Propolis reduces oxidative stress in l‐NAME‐induced hypertension rats

Abstract

The inhibition in the synthesis or bioavailability of nitric oxide (NO) has an important role in progress of hypertension. The blocking of nitric oxide synthase activity may cause vasoconstriction with the formation of reactive oxygen species (ROS). Propolis is a resinous substance collected by honey bees from various plants. Propolis has biological and pharmacological properties. The aim of this study was to examine the effect of propolis on catalase (CAT) activity, malondialdehyde (MDA) and NO levels in the testis tissues of hypertensive rats by Nω-nitro-l-arginine methyl ester (l-NAME). Rats have received nitric oxide synthase inhibitor (l-NAME, 40 mg kg(-1) , intraperitoneally) for 15 days to produce hypertension and propolis (200 mg kg(-1) , by gavage) during the last 5 days. MDA level in l-NAME-treated group significantly increased compared with control group (P < 0.01). MDA level of l-NAME + propolis-treated rats significantly reduced (P < 0.01) compared with l-NAME-treated group. CAT activity and NO level significantly reduced (P < 0.01) in l-NAME group compared with control group. There were no statistically significant increases in the CAT activity and NO level of the l-NAME + propolis group compared with the l-NAME-treated group (P > 0.01). These results suggest that propolis changes CAT activity, NO and MDA levels in testis of l-NAME-treated animals, and so it may modulate the antioxidant system.

L-NAME releases nitric oxide and potentiates subsequent nitroglycerin-mediated vasodilation

“…Besides, the nitrodilator-potentiating effect of L-NAME is also unlikely associated with alterations in redox signaling. Prolonged treatment of L-NAME may result in increase of ROS [4]. However, oxidative stress generally hampers NO-cGMP dependent vasodilation.…”

“…Despite its use as a NOS antagonist, there are numerous reports of L-NAME inducing responses that are inconsistent with NOS inhibition [2]. Several non-canonical actions of L-NAME have been proposed, including sympathetic activation [3], reactive oxygen species (ROS) generation [4], and paradoxically, increased NO production [2,5]. Supported by the up-regulation of NOS expression and activity measured in vitro, feedback NO production via NOS activation by L-NAME has been proposed, although it is unlikely that L-NAME increases the overall NO production from NOS in vivo [2].…”

Flavonoid Extract from Propolis Inhibits Cardiac Fibrosis Triggered by Myocardial Infarction through Upregulation of SIRT1

“…Propolis was accepted as a traditional medicine; proven to be beneficial to human health [ 27 ] and possess a wide range of biological and pharmacological activities, including antiatherosclerosis [ 28 ], antioxidative stress, and antihypertensive [ 29 ]. FP, the main bioactive compound of propolis [ 30 , 31 ], has been shown to exhibit several cellular activities. For example, Maruyama et al have demonstrated that FP plays a role in controlling the dilation of blood vessels, thereby decreasing blood pressure [ 32 ]; and research from our group has revealed that FP decreases the expression of collagen I and collagen III via the PI3K/AKT pathway in the hypertrophic ventricles of rats given isoproterenol [ 14 ].…”

Chronic NOS Inhibition Affects Oxidative State and Antioxidant Response Differently in the Kidneys of Young Normotensive and Hypertensive Rats

“…Short- and long-term administrations of L-NAME (nonselective inhibitor of NOS) in moderate and high doses cause persistent hypertension associated with multiple renal functional and morphological damage [15–17]. Studies show that the L-NAME-induced inhibition of NOS can lead to stimulation of RAS [18–20] and may result in an increase of ROS production [21, 22]. Oxidative injury of the kidney present in L-NAME-treated normotensive rats is probably mediated by Ang II.…”