Caffeic acid phenethyl ester (CAPE) attenuates cerebral vasospasm after experimental subarachnoidal haemorrhage by increasing brain nitric oxide levels

Aladağ, Murat; Türköz, Yusuf; Özcan, Cemal; Şahna, Engin; Parlakpınar, Hakan; Akpolat, Nusret; Çiğremiş, Yılmaz

doi:10.1016/j.ijdevneu.2005.12.002

Cited by 24 publications

(15 citation statements)

References 41 publications

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“…57,58 Previous studies implicated that both ferulic acid and caffeic acid modulated NO pathways in the central nervous system. [59][60][61] Increased central NO had a role of restraining sympathetic outflow, 50,62,63 thereby attenuating reflex tachycardia when arterial baroreceptors were unloaded due to blood pressure reduction. 58 Although the current data on CGAs are promising, gaps in knowledge remain to be filled.…”

Section: Molecular Targets Of Chlorogenic Acid In Blood-pressure Regumentioning

confidence: 99%

Antihypertensive effects and mechanisms of chlorogenic acids

et al. 2011

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Chlorogenic acids (CGAs) are potent antioxidants found in certain foods and drinks, most notably in coffee. In recent years, basic and clinical investigations have implied that the consumption of chlorogenic acid can have an anti-hypertension effect. Mechanistically, the metabolites of CGAs attenuate oxidative stress (reactive oxygen species), which leads to the benefit of blood-pressure reduction through improved endothelial function and nitric oxide bioavailability in the arterial vasculature. This review article highlights the physiological and biochemical findings on this subject and highlights some remaining issues that merit further scientific and clinical exploration. In the framework of lifestyle modification for the management of cardiovascular risk factors, the dietary consumption of CGAs may hold promise for providing a non-pharmacological approach for the prevention and treatment of high blood pressure.

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Section: Molecular Targets Of Chlorogenic Acid In Blood-pressure Regumentioning

confidence: 99%

Antihypertensive effects and mechanisms of chlorogenic acids

et al. 2011

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“…Thus, the use of free radical scavengers in animal models of SAH [11,12] and some clinical trials [13,14] have demonstrated beneficial effects of these agents on ischemic neurological deficits due to SAH-induced vasospasms. We have recently shown that melatonin, which is a potent free radical scavenger, reversed SAH-induced histopathological and biochemical alterations [15].…”

Section: Introductionmentioning

confidence: 99%

Alpha Lipoic Acid Alleviates Oxidative Stress and Preserves Blood Brain Permeability in Rats with Subarachnoid Hemorrhage

et al. 2009

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The neuroprotective effect of alpha lipoic acid (ALA; 100 mg/kg, po), a dithiol antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) was assessed in Wistar albino rats. Neurological examination scores recorded at the 48th h of SAH induction were increased in SAH groups, which were accompanied with significant increases in the formation of reactive oxygen species, DNA fragmentation ratios, malondialdehyde levels and myeloperoxidase activity, while significant decreases in the brain glutathione content and Na(+), K(+)-ATPase activity were observed. On the other hand, ALA treatment reversed all these biochemical indices as well as SAH-induced histopathological alterations. Increased brain edema, impaired blood-brain-barrier permeability and neurological scores were also improved by ALA treatment. The results demonstrate that ALA exerts neuroprotective effects via the enhancement of endogenous antioxidant enzyme activity, the inhibition of neutrophil accumulation and free radical generation, suggesting a therapeutic potential in reducing secondary injury after SAH in patients.

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“…1 It is plausible that the inflammatory response to oxidant stress represent a critical step in the pathogenesis of cerebral vasospasm (CVS) pursuant to SAH. [2][3][4] In addition, glutamate plays an important role in the pathogenesis of neuronal injury after ischemic injury. 5 Glutamate transporter-1 (GLT-1) predominates among the functional glutamate transporters, which are essential for maintaining a low extracellular glutamate concentration and for preventing glutamate neurotoxcity.…”

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confidence: 99%