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抗高血压药物依那普利对自发性高血压大鼠肾脏氧化应激标志物和抗氧化酶的影响。

Effect of the antihypertensive drug enalapril on oxidative stress markers and antioxidant enzymes in kidney of spontaneously hypertensive rat.

作者信息

Chandran G, Sirajudeen K N S, Yusoff Nik Syamimi Nik, Swamy M, Samarendra Mutum S

机构信息

Department of Chemical Pathology, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, 16150 Kubang Kerian, Kelantan, Malaysia.

Department of Pathology, School of Medical Sciences, Universiti Sains Malaysia, Health Campus, 16150 Kubang Kerian, Kelantan, Malaysia.

出版信息

Oxid Med Cell Longev. 2014;2014:608512. doi: 10.1155/2014/608512. Epub 2014 Aug 28.

Abstract

Oxidative stress has been suggested to play a role in hypertension and hypertension induced organ damage. This study examined the effect of enalapril, an antihypertensive drug, on oxidative stress markers and antioxidant enzymes in kidney of spontaneously hypertensive rat (SHR) and Nω -nitro-L-arginine methyl ester (L-NAME) administered SHR. Male rats were divided into four groups (SHR, SHR+enalapril, SHR+L-NAME, and SHR+enalapril+L-NAME). Enalapril (30 mg kg(-1) day(-1)) was administered from week 4 to week 28 and L-NAME (25 mg kg(-1) day(-1)) was administered from week 16 to week 28 in drinking water. Systolic blood pressure (SBP) was measured during the experimental period. At the end of experimental periods, rats were sacrificed; urine, blood, and kidneys were collected for the assessment of creatinine clearance, total protein, total antioxidant status (TAS), thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), and catalase (CAT), as well as histopathological examination. Enalapril treatment significantly enhanced the renal TAS level (P < 0.001) and SOD activity (P < 0.001), reduced the TBARS levels (P < 0.001), and also prevented the renal dysfunction and histopathological changes. The results indicate that, besides its hypotensive and renoprotective effects, enalapril treatment also diminishes oxidative stress in the kidneys of both the SHR and SHR+L-NAME groups.

摘要

氧化应激被认为在高血压及高血压所致器官损伤中起作用。本研究检测了抗高血压药物依那普利对自发性高血压大鼠(SHR)以及给予Nω-硝基-L-精氨酸甲酯(L-NAME)的SHR肾脏中氧化应激标志物和抗氧化酶的影响。雄性大鼠被分为四组(SHR、SHR+依那普利、SHR+L-NAME以及SHR+依那普利+L-NAME)。依那普利(30 mg kg⁻¹ 天⁻¹)从第4周给药至第28周,L-NAME(25 mg kg⁻¹ 天⁻¹)在第16周开始通过饮水给药至第28周。在实验期间测量收缩压(SBP)。实验期末,处死大鼠;收集尿液、血液和肾脏用于评估肌酐清除率、总蛋白、总抗氧化状态(TAS)、硫代巴比妥酸反应性物质(TBARS)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT),以及进行组织病理学检查。依那普利治疗显著提高了肾脏TAS水平(P < 0.001)和SOD活性(P < 0.001),降低了TBARS水平(P < 0.001),还预防了肾功能障碍和组织病理学变化。结果表明,除了其降压和肾脏保护作用外,依那普利治疗还可减轻SHR和SHR+L-NAME组大鼠肾脏中的氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1825/4164806/9f5864532dc4/OMCL2014-608512.001.jpg

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