ZHANG Zhe, CHEN Xinyi, ZHENG Zhi. Effect of Fufang Zhebei Granules Drug-Containing Serum on Proliferation and Apoptosis of Human Colorectal Cancer HCT-116 Cells[J]. Journal of Traditional Chinese Medicine2015, 56(1): 55-58.
ZHANG Zhe, CHEN Xinyi, ZHENG Zhi. Effect of Fufang Zhebei Granules Drug-Containing Serum on Proliferation and Apoptosis of Human Colorectal Cancer HCT-116 Cells[J]. Journal of Traditional Chinese Medicine2015, 56(1): 55-58.DOI: 10.13288/j.11-2166/r.2015.01.015.
Objective To observe influence of Fufang Zhebei Granules( FFZBG) on proliferation and apoptosis of human colorectal cancer HCT-116 cells and discuss the possible mechanism. Methods A total of 40 Wistar rats were randomly assigned to control group and high
middle
low-dose FFZBG group
with 10 in each. For 7 days
high
middle
low-dose FFZBG group were given 8
4
2 g /( kg · d) drug solution by gavage
while the control group was given 0. 1 ml /10 g normal saline. One hour after the last gavage
drug-containing serum was prepared. MTT method was applied to detect cell inhibitory rate of HCT-116 cells intervened by drug-containing serum of different dosage. The apoptosis rates of HCT-116 cells were detected quatitatively by flow cytometry. Western blot was used to examine the influence on expression of MDM2
p53
p21 proteins. Results The cell inhibitory rates of high
middle
low-dose FFZBG group were 40. 00%
42. 37% and 26. 78% respectively
while apoptosis rates were18. 75%
20. 00% and 15. 32% respectively
which were higher than that of the control group( P < 0. 05). At 48 h
the expression of MDM2
p53
p21 protein in high-dose FFZBG group
MDM2 protein in middle-dose FFZBG group and MDM2
p53 protein in low-dose FFZBG group were higher than that of the control group( P < 0. 01). At 96 h
the expression of MDM2 protein of high
middle
low-dose FFZBG group was significantly lower than that at 48 h
while the expression of p53 protein was higher( P < 0. 01). Conclusion Fufang Zhebei Granules can inhibit the proliferation of HCT-116 cells and promote apoptosis
with the possible mechanism of up-regulating the MDM2-p53 signal pathway.