Open AccessEffects of Ginkgo biloba leaf extract, shenmai and matrine on a human embryonic lung fibroblast fibrosis model
Author(s) -
Xingcai Zhang,
Yuli Cai
Publication year - 2018
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2018.6698
Subject(s) - ginkgo biloba , matrine , oncogene , molecular medicine , embryonic stem cell , fibroblast , biology , traditional medicine , cell cycle , pharmacology , apoptosis , cancer research , medicine , cell culture , neuroscience , biochemistry , genetics , gene
The aim of the present study was to investigate the effects of Ginkgo biloba leaf extract (GBLE), shenmai (S), and matrine (M) on human embryonic lung fibroblasts (HELFs). HELFs were allocated into the following groups: Group A (control group), group B [transforming growth factor β1 (TGF-β1) model group], groups C1-3 (TGF-β1 + low-, moderate- and high-dose GBLE), groups D1-3 (TGF-β1 + low-, moderate- and high-dose S) and groups E1-3 (TGF-β1 + low-, moderate- and high-dose oM). Cell proliferation was assessed with an MTT assay and apoptosis was measured by annexin V/propidium iodide double staining and flow cytometry analysis. Collagen type I (COL-I), collagen type III (COL-III), α-smooth muscle actin (α-SMA) and extracellular superoxide dismutase (ECSOD) mRNA expression levels were measured using semi-quantitative reverse transcription-polymerase chain reaction, and protein content was measured using ELISA. The cell growth inhibition rates of the S groups were significantly higher than those of the other treatment groups (P<0.05). The rate of apoptosis was significantly increased in the treatment groups compared with the model group (P<0.05), and S induced a significant increase in HELF apoptosis compared with the other treatment groups (P<0.05). The mRNA and protein expressions of COL-III, COL-I and α-SMA in the GBLE, S and M groups were significantly decreased, while the expression of ECSOD was significantly increased when compared with the model group (P<0.05). In conclusion, GBLE, S and M inhibited the pro-fibrotic role of TGF-β1 by targeting different steps in TGF-β1-mediated fibrosis.