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Gastrodin Promotes SGC7901 Apoptosis by Up‐regulating the ProBDNF Signaling Pathway
Author(s) -
jianhui Guo,
jinwei Yang,
wei Ma,
bin Du,
jingru Cheng,
liyan Li
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.983.12
Subject(s) - gastrodin , apoptosis , tunel assay , viability assay , gastrodia elata , terminal deoxynucleotidyl transferase , chemistry , signal transduction , microbiology and biotechnology , messenger rna , biology , biochemistry , medicine , pathology , gene , alternative medicine , chromatography , traditional chinese medicine
Objective To investigate the affect of Gastrodin on human gastric cancer cells (SGC7901) and its relationship with precursor brain‐derived neurotrophic factor proBDNF signal pathway. Methods SGC‐7901 was cutured in vitro and randomly divided into normal, control and experimental groups, and then, each group was divided into 6, 12, 24, 48 and 72 h groups. The experimental group cells were co‐cultured with Gastrodin at 2 mg/ml, but saline in control groups, and normal groups had no other treatment. After that, 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay was used to detect the cell activity and terminal dexynucleotidyl transferase(TdT)‐mediated dUTP nick end labeling (TUNEL) was used to detect the apoptosis of the cells. Immunofluorescence was used to locate the proBDNF, p75 and Sortilin positive cells, and the expression of proBDNF, p75 and Sortilin mRNA was detected by Real time Polymerase Chain Reaction (PCR). Results 1, SGC7901 was successfully cultured. 2, Cell viability in experimental groups was decreased compared with normal or control groups, but the apoptosis was increased. 3, proBDNF, p75 and Sortilin mRNA was up‐regulated in experimental groups. Conclusion Gastrodin can decrease the biological activity and increase the apoptosis of SGC7901, and the mechanism may be by increasing the proBDNF apoptosis signal pathway. Corresponding author: Li‐yan Li.