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Title 

Delayed occurrence of H-ras12V-induced hepatocellular carcinoma with long-term treatment with cinnamaldehydes

Authors 

Eun Yi MoonMi Ran LeeAi Guo WangJun Hee LeeHyoung-Chin KimHwan Mook KimJ M KimByoung-Mog KwonDae Yeul Yu

Publisher 

Elsevier

Issue Date 

2006

Citation 

European Journal of Pharmacology, vol. 530, no. 3, pp. 270-275

Keywords 

cinnamaldehydeH-ras12Vhepatocellular carcinomalong-term treatment2' benzoyloxycinnamaldehyde2' hydroxycinnamaldehydecinnamaldehyde derivativelipopolysaccharidechemoprophylaxisdrug inhibition

Abstract 

Cinnamaldehyde from the bark of Cinnamomum cassia has been reported to have antitumor activity mediated by the inhibition of farnesyl transferase. We assessed in vivo the chemo-preventive effect of cinnamaldehydes on H-ras12V-induced hepatocellular carcinoma formation. A mouse model of hepatocellular carcinoma was established by using the transgene of mutated H-ras12V under the regulation of albumin enhancer/promoter. When treated with cinnamaldehyde for 10 weeks, hepatic tumor development was delayed with 2′-benzoyloxycinnamaldehyde (BCA) compared with control hepatocellular carcinoma formation. The effect of 2′-hydroxycinnamaldehyde (HCA) was comparable. The number of lesions and the size of each lesion were significantly reduced by BCA. Cell proliferation in the lesion was detected by incorporation of 5-bromo-2′-deoxyuridine (BrdU). BCA increased the number of splenocytes, concanavalin A-stimulated splenocyte proliferation and the infiltration of lymphocytes into liver. Data suggest that the delayed hepatic tumor development observed with BCA could be mediated by a long-term immunostimulating effect on T cells.

ISSN 

0014-2999

Link 

http://dx.doi.org/10.1016/j.ejphar.2005.11.053

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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