Title

丁酸鈉抑制二甲基肼誘發小鼠大腸癌的實驗研究

Translated Titles

Inhibitory Effect of Sodium Butyrate on 1, 2-Dimethylhydrazine-induced Tumorigenesis of Colorectal Cancer in Mice

Authors

劉成霞(Cheng-Xia Liu);張尚忠(Shang-Zhong Zhang);張孝衛(Xiao-Wei Zhang);耿秀蘭(Xiu-Lan Geng);李鐵軍(Tie-Jun Li);黃麗華(Li-Hua Huang);王兵(Bing Wang)

Key Words

丁酸鈉/拮抗劑和抑制劑 ; 二甲基肼/毒性 ; 大腸腫瘤/化學誘導 ; 大腸腫瘤/預防和控制 ; 小鼠 ; Sodium butyrate/antagonist and inhibitor ; 1, 2-Dimethylhydra-zine (DMH)/Toxicity ; Colorectal neoplasms/chemomorphosis ; Colorectal neoplasms/prophylaxis and control ; Mouse

PublicationName

癌症

Volume or Term/Year and Month of Publication

24卷8期(2005 / 08 / 05)

Page #

930 - 934

Content Language

簡體中文

Chinese Abstract

Background & Objective: In vitro studies proved that sodium butyrate (NaB) could stimulate cell differentiation, inhibit cell proliferation, and induce cell apoptosis in various tumors. This study was to evaluate the preventive effects of coloclysis of NaB on 1, 2-dimethylhydrazine (DMH)-induced tumorigenesis of colorectal cancer in mice. Methods: The mice of Kunming species were divided into 5 groups and received relevant treatments: DMH alone group (with subcutaneous injection of 30mg/kg of DMH weekly for 11 weeks), control (normal saline, NS) group, DMH plus low dose of NaB (1.25mol/kg, 24-week coloclysis) group, DMH plus high dose of NaB (2.5mol/kg, 24-week coloclysis) group, and high dose of NaB group. The mice were killed in batches at the 12(superscript th), 18(superscript th), and 24(superscript th) weeks of carcinoma induction separately. The incidence of colorectal tumor in each group was observed. Meanwhile, the general condition, body weight increasing, liver and renal functions, and pathologic changes of liver, kidney, lungs, and pancreas of the mice in DMH plus high dose of NaB group were also observed. Results: No tumor was observed at the 12(superscript th) week in each group. At the l8(superscript th) week, the tumor incidence was significantly higher in DMH alone group and DMH plus low dose of NaB group than in DMH plus high dose of NaB group (58.3%, and 25.0% vs. 0, P<0.01). At the 24(superscript th) week, the tumor incidence was 95.0% in DMH alone group, 45.0% in DMH plus low dose of NaB group, and 15.0% in DMH plus high dose of NaB group; the differences among the 3 groups were significant (P=0.01, P<0.01). No tumor was observed in control group and high dose of NaB group. There was no difference in the general condition, body weight increasing, and liver and renal functions of the mice between control group and high dose of NaB group (P>0.05); no pathologic changes in liver, kidney, lungs, and pancreas were observed in the mice in high dose of NaB group. Conclusion: NaB could inhibit DMH-induced tumorigenesis of colorectal cancer in mice with no obvious toxicity.

English Abstract

Background & Objective: In vitro studies proved that sodium butyrate (NaB) could stimulate cell differentiation, inhibit cell proliferation, and induce cell apoptosis in various tumors. This study was to evaluate the preventive effects of coloclysis of NaB on 1, 2-dimethylhydrazine (DMH)-induced tumorigenesis of colorectal cancer in mice. Methods: The mice of Kunming species were divided into 5 groups and received relevant treatments: DMH alone group (with subcutaneous injection of 30mg/kg of DMH weekly for 11 weeks), control (normal saline, NS) group, DMH plus low dose of NaB (1.25mol/kg, 24-week coloclysis) group, DMH plus high dose of NaB (2.5mol/kg, 24-week coloclysis) group, and high dose of NaB group. The mice were killed in batches at the 12(superscript th), 18(superscript th), and 24(superscript th) weeks of carcinoma induction separately. The incidence of colorectal tumor in each group was observed. Meanwhile, the general condition, body weight increasing, liver and renal functions, and pathologic changes of liver, kidney, lungs, and pancreas of the mice in DMH plus high dose of NaB group were also observed. Results: No tumor was observed at the 12(superscript th) week in each group. At the l8(superscript th) week, the tumor incidence was significantly higher in DMH alone group and DMH plus low dose of NaB group than in DMH plus high dose of NaB group (58.3%, and 25.0% vs. 0, P<0.01). At the 24(superscript th) week, the tumor incidence was 95.0% in DMH alone group, 45.0% in DMH plus low dose of NaB group, and 15.0% in DMH plus high dose of NaB group; the differences among the 3 groups were significant (P=0.01, P<0.01). No tumor was observed in control group and high dose of NaB group. There was no difference in the general condition, body weight increasing, and liver and renal functions of the mice between control group and high dose of NaB group (P>0.05); no pathologic changes in liver, kidney, lungs, and pancreas were observed in the mice in high dose of NaB group. Conclusion: NaB could inhibit DMH-induced tumorigenesis of colorectal cancer in mice with no obvious toxicity.

Topic Category 醫藥衛生 > 內科