The effects of Berberine on growth of Immorto-Min colonic epithelial cell line
10.3760/cma.j.issn.0578-1426.2011.05.016
- VernacularTitle:小檗碱对永生化结肠细胞系生长的影响及其机制
- Author:
Hailong CAO
;
Bangmao WANG
;
Fang YAN
;
Xin CHEN
- Publication Type:Journal Article
- Keywords:
Berberine;
Cell proliferation;
Apoptosis;
Receptor,epidermal growth factor
- From:
Chinese Journal of Internal Medicine
2011;50(5):420-423
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of Berberine on growth of Immorto-Min colonic epithelial cell line (IMCE) and explore its possible mechanisms. Methods IMCE cells were treated with Berberine in the absence or presence of epidermal growth factor (EGF) and TNFα. Ki-67 staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay were used to identify the cell proliferation and apoptosis respectively. Furthermore, Western blot analysis was performed to detect the epidermal growth factor receptor ( EGFR), protein kinase B (Akt) and their phosphorylation.Results ( 1 ) Proliferating activity of IMCE cells was increased after adding EGF and the proportion of cell proliferation was ( 10. 64 ± 1.41 ) %. The proportion was significantly lowed in EGF plus Berberine group [(1.81 ±0. 85)%] compared to the EGF group(P ＜0. 01 ), while the lowest was the Berberine group [(0.49 ± 0.42) %]. (2) The proportions of cell apoptosis were ( 8.47 ± 2. 52 ) % and (9. 39 ± 2. 13 ) %in the Berberine group and TNFt group respectively which were significantly higher compared to the normal control [(0. 27 ± 0. 30)%], both P ＜ 0. 01. (3) The phosphorylation of EGFR was significantly increased after adding EGF and p-EGFR was decreased in EGF plus Berberine group at a concentration-dependent manner. (4) Moreover, the phosphorylation of Akt was enhanced after addition of TNFα , while the phosphorylation in the TNFα and Berberine group was inhibited compared to the TNFα group. Conclusions Berberine may suppress the proliferation and promote the apoptosis of IMCE cells. The mechanisms may relate to the inhibition of the phosphorylation of EGFR and Akt.
