Research on Ginsenoside Re inhibition of CFs proliferation by regulating Wnt/β-catenin signaling pathway
10.3760/cma.j.cn115398-20210628-00253
- VernacularTitle:人参皂苷Re调控Wnt/β-catenin信号通路抑制心肌成纤维细胞增殖研究
- Author:
Lutuo HAN
1
;
Hongwei GUO
;
Junguo REN
;
Jianxun LIU
;
Pan WANG
;
Jiamei YANG
Author Information
1. 黑龙江中医药大学中医药博物馆，哈尔滨 150040
- Keywords:
Ginsenoside Re;
Wnt signaling pathway;
Cell proliferation;
Transforming growth factor beta1;
Fibroblasts
- From:
International Journal of Traditional Chinese Medicine
2022;44(3):298-304
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the effect of Ginsenoside Re on the proliferation and protein secretion of primary cardiac fibroblasts (CFs) cultured in high glucose by vitro, and the regulation of Wnt/β-catenin signaling pathway.Methods:The myocardial fibroblast proliferation model induced by high glucose in vitro was used. Cell proliferation was detected by MTT method, cell cycle was measured by flow cytometry, concentration of type Ⅰ,Ⅲ collagens and TGF-β 1 protein were tested by ELISA assay. Protein expression of β-catenin, GSK-3β and p-GSK-3β were determined by Western blot. Results:Compared with the model group, the cell proliferation in Ginsenoside Re high, medium, low group were significantly decreased ( P<0.01), the percentage of cells in G 0 + G 1 phase was increased ( P<0.01), and the percentage of cells in S + G 2 + M phase was decreased ( P<0.01), the content of TGF-β 1 was significantly decreased( P<0.01). The content of type Ⅲ collagen [(6.566±1.620)ng/ml,(7.170±0.470)ng/ml vs. (11.241±2.234)ng/ml] in Ginsenoside Re high, medium group were significantly decreased ( P<0.01). The expression of β-catenin (0.281±0.016, 0.301±0.021 vs. 0.409±0.037) was significantly decreased and the expression of p-GSK-3β (0.369±0.049 vs. 0.268±0.048) in Ginsenoside Re high, medium group were significantly increased ( P<0.01). Conclusion:Ginsenoside Re plays an important role in inhibiting CFs proliferation and reducting the synthesis of collagen and TGF-β 1 by regulating abnormal expression of Wnt/β-catenin signaling pathway. It has the potential to delay the myocardial fibrosis of diabetes mellitus.
