NIS - libdoc.who.int - World Health Organization

WHO monographs on medicinal plants commonly used in the Newly Independent States (NIS)
(43). Serum fibrinolytic activity increased after administration of dry garlic
or garlic extracts to animals that were artificially rendered arteriosclerotic
(79, 80). Although adenosine was thought to be the active constituent,
it did not affect whole blood (43).
Garlic inhibited platelet aggregation in both in vitro and in vivo studies.
A water, chloroform, or methanol extract of the drug inhibited collagen-,
ADP-, arachidonic acid-, epinephrine-, and thrombin-induced platelet aggregation
in vitro (81–87). Prolonged administration (intragastric, 3
months) of the essential oil or a chloroform extract of Bulbus Allii Sativi
inhibited platelet aggregation in rabbits (88–90). Adenosine, alliin, allicin,
and the transformation products of allicin, the ajoenes; the vinyldithiins;
and the dialkyloligosulfides are responsible for inhibition of platelet adhesion
and aggregation (4, 42, 91–93). In addition methyl allyl trisulfide, a
minor constituent of garlic oil, inhibited platelet aggregation at least 10
times as effectively than allicin (94). Inhibition of the arachidonic acid cascade
appears to be one of the mechanisms by which the various constituents
and their metabolites affect platelet aggregation. Inhibition of platelet
cyclic AMP phosphodiesterase may also be involved (91).
Ajoene, one of the transformation products of allicin, inhibited in vitro
platelet aggregation induced by the platelet stimulators—ADP, arachidonic
acid, calcium ionophore A23187, collagen, epinephrine, platelet
activating factor, and thrombin (95, 96). Ajoene inhibited platelet aggregation
in cows, dogs, guinea-pigs, horses, monkeys, pigs, rabbits, and rats
(95, 96). The antiplatelet activity of ajoene is potentiated by prostacyclin,
forskolin, indometacin, and dipyridamole (95). The mechanism of action
involves the inhibition of the metabolism of arachidonic acid by both cyclooxygenase
and lipoxygenase, thereby inhibiting the formation of
thromboxane A2 and 12-hydroxyeicosatetraenoic acid (95). Two mechanisms
have been suggested for ajoene’s antiplatelet activity. First, ajoene
may interact with the primary agonist–receptor complex with the exposure
of fibrinogen receptors through specific G-proteins involved in the
signal transduction system on the platelet membrane (92). Or it may interact
with a haemoprotein involved in platelet activation that modifies
the binding of the protein to its ligands (96).
Hypoglycaemic effects of Bulbus Allii Sativi have been demonstrated
in vivo. Oral administration of an aqueous, ethanol, petroleum ether, or
chloroform extract, or the essential oil of garlic, lowered blood glucose
levels in rabbits and rats (24, 97–104). However, three similar studies reported
negative results (105– 107). In one study, garlic bulbs administered
orally (in feed) to normal or streptozotocin-diabetic mice reduced hyperphagia
and polydipsia but had no effect on hyperglycaemia or hypoinsu-
16