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- Delayed occurrence of H-ras12V-induced hepatocellular carcinoma with long-term treatment with cinnamaldehydes
- Eun Yi Moon; Mi Ran Lee; Ai Guo Wang; Jun Hee Lee; Hyoung-Chin Kim; Hwan Mook Kim; J M Kim; Byoung-Mog Kwon; Dae Yeul Yu
- Bibliographic Citation
- European Journal of Pharmacology, vol. 530, no. 3, pp. 270-275
- Publication Year
- 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.
- Cinnamaldehyde; H-ras12V; Hepatocellular carcinoma; Long-term treatment
- Appears in Collections:
- Ochang Branch Institute > Division of Bioinfrastructure > 1. Journal Articles
Division of Biomedical Research > Genome Editing Research Center > 1. Journal Articles
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