Roselle Polyphenols Exert Potent Negative Inotropic Effects via Modulation of Intracellular Calcium Regulatory Channels in Isolated Rat Heart

Lim, Yi Cheng; Budin, Siti Balkis; Othman, Faizah; Latip, Jalifah; Zainalabidin, Satirah

doi:10.1007/s12012-016-9379-6

Cited by 30 publications

(23 citation statements)

References 27 publications

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“…The present data supports previous findings demonstrating that olive pomace improves endothelial dysfunction in hypertensive animals by enhancing eNOS expression [ 100 ]. Moreover, HS was found to ameliorate hypertension by mechanisms associated with endothelium-derived NO-cGMP pathway and inhibition of Ca2 + influx into VSMCs [ 101 , 102 ].…”

Section: Resultsmentioning

confidence: 99%

Antihypertensive Effects of Roselle‐Olive Combination in L‐NAME‐Induced Hypertensive Rats

Abdel-Rahman

Hessin

Abdelbaset

et al. 2017

Oxidative Medicine and Cellular Longevity

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This study aimed to evaluate the antihypertensive efficacy of a new combination therapy of Hibiscus sabdariffa and Olea europaea extracts (2 : 1; Roselle-Olive), using N(G)-nitro-L-arginine-methyl ester- (L-NAME-) induced hypertensive model. Rats received L-NAME (50 mg/kg/day, orally) for 4 weeks. Concurrent treatment with Roselle-Olive (500, 250, and 125 mg/kg/day for 4 weeks) resulted in a dose-dependent decrease in both systolic and diastolic blood pressure, reversed the L-NAME-induced suppression in serum nitric oxide (NO), and improved liver and kidney markers, lipid profile, and oxidative status. Furthermore, Roselle-Olive significantly lowered the elevated angiotensin-converting enzyme activity (ACE) and showed a marked genoprotective effect against oxidative DNA damage in hypertensive rats. Roselle-Olive ameliorated kidney and heart lesions and reduced aortic media thickness. Real-time PCR and immunohistochemistry showed an enhanced endothelial nitric oxide synthase (eNOS) gene and protein expression in both heart and kidney of Roselle-Olive-treated rats. To conclude, our data revealed that Roselle-Olive is an effective combination in which H. sabdariffa and O. europaea synergistically act to control hypertension. These effects are likely to be mediated by antioxidant and genoprotective actions, ACE inhibition, and eNOS upregulation by Roselle-Olive constituents. These findings provide evidences that Roselle-Olive combination affords efficient antihypertensive effect with a broad end-organ protective influence.

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Section: Resultsmentioning

confidence: 99%

Antihypertensive Effects of Roselle‐Olive Combination in L‐NAME‐Induced Hypertensive Rats

Abdel-Rahman

Hessin

Abdelbaset

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…Specifically, mangiferin prevented methylmercury-mediated Ca 2+ influx in a human neuroblastoma cell line, showing a neuroprotective potential activity [ 40 ]. According to these findings, Roselle polyphenols elicited a negative ionotropic response of agonists for L-type Ca 2+ channels by possibly modulating calcium entry in cardiac cells [ 41 ]. However, in cancer cells, resveratrol and picetannol strongly enhanced the mitochondrial Ca 2+ uptake by mechanisms involving SERCA activity reduction [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Mangiferin and Morin Attenuate Oxidative Stress, Mitochondrial Dysfunction, and Neurocytotoxicity, Induced by Amyloid Beta Oligomers

Alberdi

Sánchez‐Gómez

Ruiz

et al. 2018

Oxidative Medicine and Cellular Longevity

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Amyloid beta- (Aβ-) mediated ROS overproduction disrupts intraneuronal redox balance and exacerbates mitochondrial dysfunction which leads to neuronal injury. Polyphenols have been investigated as therapeutic agents that promote neuroprotective effects in experimental models of brain injury and neurodegenerative diseases. The aim of this study was to identify the neuroprotective effects of morin and mangiferin against Aβ oligomers in cultured cortical neurons and organotypic slices as well as their mechanisms of action. Cell death caused by Aβ oligomers in neuronal cultures was decreased in the presence of micromolar concentrations of mangiferin or morin, which in turn attenuated oxidative stress. The neuroprotective effects of antioxidants against Aβ were associated with the reduction of Aβ-induced calcium load to mitochondria; mitochondrial membrane depolarization; and release of cytochrome c from mitochondria, a key trigger of apoptosis. Additionally, we observed that both polyphenols activated the endogenous enzymatic antioxidant system and restored oxidized protein levels. Finally, Aβ induced an impairment of energy homeostasis due to a decreased respiratory capacity that was mitigated by morin and mangiferin. Overall, the beneficial effects of polyphenols in preventing mitochondrial dysfunction and neuronal injury in AD cell models suggest that morin and mangiferin hold promise for the treatment of this neurological disorder.

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“…For Langendorff heart studies, rats from each group were given sodium heparin (500 U/kg) as anticoagulant and urethane (1.2 g/kg) for anesthesia via intraperitoneal injections (Lim et al, 2016). Hearts were rapidly excised and subjected to retrograde perfusion via the aortic cannula under constant pressure of ~60-70 mmHg, with Krebs-Henseleit buffer (containing 118 mM NaCl, 25 mM NaHCO 3 , 4.7 mM KCl, 1.2 mM KH 2 PO 4 , 1.2 mM MgSO 4 , 1.25 mM CaCl 2 , 11 mM glucose; 95% O 2 /5% CO 2 maintained at 37°C).…”

Section: Langendorff Perfusion and Ischemia-reperfusion Injury Ex Vivomentioning

confidence: 99%

Angiotensin II Type I Receptor Antagonism Attenuates Nicotine-Induced Cardiac Remodeling, Dysfunction, and Aggravation of Myocardial Ischemia-Reperfusion Injury in Rats

et al. 2019

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Increased exposure to nicotine contributes to the development of cardiac dysfunction by promoting oxidative stress, fibrosis, and inflammation. These deleterious events altogether render cardiac myocytes more susceptible to acute cardiac insults such as ischemia-reperfusion (I/R) injury. This study sought to elucidate the role of angiotensin II type I (AT1) receptors in cardiac injury resulting from prolonged nicotine administration in a rat model. Male Sprague-Dawley rats were given nicotine (0.6 mg/kg ip) for 28 days to induce cardiac dysfunction, alone or in combination with the AT1 receptor antagonist, irbesartan (10 mg/kg, po). Vehicle-treated rats were used as controls. Rat hearts isolated from each experimental group at study endpoint were examined for changes in function, histology, gene expression, and susceptibility against acute I/R injury determined ex vivo. Rats administered nicotine alone exhibited significantly increased cardiac expression of angiotensin II and angiotensin-converting enzyme (ACE) in addition to elevated systolic blood pressure (SBP) and heart rate. Furthermore, nicotine administration markedly reduced left ventricular (LV) performance with concomitant increases in myocardial oxidative stress, fibrosis, and inflammation. Concomitant treatment with irbesartan attenuated these effects, lowering blood pressure, heart rate, oxidative stress, and expression of fibrotic and inflammatory genes. Importantly, the irbesartan-treated group also manifested reduced susceptibility to I/R injury ex vivo. These findings suggest that AT1 receptors play an important role in nicotine-induced cardiac dysfunction, and pharmacological approaches targeting cardiac AT1 receptors may thus benefit patients with sustained exposure to nicotine.

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Roselle Polyphenols Exert Potent Negative Inotropic Effects via Modulation of Intracellular Calcium Regulatory Channels in Isolated Rat Heart

Cited by 30 publications

References 27 publications

Antihypertensive Effects of Roselle‐Olive Combination in L‐NAME‐Induced Hypertensive Rats

Antihypertensive Effects of Roselle‐Olive Combination in L‐NAME‐Induced Hypertensive Rats

Mangiferin and Morin Attenuate Oxidative Stress, Mitochondrial Dysfunction, and Neurocytotoxicity, Induced by Amyloid Beta Oligomers

Angiotensin II Type I Receptor Antagonism Attenuates Nicotine-Induced Cardiac Remodeling, Dysfunction, and Aggravation of Myocardial Ischemia-Reperfusion Injury in Rats

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