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l histidine/beroerte

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LidwoordKlinische proevenOctrooien
8 resultaten

Differential neuroprotective effects of carnosine, anserine, and N-acetyl carnosine against permanent focal ischemia.

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Carnosine (beta-alanyl-L-histidine) has been shown to exhibit neuroprotection in rodent models of cerebral ischemia. In the present study, we further characterized the effects of carnosine treatment in a mouse model of permanent focal cerebral ischemia and compared them with its related peptides
Glial scar formation resulted from excessive astrogliosis limits axonal regeneration and impairs recovery of function, thus an intervention to ameliorate excessive astrogliosis is crucial for the recovery of neurological function after cerebral ischemia. In this study we investigated the effects of
The brain endothelial large neutral amino acid carrier (L-system) is well suited for facilitated drug transport to the brain because of its high transport capacity and relatively broad structural substrate tolerance. The authors have examined the potential of this transporter for central nervous

Physiological and therapeutic effects of carnosine on cardiometabolic risk and disease.

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Obesity, type 2 diabetes (T2DM) and cardiovascular disease (CVD) are the most common preventable causes of morbidity and mortality worldwide. They represent major public health threat to our society. Increasing prevalence of obesity and T2DM contributes to escalating morbidity and mortality from CVD

Carnosine as a natural antioxidant and geroprotector: from molecular mechanisms to clinical trials.

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Carnosine is a neuroprotective dipeptide consisting of beta-alanine and L-histidine. It demonstrates a number of useful features, including stimulation of brain and muscle microcirculation and a rejuvenating effect on cultured cells. Its activity is based on its antioxidant and antiglycating action

Carnosine: can understanding its actions on energy metabolism and protein homeostasis inform its therapeutic potential?

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The dipeptide carnosine (β-alanyl-L-histidine) has contrasting but beneficial effects on cellular activity. It delays cellular senescence and rejuvenates cultured senescent mammalian cells. However, it also inhibits the growth of cultured tumour cells. Based on studies in several organisms, we

Histidine, cystine, glutamine, and threonine collectively protect astrocytes from the toxicity of zinc.

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In epilepsy, traumatic brain injury, and ischemic stroke, toxic levels of zinc released from neurons contribute to the brain damage associated with these disorders. Zinc causes oxidative stress by increasing the generation of reactive oxygen species and by inhibiting glutathione reductase (GR). This
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