Ginger extract mitigates ethanol-induced changes of alpha and beta – myosin heavy chain isoforms gene expression and oxidative stress in the heart of male wistar rats

Shirpoor, Alireza; Zerehpoosh, Mitra; Ansari, M H Khadem; Kheradmand, Fatemeh; Rasmi, Yousef

doi:10.1016/j.dnarep.2017.06.023

Cited by 14 publications

(9 citation statements)

References 29 publications

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“…Moreover, the current findings showed that chronic ethanol exposure caused oxidative stress in the epididymis tissue, as indicated by an increase in NADPH‐oxidase and 8‐OHdG levels. Our previous laboratory studies (Shirpoor, Barmaki, Khadem Ansari, Lkhanizadeh, & Barmaki, ; Shirpoor et al, ; Shirpoor, Nemati, Ansari, & Ilkhanizadeh, ; Shirpoor, Zerehpoosh, Ansari, Kheradmand, & Rasmi, ), as well as other similar studies in the literature (Abarikwu et al, ; Teixeira et al, ), have revealed that chronic ethanol consumption in male rats leads to oxidative stress and inflammatory changes in the testis, heart, lung, and kidney.…”

Section: Discussionmentioning

confidence: 65%

Long‐term ethanol consumption promotes changes in β‐defensin isoform gene expression and induces structural changes and oxidative DNA damage to the epididymis of rats

Sadeghzadeh

Shirpoor

Naderi

et al. 2019

Molecular Reproduction Devel

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Chronic alcohol ingestion causes sexual dysfunction, impairs sperm motility and fertility, and changes semen quality. Considering the key role of epididymis in sperm development, the aim of the present study was to evaluate the effects of long‐term ethanol consumption on epididymis changes, including alterations in β‐defensin isoform gene expression, oxidative stress, and pathological changes, such as cell proliferation and fibrosis in the epididymis of rats. In this study, male Wistar rats were equally divided into control and ethanol (4.5 g/kg BW) groups. After six weeks of treatment, the results revealed the proliferation of epididymis cells, fibrosis in the epididymis tissue, and a significant rise in the level of 8‐OHdG and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in the ethanol group, compared with the control group. Moreover, the ethanol group showed an increase in the gene expression of epididymal β‐defensin isoforms 15 and 21 and a reduction in the gene expression of β‐defensin isoforms 27 and 30, compared with the controls. These findings indicate that ethanol‐induced epididymal damage and sperm abnormalities might be partly associated with changes in β‐defensin isoforms and epididymal structure, mediated by the increased activities of 8‐OHdG and NADPH oxidase.

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Section: Discussionmentioning

confidence: 65%

Long‐term ethanol consumption promotes changes in β‐defensin isoform gene expression and induces structural changes and oxidative DNA damage to the epididymis of rats

Sadeghzadeh

Shirpoor

Naderi

et al. 2019

Molecular Reproduction Devel

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“…Marrs et al reported that supplementation with retinoic acid (10 −9 M) could partially rescue the development of disorders, including cardiovascular malformation in zebrafish embryos exposed to ethanol (100 mM) (Marrs et al, 2010). Shirpoor et al, conducted an animal experiment with male Wistar rats, in which ethanol led to cardiac defects by inducing decreased α‐myosin heavy chain (MHC)/β‐MHC expression, an effect that was mitigated by ginger extract as an antioxidant molecule (Shirpoor, Zerehpoosh, Ansari, Kheradmand, & Rasmi, 2017). Gao et al found that U0126 successfully attenuated Gata4 and Mef2c over‐expression via the ERK1/2 – H 3 hyperacetylation pathway (Gao et al, 2015) suggesting its potential to prevent or reduce CHDs caused by intended or unintended alcohol exposure (Figure 2).…”

Section: Early Diagnosis and Preventive Measures For Chds Caused By Paementioning

confidence: 99%

Prenatal alcohol exposure induced congenital heart diseases: From bench to bedside

Chen

Guo

et al. 2020

Birth Defects Research

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Alcohol consumption is increasing worldwide. Many child-bearing-aged women consume alcohol during pregnancy, intentionally or unintentionally, thereby increasing the potential risk for severe congenital diseases. Congenital heart disease (CHD) is the most common birth defect worldwide and can result from both hereditary and acquired factors. Prenatal alcohol exposure (PAE) is considered a key factor that leads to teratogenesis in CHD and its specific phenotypes, especially defects of the cardiac septa, cardiac valves, cardiac canals, and great arteries, adjacent to the chambers, both in animal experiments and clinical retrospective studies. The mechanisms underlying CHD and its phenotypes caused by PAE are associated with changes in retinoic acid biosynthesis and its signaling pathway, apoptosis and defective function of cardiac neural crest cells, disturbance of the Wntβ-catenin signaling pathway, suppression of bone morphogenetic protein (BMP) signaling, and other epigenetic mechanisms. Drug supplements and early diagnosis can help prevent PAE from inducing CHDs.

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“…[26] indicated that advanced oxidation protein products decrease expression of nephrin and podocin in podocytes through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species generation that activated p38 mitogen-activated protein kinase pathway. Interestingly, previous studies had demonstrated that ethanol exposure led to increase the level of NADPH oxidase in the kidney tissue, as well as in the cardiac tissue concurrent alteration of fetal gene expression [15, 27, 28]. Based on the results of this study and the previous ones, we suggest that ethanol induces NADPH oxidase to mediate oxidative stress, may trigger decreasing expression of nephrin and podocin in podocytes, and contribute, at least in part, to glomerular disease and kidney injury.…”

Section: Discussionmentioning

confidence: 99%

“…Sixteen male Wistar rats initially weighing 220 ± 10 g were randomly divided into two groups: (1) control and (2) ethanol groups. Similar to our previous study, rats in the ethanol group received ethanol with a dose of 4.5 g/kg body weight (Merck KGaA, Darmstadt, Germany) saluted in tap water (20% w/v) intragastrically by gavage once a day, for 6 weeks [15]. The control group was treated with tap water only.…”

Section: Methodsmentioning

confidence: 99%

Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats

Samadi

Shirpoor

Afshari

et al. 2018

IMAS

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BackgroundChronic alcohol ingestion-induced kidney structure and function alterations are very well known, but the precise underlying molecular mediators involved in ethanol-induced kidney abnormalities remain elusive. The aim of this study was to investigate the effect of chronic ethanol exposure on matrix metalloproteinase 2, 9 (MMP), glomerular filtration barrier proteins (nephrin and podocin), as well as vascular endothelial growth factor receptor 1, 2 (VEGFRs) isoforms gene expression in the kidney of rats.MethodsSixteen male Wistar rats with an initial body weight of 220 ± 10 g were divided into the following two groups: (1) control and (2) ethanol (4.5 g/kg BW).ResultsAfter 6 weeks of treatment, the results revealed a significant increase in isoforms VEGFR1 and VEGFR2 of VEGFR gene expression, significant increases of MMP2 and MMP9 activities, as well as significant decrease of nephrin and podocin gene expressions in the ethanol group, compared with that in the control group.ConclusionThese findings indicate that ethanol-induced kidney abnormalities may be in part associated with alteration in expressions of VEGFRs, nephrin, and podocin and in increasing activities of MMP2 and MMP9 as key molecular mediators in the kidney function.

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Ginger extract mitigates ethanol-induced changes of alpha and beta – myosin heavy chain isoforms gene expression and oxidative stress in the heart of male wistar rats

Cited by 14 publications

References 29 publications

Long‐term ethanol consumption promotes changes in β‐defensin isoform gene expression and induces structural changes and oxidative DNA damage to the epididymis of rats

Long‐term ethanol consumption promotes changes in β‐defensin isoform gene expression and induces structural changes and oxidative DNA damage to the epididymis of rats

Prenatal alcohol exposure induced congenital heart diseases: From bench to bedside

Chronic ethanol ingestion induces glomerular filtration barrier proteins genes expression alteration and increases matrix metalloproteinases activity in the kidney of rats

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