Chemical constituents of liquid culture of symbiotic Chaetomium globosum ML-4 of oyster and their in vitro antitumor activity.
10.19540/j.cnki.cjcmm.20170905.005
- Author:
Dan WAN
1
;
Xi CHEN
1
;
Li ZHU
1
;
Feng-Wu WANG
2
;
Gui-Mei KONG
1
;
Gui-Yun CAO
1
;
Li SHEN
1
Author Information
1. Medical College, Yangzhou University, Yangzhou 225001, China.
2. College of Food Science and Engineering, Qingdao Agricultural University, Qingdao 266109, China.
- Publication Type:Journal Article
- Keywords:
Chaetomium globosum;
antitumor activity;
chemical constituents;
oyster;
symbiotic microorganism
- From:
China Journal of Chinese Materia Medica
2017;42(21):4142-4149
- CountryChina
- Language:Chinese
-
Abstract:
Isolation and purification of chemical constituents of liquid culture of symbiotic Chaetomium globosum ML-4 of oyster was performed through silica gel column chromatography, gel filtration over Sephadex LH-20, preparative TLC and HPLC. Five compounds were obtained and their structures were determined as chaetoglobosin V(1), chaetoglobosin Vb(2), tyrosol(3), 5-methyluracil(4)and uracil(5), respectively, based on HR-MS and NMR data and comparison with literatures. In vitro cytotoxicity of compounds against human hepatocellular carcinoma cell line SMMC-7721 were measured byMTT method, and results showed that compound 1 could obviously inhibit the proliferation of SMMC-7721 cells with an IC₅₀ value of 60.5 mg•L⁻¹, while the IC₅₀ value of positive control cisplatin was 19.96 mg•L⁻¹. Further studies discovered that compound 1 could lead to G2 phase arrest in SMMC-7721 cells and induce SMMC-7721 cells apoptosis. The ratio of Bcl-2/Bax in SMMC-7721 cells was decreased. The expression of protein Caspases-3,-8,-9 was improved and the expression and phosphorylation level of Akt were reduced. Aforementioned results revealed that in vitro antitumor activity of compound 1 against SMMC-7721 cells were related to G2 phase cell cycle arrest and induced-apoptosis. The induced-apoptosis was involved in both the mitochondrial pathway and the death receptor pathway and connected with activity decline of PI3K/Akt signaling pathway.