2019
DOI: 10.1016/j.ejphar.2019.172707
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Chronic administration of NaHS and L-Cysteine restores cardiovascular changes induced by high-fat diet in rats

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Cited by 20 publications
(8 citation statements)
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“…It has been indicated that L-cysteine can upregulate GSH levels and improve oxidative stress in a high-glucose cultured hepatocyte model and in diabetic fatty liver rats [94]. Longterm supplementation with L-cysteine restores cardiovascular lesions caused by a high-fat diet in rats [95]. Dietary supplementation with L-cysteine dose-dependently promoted the antioxidant enzyme activity and decreased lipid levels in the serum and rat liver [96].…”
Section: Cysteine and Methionine Metabolismmentioning
confidence: 99%
“…It has been indicated that L-cysteine can upregulate GSH levels and improve oxidative stress in a high-glucose cultured hepatocyte model and in diabetic fatty liver rats [94]. Longterm supplementation with L-cysteine restores cardiovascular lesions caused by a high-fat diet in rats [95]. Dietary supplementation with L-cysteine dose-dependently promoted the antioxidant enzyme activity and decreased lipid levels in the serum and rat liver [96].…”
Section: Cysteine and Methionine Metabolismmentioning
confidence: 99%
“…L‐Cysteine is involved in the reduction process of cells and the metabolism of phospholipids in the liver, which can protect liver cells from damage, restore liver function and promote the detoxification effect of liver. Chronic treatment with L‐cysteine can reduce adipose tissue and ameliorate the cardiovascular changes induced by obesity 38 . Furthermore, alanine, a metabolite of L‐cysteine, increases from juvenile to adult stages.…”
Section: Discussionmentioning
confidence: 99%
“…L-cysteine can reduce adipose tissue and ameliorate the cardiovascular changes induced by obesity. 38 Furthermore, alanine, a metabolite of L-cysteine, increases from juvenile to adult stages.…”
Section: Con Clus Ionmentioning
confidence: 99%
“…It has been suggested that high concentrations of H 2 S may exert a rapid “knockdown” effect, perhaps because high concentrations of H 2 S cause transient inhibition of complex IV, resulting in inhibition of mitochondrial respiration [ 161 ]. In previous studies, NaHS treatment (100 µmol kg −1 day −1 ) for 4 weeks reversed diabetes–induced vascular dysfunction in mouse aortas [ 100 ] and ameliorated the cardiovascular changes induced by obesity [ 164 ]. However, it is worth noting that the NaHS was injected intraperitoneally, which may have led to a high initial circulating concentration of H 2 S followed by a decline and would not have provided 24–hour “coverage” for H 2 S delivery in vivo [ 161 ].…”
Section: Methodology Of Preclinical Workmentioning
confidence: 99%