Propolis protects against high glucose-induced vascular endothelial dysfunction in isolated rat aorta

El‐Awady, Mohammed S.; El‐Agamy, Dina S.; Suddеk, Ghada M.; Nader, Manar A.

doi:10.1007/s13105-013-0299-7

Cited by 15 publications

(19 citation statements)

References 30 publications

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“…In this context, we analyzed the role of AMPK in regulation of autophagy, a pathological process implicated in atherogenesis. Consistent with the role of these nutrients in endothelial dysfunction (22,47) as well as previous studies in HUVECs (8,9,41), we found that the combination of glucose and palmitate both predisposed HAECs to apoptosis and increased their inflammatory profile. The subsequent novel findings from our work were as follows: 1) Incubation of HAECs with the same high concentrations of glucose and palmitate that increased apoptosis and inflammation also impaired autophagy.…”

Section: Discussionsupporting

confidence: 91%

Glucose and palmitate uncouple AMPK from autophagy in human aortic endothelial cells

Weikel

Cacicedo

Ruderman

et al. 2015

American Journal of Physiology-Cell Physiology

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Weikel KA, Cacicedo JM, Ruderman NB, Ido Y. Glucose and palmitate uncouple AMPK from autophagy in human aortic endothelial cells. Am J Physiol Cell Physiol 308: C249 -C263, 2015. First published October 29, 2014 doi:10.1152/ajpcell.00265.2014.-Dysregulated autophagy and decreased AMP-activated protein kinase (AMPK) activity are each associated with atherogenesis. Atherogenesis is preceded by high circulating concentrations of glucose and fatty acids, yet the mechanism by which these nutrients regulate autophagy in human aortic endothelial cells (HAECs) is not known. Furthermore, whereas AMPK is recognized as an activator of autophagy in cells with few nutrients, its effects on autophagy in nutrient-rich HAECs has not been investigated. We maintained and passaged primary HAECs in media containing 25 mM glucose and incubated them subsequently with 0.4 mM palmitate. These conditions impaired basal autophagy and rendered HAECs more susceptible to apoptosis and adhesion of monocytes, outcomes attenuated by the autophagy activator rapamycin. Glucose and palmitate diminished AMPK activity and phosphorylation of the uncoordinated-51-like kinase 1 (ULK1) at Ser555, an autophagy-activating site targeted by AMPK. 5-Aminoimidazole-4-carboxamide-1-␤-D-ribofuranoside (AICAR)-mediated activation of AMPK phosphorylated acetyl-CoA carboxylase, but treatment with AICAR or other AMPK activators (A769662, phenformin) did not restore ULK1 phosphorylation or autophagosome formation. To determine whether palmitate-induced ceramide accumulation contributed to this finding, we overexpressed a ceramidemetabolizing enzyme, acid ceramidase. The increase in acid ceramidase expression ameliorated the effects of excess nutrients on ULK1 phosphorylation, without altering the effects of the AMPK activators. Thus, unlike low nutrient conditions, AMPK becomes uncoupled from autophagy in HAECs in a nutrient-rich environment, such as that found in patients with increased cardiovascular risk. These findings suggest that combinations of AMPK-independent and AMPK-dependent therapies may be more effective alternatives than either therapy alone for treating nutrient-induced cellular dysfunction. endothelium; autophagy; palmitate; glucose; AMPK PATIENTS WITH THE METABOLIC SYNDROME or type 2 diabetes are more likely to develop cardiovascular complications such as atherosclerosis (26,44,54,62,77). Many cellular processes have been implicated in driving this pathology, but the predominant mechanisms remain unclear. Intriguing reports from humans and murine models of vascular disease indicate that dysregulation of macroautophagy, a pathway by which cellular components are recycled for energy utilization, may play a prominent role in this disease progression. Thus it has been shown that impairment of macroautophagy contributes to arterial aging (56), cardiomyocyte apoptosis (34), and aortic lesion formation (74).Macroautophagy (hereinafter referred to as "autophagy") is a process by which cellular components are engulfed in a double-membraned vesicle, the au...

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Section: Discussionsupporting

confidence: 91%

Glucose and palmitate uncouple AMPK from autophagy in human aortic endothelial cells

Weikel

Cacicedo

Ruderman

et al. 2015

American Journal of Physiology-Cell Physiology

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“…For instance, it is reported that mollugin has potential antioxidant and anti-inflammatory effects (21) that may involve in aortic endothelial protection against hyperglycemic environment. Similarly, it is reported that many agents such as, Propolise, Ramipril, and Hespiridin protect endothelium against damage induced by hyperglycemic environment through their antioxidant activities (22)(23)(24).…”

Section: Discussionmentioning

confidence: 97%

The Contractive Effect of Rubia tinctorum L. Extract on the Isolated Aorta Smooth Muscle and Its Protective Effect Against the Damage Caused by Hyperglycemic Solution in Rat

Nejat

Sedaghat

Vakili

et al. 2017

Jundishapur J Nat Pharm Prod

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Background: Few past studies have indicated antispasmodic and anti-oxidative effects of some species of Rubiaceae. Objectives: This study aimed to investigate the effect of hydroalcoholic extract of Rubia tinctorum L. (madder) root on the rat-isolated aorta and possible protective effects against the damage caused by hyperglycemic environment. Methods: The isolated thoracic aorta ring (with or without endothelium) was treated with phenylephrine (10 -6 M) or KCl (80 mM)

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“…The effects of HG on PhE-induced contraction vary depending on the experimental conditions [1415162324]. Although long term exposure to high glucose inhibits EDR in a majority of studies [252627], several studies show conflicting results with regard to the effects of short-term exposure to high glucose [14151628].…”

Section: Discussionmentioning

confidence: 99%

“…The majority of previous studies demonstrated effects of hyperglycemia on vascular functions with long-term exposure; however, a few studies have been conducted to determine the effects of high glucose with short-term exposure. The results of those studies varied with the different experimental conditions [141516]. The incubation of high glucose (20 mM) for 2 h induced impairment of bradykinin-induced relaxation in human subcutaneous arteries whereas induced opposite result in human mesenteric arteries (MAs) [15].…”

Section: Introductionmentioning

confidence: 99%

“…The incubation of high glucose (20 mM) for 2 h induced impairment of bradykinin-induced relaxation in human subcutaneous arteries whereas induced opposite result in human mesenteric arteries (MAs) [15]. Also, exposure of high glucose (44 mM) for 3h produced the attenuation of phenylephrine (PhE)-induced contraction in rat aortic rings [14]. …”

Section: Introductionmentioning

confidence: 99%

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Effects of high glucose with or without other metabolic substrates on alpha-adrenergic contractions in rat mesenteric and femoral arteries

Vorn

Yoo

2017

Korean J Physiol Pharmacol

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Hyperglycemia is associated with an increased risk of cardiovascular diseases. It has been demonstrated that chronic exposure to high glucose impaired endothelial functions. However, specific effects of short-term exposure to high glucose on vascular reactivity are controversial. Moreover, the combined effects of other metabolic substrates such as free fatty acids (FFA) on vascular reactivity remain poorly understood. Here we investigate the effects of short-term exposure to high glucose with or without other metabolic substrates including FFAs termed “nutrition full” (NF) solution, on mesenteric (MA) and deep femoral arteries (DFA) of rats. Arterial ring segments were mounted in a double-wire myograph. Contraction in response to phenylephrine (PhE) was determined in control (5 mM) and high glucose (23 mM, HG) environments over a 30 min period. In both arteries, PhE-inducedvasocontraction was enhanced by pre-incubation of HG solution. A combined incubation with HG and palmitic acid (100 µM) induced similar sensitization of PhE-contractions in both arteries. In contrast, high K+-induced contractions were not affected by HG. Interestingly, pre-incubation with NF solution decreased PhE-induced contraction in MA but increased the contraction in DFA. In NF solution, the HG-induced facilitation of PhE-contraction was not observed in MA. Furthermore, the PhE-induced contraction of DFA was attenuated by HG in NF solution. Our results demonstrate that the sensitization of PhE-induced arterial contraction by HG is differentially affected by other metabolic substrates. The conversation of skeletal arterial contractility by HG in NF solution requires careful interpretation of the previous in vitro studies where only glucose is included in physiological salt solutions. Further studies are required to elucidate the mechanism underlying the inconsistent effect of NF solution on MA and DFA.

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Propolis protects against high glucose-induced vascular endothelial dysfunction in isolated rat aorta

Cited by 15 publications

References 30 publications

Glucose and palmitate uncouple AMPK from autophagy in human aortic endothelial cells

Glucose and palmitate uncouple AMPK from autophagy in human aortic endothelial cells

The Contractive Effect of Rubia tinctorum L. Extract on the Isolated Aorta Smooth Muscle and Its Protective Effect Against the Damage Caused by Hyperglycemic Solution in Rat

Effects of high glucose with or without other metabolic substrates on alpha-adrenergic contractions in rat mesenteric and femoral arteries

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