Melatonin attenuates homocysteine‐induced injury in human umbilical vein endothelial cells

Aminzadeh, Azadeh; Mehrzadi, Saeed

doi:10.1111/fcp.12355

Cited by 18 publications

(8 citation statements)

References 35 publications

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“…MDA is one of the toxic products of free radical‐mediated lipid peroxidation and is a sensitive marker of oxidative stress and lipid peroxidation . Our results demonstrated that myricetin decreased lipid peroxidation in HUVECs in high glucose condition.…”

Section: Discussionsupporting

confidence: 55%

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Aminzadeh

Bashiri

2019

Cell Biochemistry & Function

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Endothelial dysfunction is recognized as the initial detectable stage of cardiovascular disease, a serious complication of diabetes. In this study, we evaluated effects of myricetin on high glucose (HG)-elicited oxidative damage in human umbilical vein endothelial cells (HUVECs). The cells were pre-incubated with myricetin and then treated with HG to induce apoptosis. The effect of myricetin on viability was investigated by MTT assay. The levels of lipid peroxidation (LPO) were determined by thiobarbituric acid (TBA) method. The protein expression of Bax, Bcl-2 and caspase-3 was measured by western blot analysis. Moreover, the effect of myricetin on total antioxidant capacity (TAC) and total thiol molecules was also determined.Our results showed that myricetin was able to markedly restore the viability of endothelial cells under oxidative stress. Myricetin reduced HG-caused increase in LPO levels. Also, TAC and total thiol molecules were notably elevated by myricetin.Incubation with myricetin decreased the protein expression levels of Bax, whereas it increased the expression levels of the Bcl-2, compared with HG treatment alone.Furthermore, myricetin significantly decreased cleaved caspase-3 protein expression. It is concluded that myricetin may protect HUVECs from oxidative stress induced by HG via increasing cell TAC and reducing Bax/Bcl-2 protein ratio, and caspase-3 expression.

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Section: Discussionsupporting

confidence: 55%

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Aminzadeh

Bashiri

2019

Cell Biochemistry & Function

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“…Moreover, the total antioxidant power was significantly attenuated in H9C2 cardiac cells treated with Hcy [ 69 ]. Homocysteine-induced decreases in antioxidant defense were documented in vascular injury [ 4 , 70 , 71 , 72 , 73 ]. Studies on aorta have shown decreased expression of thioredoxin (Trx) and peroxiredoxin (Prx) [ 74 ].…”

Section: Homocysteine and Mitochondrial Oxidative Stressmentioning

confidence: 99%

Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems

Kaplán

Tatarková

Sivoňová

et al. 2020

IJMS

125

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Elevated concentration of homocysteine (Hcy) in the blood plasma, hyperhomocysteinemia (HHcy), has been implicated in various disorders, including cardiovascular and neurodegenerative diseases. Accumulating evidence indicates that pathophysiology of these diseases is linked with mitochondrial dysfunction. In this review, we discuss the current knowledge concerning the effects of HHcy on mitochondrial homeostasis, including energy metabolism, mitochondrial apoptotic pathway, and mitochondrial dynamics. The recent studies suggest that the interaction between Hcy and mitochondria is complex, and reactive oxygen species (ROS) are possible mediators of Hcy effects. We focus on mechanisms contributing to HHcy-associated oxidative stress, such as sources of ROS generation and alterations in antioxidant defense resulting from altered gene expression and post-translational modifications of proteins. Moreover, we discuss some recent findings suggesting that HHcy may have beneficial effects on mitochondrial ROS homeostasis and antioxidant defense. A better understanding of complex mechanisms through which Hcy affects mitochondrial functions could contribute to the development of more specific therapeutic strategies targeted at HHcy-associated disorders.

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“…Cells can protect themselves against oxidative stress-induced cell death through their internal antioxidant defense systems. The best known antioxidant defense systems are superoxide dismutase (SOD), catalase (CAT), and GSH (Aminzadeh and Mehrzadi, 2018b; He et al, 2017). In present study, Pb decreased cardiac TAP.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of deferoxamine on lead-induced cardiotoxicity in rats

Gazeri

Aminzadeh

2020

Toxicol Ind Health

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Because of the numerous industrial applications of lead (Pb), Pb poisoning is an important public health threat in the world particularly in developing and industrialized countries. Oxidative stress is one of the important mechanisms of Pb-mediated toxicity. Deferoxamine (DFO) is an iron chelating agent that has recently shown antioxidant and antiapoptotic effects. This study investigated the protective capacity of DFO against Pb-induced cardiotoxicity in rats. We used five groups in this study: control, DFO (300 mg/kg), Pb (50 mg/kg), DFO (150 mg/kg) + Pb, DFO (300 mg/kg) + Pb. DFO was administered intraperitoneally 30 min before intraperitoneal injection of Pb for 5 days. After drug treatment, the levels of lactate dehydrogenase (LDH), lipid peroxidation (LPO), glutathione (GSH), and antioxidant enzymes were measured in serum and heart samples. The results showed that pretreatment with DFO reduced Pb-induced oxidative stress markers in serum and cardiac tissues. We found that LDH and LPO levels were significantly increased in Pb-treated rats and decreased with DFO pre-administration. Furthermore, the decreased activities of total antioxidant capacity, and GSH were observed after Pb treatment. However, DFO administration effectively prevented the Pb-induced alterations of these antioxidant enzymes activities. In conclusion, the results presented here indicate that DFO has protective effects in Pb-induced cardiotoxicity in rats, probably due to its antioxidant action and inhibition of oxidative stress.

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Melatonin attenuates homocysteine‐induced injury in human umbilical vein endothelial cells

Cited by 18 publications

References 35 publications

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems

Protective effects of deferoxamine on lead-induced cardiotoxicity in rats

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