Inhibitory effect of baicalin on fluorouracil resistant HCC cell line BEL-7402/5-Fu and its possible mechanism
10.3724/SP.J.1008.2008.00024
- Author:
Xia GUO
1
Author Information
1. Department of Gastroenterology
- Publication Type:Journal Article
- Keywords:
Antineoplastic drug resistance;
Baicalin;
Fluorouracil;
Liver neoplasm
- From:
Academic Journal of Second Military Medical University
2010;29(1):24-29
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the inhibitory effect of baicalin on the fluorouracil (Fu) resistant hepatocarcinoma cell (HCC) BEL-7402/5-Fu and its possible mechanism. Methods: Hepatocarcinoma cell line BEL-7402 and Fu-resistant hepatocarcinoma cell line BEL-7402/5-Fu were cultured in vitro. The inhibitory effect of baicalin on the BEL-7402/5-Fu cells was assessed by MTT assay; the intracellular rhodamine fluorescence intensity was observed by flow cytometry; the expression of MDR1 gene was detected by RT-PCR; and the expression of protein P-glycoprotein (P-gp) was analyzed by Western blotting assay. Adhesion assay was conducted using Matrigel model. Expression of beta 1-integrin and E-CD protein was detected by immuno-fluorescence technique. Results: Baicalin inhibited the proliferation of both BEL-7402 and BEL-7402/5-Fu cells, with IC50 of baicalin being 34.2 mg/L and 36.6 mg/L, respectively. Baicalin (5 mg/L and 10 mg/L) partially reversed the resistance of BEL-7402/5-Fu to Fu, with the reversal folds being 28.6 and 46.7, respectively. Baicalin (5 mg/L and 10 mg/L) increased the sensitivity of BEL-7402 cells to Fu, with the sensitivity-enhancing folds being 1.4 and 2.1, respectively. Baicalin also increased the concentration of rhodamine and expression of integrin β1, inhibited the expression of MDR1 gene and P-gp, E-CD protein, and reduced the adhesion capacity, with the effect of 10 mg/L baicalin significantly effective than that of 5 mg/L baicalin (all P<0.05). Conclusion: Baicalin can inhibit the proliferation of BEL-7402/5-Fu in vitro, and partially reverse the resistance to Fu, which is attributable to the increased accumulation of intracellular drug concentration, inhibited expression of MDR1 gene.
