Abstract
Platelet aggregation is one of the major causes of cardiovascular diseases. Our search for bioactive molecules from nature, led to the isolation of betulinic acid (BA) and structural modification of BA to 3β-acetoxybetulinic acid (BAA). Both inhibited blood platelet aggregation induced by thrombin, adenosine diphosphate (ADP) and epinephrine. BAA showed an enhance inhibition of platelet aggregation, in the thrombin-induced platelet aggregation (54.5±0.01 at 1 mg/ml, 63.5±0.17 at 3 mg/ml and 73.5±0.15 at 10 mg/ml; IC50 0.81 mg/ml) which was observed to be significantly (p<0.05) similar to that of the standard aspirin (65.4±0.07 at 1 mg/ml, 72.1±0.03 at 3 mg/ml and 76.5±1.22 at 10 mg/ml; IC50 0.33 mg/ml). The results clearly shows that functional group modification of BA to give BAA led to enhanced activity, hence BAA provides a better option as lead in the search for anti-platelet aggregation agents from nature. Key words: Anti-platelet aggregation, aggregation inducer, Betulinic acid, acetoxybetulinic acid, Melalueca bracteata.
Highlights
Platelets are cells in the blood that help in the formation of clot
The results clearly shows that functional group modification of betulinic acid (BA) to give BA to 3βacetoxybetulinic acid (BAA) led to enhanced activity, BAA provides a better option as lead in the search for anti-platelet aggregation agents from nature
The present study reports our findings on blood platelet aggregation (BPA) inhibition of BA and the effect of change in the functionality of BA on BPA
Summary
Platelets are cells in the blood that help in the formation of clot. They play an important role in the hemostasis and in pathophysiological processess such as thrombosis (Shattil et al, 1998; Stouffer and Smyth, 2003). Platelet over aggregation is usually the main cause of internal blood clot formation and if not checked, can be fatal leading to artherothrombotic diseases such as strokes and heart attack (Valko et al, 2005). Antiplatelet drugs help stop blood clot formation and this significantly contributes to the management of pathogennesis of cardiovascular diseases. The present study reports our findings on blood platelet aggregation (BPA) inhibition of BA and the effect of change in the functionality of BA on BPA
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