The genus Cinnamomum

Chinese Cassia 177
(3–5°C) or due to water immersion. It also inhibited serotonin induced gastric ulcers
in rats. Antiulcerative properties were noted for the following compounds from cassia
bark: 3-(2-hydroxyphenyl)-propanoic acid and its O--D-glucopyranoside, cassioside,
cinnamoside, and 3,4,5-trimethoxyphenol--D-apiofuranosyl-(1: 6)--D-glucopyranoside
(Shiraga et al., 1988).
Kubo et al. (1996) have shown that 70% methanolic extract of C. cassia bark inhibited
the rise in vascular permeability induced by acetic acid and the increase of paw oedema
induced by carrageenan in mice. It was ineffective against oedema induced by histamine
and bradykinin, and exhibited a weak inhibitory effect against oedema induced
by serotonin. The extract also showed an inhibitory effect against prekallikrein enzyme
activity and ear oedema induced by arachidonic acid. It also had an inhibitory effect on
cotton pellett-induced granuloma but showed no atrophying action against the adrenal
or thymus glands. Little effect was shown on secondary lesions in the development of
adjuvant-induced arthritis.
The daily administration of 0.35 mg of sodium cinnamate to dogs for five days
increased peripheral leukocytes by 150–200%. Intraperitoneal administration of
0.35 mg of sodium cinnamate to mice and sc administration of 5.44 mg/kg of sodium
cinnamate to dogs six hours, one, two, five and six days after irradiation with a lethal
dose of 60 Co-rays increased the survival rate of the animals.
In anesthetised dogs and guinea pigs cinnamaldehyde produced a hypotensive effect
mainly due to peripheral vasodilation. In isolated ileum of guinea pigs and mice cinnamaldehyde
exhibited a papaverine-like activity. An increase in cardiac contractile
force and beating rate was exerted by cinnamaldehyde in isolated guinea pig heart
preparations. A repeated administration of cinnamaldehyde, however, led to a progressive
decrease in such effects and to cardiac inhibition (Harada and Yano, 1975).
Cinnamaldehyde induced the release of catecholamines from the adrenal glands of dogs.
The positive ionotropic and chronotropic effects of cinnamaldehyde on perfused isolated
guinea pig heart were presumably due to the release of endogenous catecholamines
(Harada and Saito, 1978).
Oral administration of 250–500 mg/kg of cinnamaldehyde reduced the spontaneous
motor activity in mice and antagonised the locomotor activity induced by methamphetamine.
Prolongation of hexobarbital-induced hypnosis was also observed.
Intraperitonial doses of 125 and 250 mg/kg produced similar effects. At an intraperitonial
dose of 500 mg/kg, cinnamaldehyde delayed tetanic convulsion and death
induced by strychnine (Wang, 1983).
Shimada et al. (2000) studied the protective effect of aqueous extract of cassia bark
on glutamate-induced neuronal death and its action on Ca influx using cultured rat
cerebellar granule cells. In a dose-dependent manner this extract significantly protected
cells from glutamate-induced death and also inhibited glutamate-induced calcium ion
influx. These results suggest that the cassia bark has a protective effect on glutamate
induced neuronal death through the inhibition of calcium ion influx.
2-hydroxycinnamaldehyde present in cassia bark inhibited farnesyl-protein transferase
(FPTase). FPTase is an enzyme that catalyses the transfer of the farnesyl group from farnesyl
pyrophosphate on to cysteine 186 at the c-terminal of the Ras-Protein, a mandatory
process before anchoring to plasma membrane which is critical for triggering the ‘ras’
ocogene toward tumour formation (Kwon et al., 1996). Kim et al. (2000a,b) have shown
that cinnamomi cortex extract exhibited strong antiallergic activity in the mouse system.
The extract inhibited anaphylactic shock and inhibited the Arthus reaction. Among the