Impact of N-acetylcysteine and Etodolac Treatment on Systolic and Diastolic Function in a Rat Model of Myocardial Steatosis Induced by High-Fat-Diet

Topal, Askin Ender; Akkoç, Hasan; Kelle, İlker; Yilmaz, Sedat; Topal, Derya; Akkuş, Murat

doi:10.2174/1871530314666141028144702

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“…Treatment with antioxidants specifically targeting mitochondria like Mito‐TEMPO attenuated obesity, glucose intolerance and diastolic dysfunction in mice fed high fat diet . Another antioxidant N ‐acetylcysteine increased the glutathione pool and subsequently antioxidant defenses and improved the cardiac function in high fat diet induced myocardial steatosis in rats . Recently, the antioxidant role of TX on diabetes‐induced vascular damage in rat aorta has been explored …”

Section: Discussionmentioning

confidence: 99%

“…28 Another antioxidant N-acetylcysteine increased the glutathione pool and subsequently antioxidant defenses and improved the cardiac function in high fat diet induced myocardial steatosis in rats. 29 Recently, the antioxidant role of TX on diabetes-induced vascular damage in rat aorta has been explored. 30 The present data suggest that high energy intake culminates in a…”

Section: Discussionmentioning

confidence: 99%

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Troxerutin attenuates diet‐induced oxidative stress, impairment of mitochondrial biogenesis and respiratory chain complexes in mice heart

Chandrasekaran

Anuradha

2016

Clin Exp Pharma Physio

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Summary Mitochondrial abnormality is thought to play a key role in cardiac disease originating from the metabolic syndrome (MS). We evaluated the effect of troxerutin (TX), a semi‐synthetic derivative of the natural bioflavanoid rutin, on the respiratory chain complex activity, oxidative stress, mitochondrial biogenesis and dynamics in heart of high fat, high fructose diet (HFFD) ‐induced mouse model of MS. Adult male Mus musculus mice of body weight 25‐30 g were fed either control diet or HFFD for 60 days. Mice from each dietary regimen were divided into two groups on the 16th day and were treated or untreated with TX (150 mg/kg body weight [bw], per oral) for the next 45 days. At the end of experimental period, respiratory chain complex activity, uncoupling proteins (UCP)‐2 and ‐3, mtDNA content, mitochondrial biogenesis and dynamics, oxidative stress markers and reactive oxygen species (ROS) generation were analyzed. Reduced mtDNA abundance with alterations in the expression of genes related to mitochondrial biogenesis and fission and fusion processes were observed in HFFD‐fed mice. Disorganized and smaller mitochondria, reduction in complexes I, III and IV activities (by about 55%) and protein levels of UCP‐2 (52%) and UCP‐3 (46%) were noted in these mice. TX administration suppressed oxidative stress, improved the oxidative capacity and biogenesis and restored fission/fusion imbalance in the cardiac mitochondria of HFFD‐fed mice. TX protects the myocardium by modulating the putative molecules of mitochondrial biogenesis and dynamics and by its anti‐oxidant function in a mouse model of MS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Troxerutin attenuates diet‐induced oxidative stress, impairment of mitochondrial biogenesis and respiratory chain complexes in mice heart

Chandrasekaran

Anuradha

2016

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

Impact of N-acetylcysteine and Etodolac Treatment on Systolic and Diastolic Function in a Rat Model of Myocardial Steatosis Induced by High-Fat-Diet

Abstract: Obesity is associated with diastolic dysfunction rather than systolic dysfunction. NAC may protect the heart against diastolic dysfunction due to obesity. NAC and etodolac treatment improve systolic function, even in the absence of systolic dysfunction.

Cited by 1 publication

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Troxerutin attenuates diet‐induced oxidative stress, impairment of mitochondrial biogenesis and respiratory chain complexes in mice heart

Troxerutin attenuates diet‐induced oxidative stress, impairment of mitochondrial biogenesis and respiratory chain complexes in mice heart

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