Rosmarinic Acid Alleviates the Endothelial Dysfunction Induced by Hydrogen Peroxide in Rat Aortic Rings via Activation of AMPK

Zhou, Hui; Fu, Baocai; Mi, Xiangquan; Li, Gang; Ma, Chunsheng; Xie, Junhua; Li, Ji; Wang, Zhenhua

doi:10.1155/2017/7091904

Cited by 21 publications

(19 citation statements)

References 29 publications

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“…Accumulating evidence obtained from in vitro, in vivo, and clinical studies supports the free radical scavenging properties of natural phenolic antioxidants [24]. In this study, we proposed that natural herbal phenolic compounds with strong antioxidant activity, such as rosmarinic acid [24] and carvacrol [29], could help to counteract the toxicity of Al.…”

Section: Discussionmentioning

confidence: 74%

“…Elevated Al 3+ concentrations lead to Al 3+ -induced formation of oxygen radicals causing lipid peroxidation, which results in cell membrane damage and oxidative stress [3][4][5][6][7]. Accumulating evidence obtained from in vitro, in vivo, and clinical studies supports the free radical scavenging properties of natural phenolic antioxidants [24]. In this study, we proposed that natural herbal phenolic compounds with strong antioxidant activity, such as rosmarinic acid [24] and carvacrol [29], could help to counteract the toxicity of Al.…”

Section: Discussionmentioning

confidence: 99%

“…Rosmarinic acid is the ester of caffeic acid and 3,4-dihydroxyphenyl-lactic acid and one of the most abundant phenols in many well-known herbs of the Lamiaceae family [23], such as rosemary, sage, basil, mint, and thyme. Among the simple phenolic compounds, rosmarinic acid has been shown to possess very strong antioxidant activity [24]. Rosmarinic acid was demonstrated to have neuroprotective properties, attenuate oxidative stress and neuronal cell death in vitro [25][26][27], and to diminish inflammatory responses in experimental models of an ischemic stroke [18,28].…”

Section: Introductionmentioning

confidence: 99%

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Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

et al. 2020

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Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al 3+ (7.5 mg/kg/day (0.15 LD 50 ) as AlCl 3 (37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Cl − control, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD 50 ), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD 50 ), 21 days, i.g.). The treatment with AlCl 3 increased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCl 3 treatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCl 3 treatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlCl 3 had no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

et al. 2020

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“…KG-501 is a small molecule inhibitor of cyclic AMP response element (CRE)-binding protein (CREB) ( Sun et al, 2008 ), and TrkB-Fc chimeric protein serves as a BDNF scavenger ( Huang et al, 2010 ). The inhibitor concentrations were referenced in previous studies ( Helan et al, 2014 ; Kang et al, 2014 ; Zhou et al, 2017 ). According to the manufacturer’s instructions, metformin, D -glucose, and TrkB-Fc were dissolved in sterile PBS, and CC and KG-501 were dissolved in dimethylsulfoxide (DMSO).…”

Section: Methodsmentioning

confidence: 99%

Metformin Modulates High Glucose-Incubated Human Umbilical Vein Endothelial Cells Proliferation and Apoptosis Through AMPK/CREB/BDNF Pathway

et al. 2018

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Cardiovascular disease (CVD) is a leading cause of mortality and morbidity among patients with diabetes. Endothelial dysfunction is an early physiological event in CVD. Metformin, a common oral antihyperglycemic agent, has been demonstrated to directly affect endothelial cell function. Brain-derived neurotrophic factor (BDNF), originally discovered in the brain as a neurotrophin, has also been reported to play a protective role in the cardiovascular system. In our study, we demonstrated that high glucose (HG) reduced cell proliferation and induced cell apoptosis via changes in BDNF expression and that metformin reversed the effects of HG injury by upregulating BDNF expression. Furthermore, we found that cyclic AMP response element binding (CREB) phosphorylation was reduced in HG-treated human umbilical vein endothelial cells (HUVECs), and this effect was reversed by the metformin treatment. However, the metformin effect on BDNF levels in HG-incubated HUVECs was blocked by a CREB inhibitor, which indicated that BDNF expression is regulated by metformin through CREB activation. In addition, we found that adenosine monophosphate-activated protein kinase (AMPK) activation is involved in CREB/BDNF regulation in HG-incubated HUVECs treated with metformin and that an AMPK inhibitor impaired the protective effects of metformin on HG-treated HUVECs. In conclusion, this study demonstrated that metformin affects cell proliferation and apoptosis via the AMPK/CREB/BDNF pathway in HG-incubated HUVECs.

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“…However, concurrent treatment with ethyl rosmarinate was shown to prevent this alteration. Other studies have shown that the parent compound of ethyl rosmarinate, rosmarinic acid, caused vasodilatory effects regulated through the endothelium-dependent pathway and against endothelial dysfunction through the 5ʹ adenosine monophosphate-activated protein kinase (AMPK)/eNOS pathway [16,22]. From the results of this study, it can be proposed that ethyl rosmarinate prevented hypertension through the up-regulation of the eNOS signaling pathway.…”

Section: Discussionmentioning

confidence: 57%

Ethyl Rosmarinate Prevents the Impairment of Vascular Function and Morphological Changes in L-NAME-Induced Hypertensive Rats

et al. 2019

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Background and Objectives: The potent, endothelium-independent, vasorelaxant effect of ethyl rosmarinate, an ester derivative of rosmarinic acid, makes it of interest as an alternative therapeutic agent for use in hypertension. This study was designed to investigate the effect of ethyl rosmarinate on N ω -nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. Materials and Methods: L-NAME was given orally to male Wistar rats for 6 weeks to induce hypertension concurrently with treatment of ethyl rosmarinate at 5, 15, or 30 mg/kgor enalapril at 10 mg/kg Systolic blood pressure (SBP), heart rate, and body weight of all experimental groups were recorded weekly, while the vascular sensitivity and histological changes of the aorta were evaluated at the end of the experiment. Results: For all treatment groups, the data indicated that ethyl rosmarinate significantly attenuated the SBP in hypertensive rats induced by L-NAME, with no significant differences in heart rate and body weight. In addition, the response of vascular sensitivity to acetylcholine (ACh) was improved but there was no significant difference in the response to sodium nitroprusside (SNP). Furthermore, the sensitivity of the aorta to phenylephrine (PE) was significantly decreased. The thickness of the aortic wall did not differ between groups but the expression of endothelial nitric oxide synthase (eNOS) was increased in ethyl rosmarinate-and enalapril-treated groups compared with the hypertensive group. Conclusions: Ethyl rosmarinate is an interesting candidate as an alternative treatment for hypertension due to its ability to improve vascular function and to increase the expression of eNOS similar to enalapril which is a drug commonly used in hypertension.

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Rosmarinic Acid Alleviates the Endothelial Dysfunction Induced by Hydrogen Peroxide in Rat Aortic Rings via Activation of AMPK

Cited by 21 publications

References 29 publications

Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

Metformin Modulates High Glucose-Incubated Human Umbilical Vein Endothelial Cells Proliferation and Apoptosis Through AMPK/CREB/BDNF Pathway

Ethyl Rosmarinate Prevents the Impairment of Vascular Function and Morphological Changes in L-NAME-Induced Hypertensive Rats

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