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Chinese Medical Journal 2002-May

Effect of Acanthopanax giraldii Harms Var. Hispidus Hoo polysaccharides on the human gastric cancer cell line SGC-7901 and its possible mechanism.

Перакладаць артыкулы могуць толькі зарэгістраваныя карыстальнікі
Увайсці / Зарэгістравацца
Спасылка захоўваецца ў буферы абмену
Xiaoying Lu
Miancheng Su
You Li
Linfu Zeng
Xinghua Liu
Jianming Li
Baochun Zheng
Shuangyin Wang

Ключавыя словы

Рэферат

OBJECTIVE

To study the inhibitory effect of Acanthopanax giraldii Harms Var. Hispidus Hoo polysaccharides (AGP) on SGC-7901 gastric cancer cells and its possible mechanism.

METHODS

Cell doubling time analysis, colony forming assay and MTT assay were adopted to study the inhibitory effect and its characteristics. We also analyzed the amount of protein expressed by oncogenes, antioncogenes and cell factors using flow cytometric analysis.

RESULTS

AGP inhibited the proliferation of SGC-7901 cells and cell colony forming ability. AGP did not inhibit the viability and function of lymphocytes of peripheral blood in healthy subjects and human embryonic tenocytes, except for the highest dosage of AGP (P < 0.05), which slightly inhibited the viability and function of the two types of normal cells. AGP inhibited the viability and function of SGC-7901 cells, except for the lowest dosages of AGP I and AGP III. There was a dose-effect relationship between the dosage of the AGP and SGC-7901 cells. The effect of the AGP at the molecular level was associated with the low protein expression of the c-myc and bcl-2 genes and the high protein expression of the p53, bax, fas and fas-L genes, as well as the cell factor TGF beta(1). The inhibitory effect of AGP was weaker than that of CDDP, but was stronger than that of Vitamin C.

CONCLUSIONS

Acanthopanax giraldii Harms Var. Hispidus Hoo polysaccharides selectively inhibited the proliferation, the colony forming ability, and the viability and function of human gastric cancer cells through the low protein expression of c-myc, bcl-2 and the high protein expression of p53, fas, fas-L and the cell factor TGF beta(1). The different inhibitory characteristics on the normal cells and cancer cells are possibly caused by gene and the cell factor expressions.

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