Pyridoxine increases nitric oxide biosynthesis in human platelets

International journal for vitamin and nutrition research. Internationale Zeitschrift für Vitamin- und Ernährungsforschung. Journal international de vitaminologie et de nutrition
Yong WuYong Ji

Abstract

Activation and aggregation of platelets are key events in the pathophysiology of thrombotic diseases. There is increasing evidence that platelet-derived nitric oxide (NO) exerts important anti-platelet actions. Pyridoxine may have beneficial therapeutic effects in cardiovascular disease states, and has previously been shown to increase endothelial NO biosynthesis. The aims of the present study were firstly to determine in vitro whether pyridoxine can increase platelet NO synthesis, and secondly to investigate the mechanism by which it does this. Platelets isolated from blood taken from healthy subjects were treated with pyridoxine or vehicle. Platelet aggregation was measured by Born aggregometry. Intraplatelet cyclic guanosine-3',5'-monophosphate (cGMP, an index of bioactive NO) was measured by radioimmunoassay. Serine-1177-specific phosphorylation of NO synthase type 3 (NOS-3) and phosphorylation of protein kinase Akt were determined in platelets by Western blotting. Phosphatidylinositol 3-kinase (PI3K) activity in platelets was ascertained by homogeneous time-resolved fluorescence (HTRF) assay. Our results showed that pyridoxine largely inhibited the aggregation of platelets in response to adenosine diphosphate (ADP) or thro...Continue Reading

Citations

Aug 7, 2016·Nutrition & Metabolism·Xunxian Liu, Zemin Yao

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