AIM:To reveal the inhibitory effects of Curcuma aromatica oil (CAO) on cell proliferation of hepatoma in mice. METHODS: Two tumor inhibitory experiments of CAO on hepatoma in mice were conducted. The inhibitory effects of CAO on proliferation of hepatoma in mice were evaluated by DNA image cytometry and immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS: The tumor inhibitory rates of CAO were 52% and 51% in two experiments, respectively. Compared with those of the saline-treated control groups, both differences were statistically significant (P < 0.01). In the group of mice treated with CAO, the cellular nuclear DNA OD value (249 plus minus 70), areas (623&mgr;m(2) plus minus 228&mgr;m(2)) and DNA (2.38 plus minus 0.67) index of hepatic carcinomas were significantly lower than those of the control group (430 plus minus 160, 1073&mgr;m(2) plus minus 101&mgr;m2and 4.48 plus minus 0.71). CAO also could increase diploidy cell rates (29.00% plus minus 9.34% vs 2.97% plus minus 5.69%, P < 0.01) and decrease pentaploidy cell exceeding rate (30.04% plus minus 15.10% vs 70.89% plus minus 14.94%, P<0.01). In the group of mice treated with CAO, the labeling indexes of proliferating cell nuclear antigen (PCNA-LI) were 30% plus minus 4%, which were significantly lower than 40% plus minus 6% of the control group (P<0.01). CONCLUSION: The inhibition of CAO on the growth of hepatoma in mice might be associated with its depression on cellular proliferative activity.
AIM:To reveal the inhibitory effects of Curcuma aromatica oil (CAO) on cell proliferation of hepatoma in mice. METHODS: Two tumor inhibitory experiments of CAO on hepatoma in mice were conducted. The inhibitory effects of CAO on proliferation of hepatoma in mice were evaluated by DNA image cytometry and immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS: The tumor inhibitory rates of CAO were 52% and 51% in two experiments, respectively. Compared with those of the saline-treated control groups, both differences were statistically significant (P < 0.01). In the group of mice treated with CAO, the cellular nuclear DNA OD value (249 plus minus 70), areas (623&mgr;m(2) plus minus 228&mgr;m(2)) and DNA (2.38 plus minus 0.67) index of hepatic carcinomas were significantly lower than those of the control group (430 plus minus 160, 1073&mgr;m(2) plus minus 101&mgr;m2and 4.48 plus minus 0.71). CAO also could increase diploidy cell rates (29.00% plus minus 9.34% vs 2.97% plus minus 5.69%, P < 0.01) and decrease pentaploidy cell exceeding rate (30.04% plus minus 15.10% vs 70.89% plus minus 14.94%, P<0.01). In the group of mice treated with CAO, the labeling indexes of proliferating cell nuclear antigen (PCNA-LI) were 30% plus minus 4%, which were significantly lower than 40% plus minus 6% of the control group (P<0.01). CONCLUSION: The inhibition of CAO on the growth of hepatoma in mice might be associated with its depression on cellular proliferative activity.
Authors: N Hino; T Higashi; K Nouso; H Nakatsukasa; Y Urabe; N Kinugasa; K Yoshida; K Ashida; S Ohguchi; T Tsuji Journal: Hepatogastroenterology Date: 1997 Jan-Feb
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