), the activity of antioxidant enzymes (superoxide dismutase, SOD and catalase, CAT), nitrite plus nitrate (NOx) production and inducible nitric oxide synthase (iNOS) protein expression.

RESULTS

Diabetic rats showed significantly increased MDA and PC levels, NOx production and iNOS expression and a reduction of SOD and CAT activity in aortic tissues. A decrease in the levels of oxidative stress markers, NOx production and iNOS expression associated with elevated activity of antioxidant enzymes in the aortic tissue were observed in quercetin-treated diabetic trained rats.

CONCLUSIONS

These findings suggest that quercetin administration in association with moderate exercise training reduces vascular complications and tissue injuries induced by diabetes in rat aorta by decreasing oxidative stress and restoring NO bioavailability.

摘要

背景

糖尿病(DM)是一种与内皮功能障碍相关的慢性内分泌代谢紊乱疾病。高血糖、血脂异常以及一氧化氮介导的血管舒张异常是糖尿病患者内皮功能障碍发生发展的主要致病因素。预防内皮功能障碍可能是对抗动脉粥样硬化和心血管疾病出现的首要目标。我们研究了槲皮素给药与适度运动训练对糖尿病诱导的胸主动脉损伤的协同保护作用。

方法

进行运动训练的糖尿病大鼠接受游泳训练计划(每天1小时,每周5天,共4周)。糖尿病大鼠接受槲皮素(30毫克/千克体重/天)治疗4周。在研究结束时,分离胸主动脉并分为两部分;一部分浸入10%福尔马林中进行组织病理学评估,另一部分冷冻用于评估氧化应激标志物(丙二醛,MDA和蛋白质羰基基团,PC)、抗氧化酶活性(超氧化物歧化酶,SOD和过氧化氢酶,CAT)、亚硝酸盐加硝酸盐(NOx)生成以及诱导型一氧化氮合酶(iNOS)蛋白表达。

结果

糖尿病大鼠主动脉组织中MDA和PC水平、NOx生成及iNOS表达显著增加,SOD和CAT活性降低。在槲皮素治疗的糖尿病训练大鼠中,观察到主动脉组织中氧化应激标志物水平降低、NOx生成及iNOS表达减少,同时抗氧化酶活性升高。

结论

这些发现表明,槲皮素给药联合适度运动训练可通过降低氧化应激和恢复NO生物利用度,减少糖尿病诱导的大鼠主动脉血管并发症和组织损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/8d4d70154f09/molecules-20-19802-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/de4bf5f5bf56/molecules-20-19802-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/a992e35e5d76/molecules-20-19802-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/354c2fb59a2c/molecules-20-19802-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/82193b8061fb/molecules-20-19802-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/ad87c8052e61/molecules-20-19802-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/310e03a5d7d3/molecules-20-19802-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/8d4d70154f09/molecules-20-19802-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/de4bf5f5bf56/molecules-20-19802-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/a992e35e5d76/molecules-20-19802-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/2f20f3435ab8/molecules-20-19802-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/5730ca8291aa/molecules-20-19802-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/354c2fb59a2c/molecules-20-19802-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/82193b8061fb/molecules-20-19802-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/ad87c8052e61/molecules-20-19802-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/310e03a5d7d3/molecules-20-19802-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c654/6331973/8d4d70154f09/molecules-20-19802-g010.jpg

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