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Biomedical subjects

S A Saeed

Publications and source records attributed to S A Saeed.

At least 55 records · Page 3Linked to original sources
PubMed1995

Phosphatidylinositol 3-kinase inhibitor, wortmannin, inhibits 5-hydroxytryptamine-mediated potentiation of platelet aggregation induced by epinephrine.

The role of phosphatidylinositol 3-kinase (PI 3-kinase) was investigated in human platelets exposed to varying doses of 5-hydroxytryptamine (5-HT) and subthreshold doses of epinephrine. The synergistic effect of 5-HT on epinephrine-induced aggregation was blocked by a specific inhibitor of PI 3-kinase, wortmannin, in a dose-dependent manner. However, there was no effect of inhibitors of protein kinase A (PKA) or protein kinase C (PKC). These studies suggest a role of PI 3-kinase in the 5-HT induced potentiation of epinephrine-mediated platelet aggregation.

Adrenergic alpha-Agonists↗
PubMed1994

Antithrombotic activity of clove oil.

Clove oil inhibited human platelet aggregation induced by arachidonic acid (AA), platelet-activating factor (PAF) or collagen. Clove oil was a more effective inhibitor for aggregation induced by AA and PAF (IC50:4 and 6 microM respectively) than collagen (IC50: 132 microM). The in vivo experiments in rabbits showed that clove oil (50-100 mg/kg) afforded 100% protection against PAF (11 mg/kg, i.v.) and 70% protection against AA (2.0 mg/kg, i.v.)-induced thrombosis and shock due to pulmonary platelet thrombosis. It also inhibited thromboxane-A2 and 12-HETE production by human platelets incubated with [C14] AA. These results are indicative that clove oil is inhibitory of platelet aggregation and thromboxane synthesis and may act as anti-thrombotic agent.

Animals↗
PubMed1993

Dual inhibition of platelet-activating factor and arachidonic acid metabolism by ajmaline and effect on carrageenan-induced rat paw oedema.

The effects of ajmaline on human platelet aggregation, arachidonate metabolism and platelet activating factor (PAF)-induced lethality in rabbits were examined. Platelet aggregation induced by several stimuli (ADP, collagen, and PAF) was inhibited by increasing concentrations of ajmaline. The potency of ajmaline was higher when PAF was employed as stimulating agent in comparison with other agonists (IC50 70, 270 and 380 microM for PAF, ADP and collagen, respectively) whereas ajmaline had no effect against arachidonic acid-induced aggregation. In contrast however, ajmaline inhibited arachidonate metabolism by platelet homogenates. The formation of both thromboxane A2 and 12-hydroxy-eicosatetraenoic acid was inhibited by ajmaline with comparable potencies. Pretreatment of rabbits with ajmaline (50 mg kg-1) completely abolished the lethal effects of PAF (11 micrograms kg-1) given intravenously (P < 0.001). In addition, ajmaline at doses ranging from 50 to 100 mg kg-1 inhibited carrageenan-induced rat paw oedema (P < 0.001). In this test ajmaline was three times more potent than aspirin. In the light of these results we conclude that ajmaline, a known anti-arrhythmic agent is a PAF antagonist and a dual inhibitor of platelet cyclo-oxygenase and lipoxygenase enzymes with anti-inflammatory properties.

Ajmaline↗
PubMed1991

Inhibition of platelet activating factor by ajmaline in platelets: in vitro and in vivo studies.

The in vitro and in vivo effects of ajmaline and its derivatives on platelet aggregation and platelet-activating factor (PAF) induced death in rabbits was studied. Ajmalinc and acetyl ajmaline selectively inhibited PAF-induced aggregation in a concentration related manner. Weak or no inhibition of aggregation was observed when ADP, collagen or arachidonic acid were used as aggregating agents. Similarly ajmaline or acetyl ajmaline also inhibited the lethal effects of PAF in the rabbit. PAF (8-11 microg/kg i.v.) caused sudden death in rabbits due to platelet aggregation and cardiac failure. Pretreatment of rabbits with ajmaline (50 mg/kg i.p.) protected conscious rabbits from PAF (11 microg/kg i.v.)-induced death. Since PAF is a powerful inducer of platelet aggregation via stimulation of specific PAF membrane receptors, our data is suggestive that ajmaline (an anti-arrhythmic agent) could emerge as a new class of PAF antagonists.

Journal Article↗
PubMed1991

Inhibition of adrenaline-induced aggregation of human platelets by Pakistani medicinal plants.

The effects of extracts of Pakistani plants claiming medicinal value were observed on adrenaline-induced aggregation of human platelets according to the method of Born (1962). The extracts manifested significant inhibitory activity in doses of 0.625 mgm(-1) to 2.5 mgml(-1) in this in vitro model. The potency of the plant extracts in inhibiting platelet aggregation induced by adrenaline is in the following order: Sida pakistanica, IC50 = 0.90 mgml(-1) > Tribulus terrestris, IC50 = 0.97 mgml(-1) > Solanum surattense, IC50 = 1.34 mgml(-1) Tephrosia subtriflora, IC50 = 1.40 mgml(-1) > Glycyrrhiza glabra (butanolic extract), IC50 = 1.66 mgml(-1) > Urtica dioica IC50 = 2.17 mgml(-1). Further studies are proposed to find out whether the inhibition of adrenaline-induced platelet aggregation is mediated through alpha-adrenoceptor blockade or suppressed synthesis of prostaglandin endoperoxides.

Journal Article↗