Honey supplementation in spontaneously hypertensive rats elicits antihypertensive effect via amelioration of renal oxidative stress.

Omotayo O Erejuwa,Salzihan Salleh,Kuttulebbai N S Sirajudeen,Mohd S Ab Wahab,Sunil Gurtu,Siti A Sulaiman

doi:10.1155/2012/374037

Abstract

Oxidative stress is implicated in the pathogenesis and/or maintenance of elevated blood pressure in hypertension. This study investigated the effect of honey on elevated systolic blood pressure (SBP) in spontaneously hypertensive rats (SHR). It also evaluated the effect of honey on the amelioration of oxidative stress in the kidney of SHR as a possible mechanism of its antihypertensive effect. SHR and Wistar Kyoto (WKY) rats were randomly divided into 2 groups and administered distilled water or honey by oral gavage once daily for 12 weeks. The control SHR had significantly higher SBP and renal malondialdehyde (MDA) levels than did control WKY. The mRNA expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione S-transferase (GST) were significantly downregulated while total antioxidant status (TAS) and activities of GST and catalase (CAT) were higher in the kidney of control SHR. Honey supplementation significantly reduced SBP and MDA levels in SHR. Honey significantly reduced the activities of GST and CAT while it moderately but insignificantly upregulated the Nrf2 mRNA expression level in the kidney of SHR. These results indicate that Nrf2 expression is impaired in the kidney of SHR. Honey supplementation considerably reduces elevated SBP via amelioration of oxidative stress in the kidney of SHR.

Highlights

Cardiovascular disease (CVD) is a main cause of death globally
This study showed that elevated blood pressure is associated with increased oxidative damage and downregulated mRNA expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) in kidney of spontaneously hypertensive rats (SHR)
For the analysis of mRNA expressions of antioxidant enzymes and Nrf2, each group consisted of four to five rats. These results indicate that cells or tissues may augment components of the antioxidant defense system in order to increase cellular resistance and protect against the deleterious effects of oxidative stress

Summary

Introduction

Cardiovascular disease (CVD) is a main cause of death globally. The high incidence of CVD is ascribed to the increasing prevalence of modifiable cardiovascular risk factors such as hypertension, diabetes mellitus, obesity, lipid abnormalities, smoking, and sedentary lifestyle [1]. Epidemiological studies indicate that hypertension is a major public health concern because of its high prevalence and being an important risk factor for the development of CVD, end-stage renal disease, stroke, and death [2,3,4]. Evidence from literature suggests that elevated levels of ROS/RNS cause oxidative stress which is an important mediator in the imbalance between vasoconstrictor and vasodilator mechanisms in both experimental and human hypertension [5, 7,8,9]. In response to various oxidants, antioxidant enzymes undergo differential regulation or modulation [10,11,12].

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