Apocynin activity in spontaneously hypertensive rats (SHR): preliminary studies in vivo

Ciarcia, Roberto; Damiano, Sara; Panico, Carolina; Scanni, Roberto; Fiorito, Filomena; Florio, Salvatore; Welch, J. W.

doi:10.1007/s11259-010-9377-2

Cited by 6 publications

(4 citation statements)

References 10 publications

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“…Subsequently, H 2 O 2 significantly increased the cell apoptosis rate ( Figures 3A, B). Previous studies showed that ROS directly reflects the level of oxidative stress in cells (Ciarcia et al, 2010). Our experiment also indicated that the intracellular ROS level is consistent with cell damage, with a significant decrease in cell viability after the ROS level is increased.…”

Section: Discussionsupporting

confidence: 84%

Squid Ink Polysaccharides Protect Human Fibroblast Against Oxidative Stress by Regulating NADPH Oxidase and Connexin43

et al. 2020

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Oxidation injury to skin is one of the main reasons for skin aging. The aim of the present study was to explore the protective effect of squid ink polysaccharides and its mechanism of action against H 2 O 2-induced dermal fibroblast damage. Our results show that squid ink polysaccharides effectively reduce the fibroblast oxidative damage mediated by the upregulation of NADPH oxidase and Connexin43. Concurrently, squid ink polysaccharides decrease the ROS induced up-regulation of MMP1 and MMP9 to decrease MMPmediated skin aging. Therefore, we hypothesize that squid ink polysaccharides play an antioxidant role by inhibiting the expression of NADPH oxidase and connexin43. This provides a new target for the effective clinical prevention and treatment of oxidative skin damage.

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Section: Discussionsupporting

confidence: 84%

Squid Ink Polysaccharides Protect Human Fibroblast Against Oxidative Stress by Regulating NADPH Oxidase and Connexin43

et al. 2020

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“…Different studies have been using apocynin [32,[60][61][62][63][64] and diapocynin [25,27,28] for treatment of experimental animal models to evaluate the role of NAD(P)H oxidase enzyme and the contribution of ROS to oxidative stress and cardiovascular disease. Then, the intent of our study was elucidating the clinical pharmacology of diapocynin on vascular system and its vasodilator and hypotensive effect, once is an active dimer from apocynin and thus our data could contribute to the progress of the field for ROS study and vascular biology.…”

Section: Discussionmentioning

confidence: 99%

Hypotensive and vasorelaxant effect of Diapocynin in normotensive rats

Potje

Troiano

Graton

et al. 2017

Free Radical Biology and Medicine

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Nicotinamide adenine dinucleotide phosphate oxidase (NAD(P)H-oxidase) is a multicomponent enzyme system that generates superoxide anion by one-electron reduction of molecular oxygen and represents the major source of reactive oxygen species (ROS) in the vascular cells. Apocynin has been extensively used as an inhibitor of NADPH oxidase (NOX) in phagocytic cells and as an antioxidant in non-phagocytic cells. In phagocytes cells, due to the presence of myeloperoxidase, apocynin can be the converted to diapocynin, which is supposed to be the active form of this phytochemical. Moreover, apocynin was shown to induce hypotension and vasodilatation in many experimental animal models. However, there are no studies showing the effects of diapocynin on blood pressure or in vascular cells. In this present study, we used chemically synthesized diapocynin and analyzed its antioxidant capacity, effect on blood pressure and vascular reactivity. Moreover, it was evaluated the levels of nitric oxide (NO), ROS and calcium in aortic endothelial cells stimulated by diapocynin. All results were compared to apocynin. We found that diapocynin showed higher antioxidant capacity than apocynin. Apocynin and diapocynin, promoted hypotensive effects without changing the heart rate, however the effects of diapocynin were reversed faster than the effects of apocynin, which was long lasting. Diapocynin and apocynin induced endothelium dependent and independent vasodilatation, but diapocynin was less potent than apocynin regarding the capacity of induction of vasodilatation in mesenteric resistance arteries and aorta from Wistar rats. The relaxation induced by apocynin or diapocynin involves sGC and potassium channels in vascular smooth muscle cells and NOS participates of relaxation induced by apocynin or diapocynin in intact mesenteric rings. Apocynin and diapocynin increased NO and decreased ROS levels in endothelial cells, however diapocynin did not alter calcium levels in these cells. In conclusion, these results demonstrated that, similarly to apocynin, diapocynin also induces hypotensive and vasodilator effects in rats and vascular endothelium improves the diapocynin vasodilator effects by increases NO bioavailability.

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“…This conclusion is further supported by findings that in isolated arteries presence of ADMA increased ethidium bromide fluorescence, an indicator of vascular oxidative stress, which was reduced by apocynin [18]. The primary cellular effect of apocynin is to inhibit the release of superoxide anion by inhibiting NADPH oxidase activity via blocking the migration of p47 phox to the plasma or microsomal membranes [50]. …”

Section: Discussionmentioning

confidence: 73%

Asymmetric Dimethylarginine Reduces Nitric Oxide Donor-Mediated Dilation of Arterioles by Activating the Vascular Renin-Angiotensin System and Reactive Oxygen Species

et al. 2012

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Introduction: We tested the hypothesis that asymmetric dimethylarginine (ADMA) interferes with other mechanisms in addition to inhibition of nitric oxide synthase (NOS). Thus, in skeletal muscle arterioles, in the presence of ADMA, we investigated the dilator effect of an NO donor and increases in flow and aimed to elucidate the underlying mechanisms, including the role of oxidative stress, which is known to reduce the bioavailability of NO. Methods and Results: In isolated rat gracilis skeletal muscle arterioles (∼160 µm at 80 mm Hg), ADMA (similarly to pyrogallol) reduced dilations to sodium nitroprusside (SNP), which was significantly prevented by the presence of superoxide dismutase (SOD) and catalase (CAT): SNP 10^–8M; control: 43.2 ± 3%, ADMA: 4.9 ± 1%, ADMA + SOD/CAT: 30.2 ± 9% (p < 0.05). Also, ADMA reduced basal diameter and flow-induced dilations, which were not restored by L-arginine, but prevented by SOD/CAT and by inhibition of NAD(P)H oxidase (but not xanthine oxidase) and by an angiotensin-converting enzyme inhibitor or an angiotensin type 1 receptor blocker (ARB). ADMA increased the production of reactive oxygen species detected by lucigenin-enhanced chemiluminescence, which was significantly inhibited by SNP or ARB. Conclusion: We suggest that by activating the vascular renin-angiotensin-NAD(P)H oxidase pathway, ADMA elicits oxidative stress, which interferes with the bioavailability of NO and consequently reduces NO-mediated dilations.

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Apocynin activity in spontaneously hypertensive rats (SHR): preliminary studies in vivo

Cited by 6 publications

References 10 publications

Squid Ink Polysaccharides Protect Human Fibroblast Against Oxidative Stress by Regulating NADPH Oxidase and Connexin43

Squid Ink Polysaccharides Protect Human Fibroblast Against Oxidative Stress by Regulating NADPH Oxidase and Connexin43

Hypotensive and vasorelaxant effect of Diapocynin in normotensive rats

Asymmetric Dimethylarginine Reduces Nitric Oxide Donor-Mediated Dilation of Arterioles by Activating the Vascular Renin-Angiotensin System and Reactive Oxygen Species

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