The genus Cinnamomum

264 K.K. Vijayan and R.V. Ajithan Thampuran
inhibitory activity on NADPH-dependant microsomal lipid peroxidation with IC 50
value of 3.4 0.1M without affecting the microsomal electron transport
of NADPH-cytochrome P-450 reductase. Both 1,1-diphenyl-2-picrilhydrazyl and
2,2 1 -azo-bis (-amidinopropane) dihydrochloride-derived peroxyl radical tests demonstrated
that cinnamophilin possessed a marked free radical scavenging capacity.
Cinnamophilin significantly protected cultured rat aortic smooth muscle cells (A7r5)
against alloxan/iron ion/H 2O 2-induced damage that would result in cytoplasmic
membranous disturbance and mitochondrial decay. Cinnamophilin inhibited coppercatalysed
oxidation of human low-density lipoprotein, as measured by fluorescence
intensity and thiobarbituric acid-reactive substance formation in a concentrationdependant
manner. On the other hand it was reactive towards superoxide anions
generated by the xanthine/xanthine oxidase system and the aortic segment from aged
spontaneously hypertensive rat.
Antiulcerogenic effects
In Ayurveda texts and other books on medicinal plants the main activity and use
attributed to cinnamon (and its related taxa) is as a curative agent for gastrointestinal
problems. In the pharmacopoeias of different countries and in ‘Martindale’ cinnamon is
included as an official drug for carminative action and for gastrointestinal problems.
The various preparations of cinnamon described in ‘Martindale’, which are employed
in the therapeutic practices of various countries, are used mainly for gastrointestinal
disorders. Cinnamon is used in traditional medicine as a cure for diarrhoea, dyspepsia
and for its carminative action. In modern medicine it is regarded as a stomachic and
carminative. In the ‘Materia Medica of India’, cinnamon is characterised as a drug active
against diarrhoea and dysentery. The effect of cinnamon oil on digestive enzymes was
studied by Yoshiki et al. (1981). An aqueous extract of Chinese cinnamon suppressed
the serotonin-induced gastric mucosal lesions in mice and rats and the antiulcerogenic
activity was attributed to the inhibition of both the gastric secretion and pepsin output.
It potentiated gastric mucosal flow (Akina, 1986). Later Tanaka et al. (1989) isolated
and identified the active compounds which prevented the ulcerogenesis. These were 3-
(2-hydroxyphenyl) propanoic acid and its o-glycoside. The former compound administered
orally or parenterally to rats at a remarkably low dose of 40g/kg body weight
produced the effect. This compound also inhibited gastric ulcers induced by other
ulcerogens such as phenylbutazone, aspirin and water immersion stress. However,
it failed in the case of indomethacin induced ulcers. The result suggests that the
antiulcerogenic effect of this compound is attributable to the potentiation of defensive
factors through the improvement of gastric blood flow and gastric cytoprotection.
Cassioside, cinnamoside and 3,4,5-trimethoxyphenol--D-apiofuranosyl (1→6)--Dglucopyranoside
were isolated as antiulcerative factors (Shiraga et al., 1988).
Sedative and anticonvulsant effects
Oral administration of cinnamaldehyde (250 mg/kg B.W.) reduced spontaneous motor
activity in mice. This also antagonised the drug-induced locomotor activity and
prolonged the hexobarbital induced sleeping time. Similar effects were produced by
an intraperitonial dose of 125–250 mg/kg (Harada and Ozaki, 1972). A Chinese