[Gambogenic acid induces mitochondria-dependent apoptosis in human gastric carcinoma cell line].

Abstract

OBJECTIVE:

To study the effects of Gambogenic acid (GNA) on the growth of human gastric carcinoma cell line MGC-803 and its underlying mechanisms.

METHODS:

MTT assay was used to measure the cell viability. Apoptosis, mitochondrial membrane potential (MMP), reactive oxygen species (ROS) were detected using flow cytometry method. Among them, Annexin V-FITC/PI double staining was employed in the analysis of apoptosis, Rh123 in analyzing MMP and H2DCFDA in analyzing ROS formation. P53 expression was confirmed by Western blot.

RESULTS:

4.0 micromol/L GNA inhibited MGC-803 cells growth in a time dependent manner from 24 to 48 h. At the concentration range from 1.0 to 12.0 micromol/L, the inhibitory effect was in a concentration dependent manner. After treatment with 4.0 micromol/L GNA for 48 h, apoptosis was obviously observed as assayed by Annexin V-FITC/PI staining. Importantly, MMP was decreased and ROS formation was increased following GNA treatment. Additionally, P53 expression was up-regulated following 4.0 micromol/ L GNA treatment in a time dependent manner.

CONCLUSION:

GNA induces mitochondria-dependent apoptosis and increases P53 expression in human gastric carcinoma cell line.

• Authors: Xun-cui Wang, Guo-qi Zhu, Hui Cheng, Qing-lin Li
• Journal: Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials (Zhong Yao Cai) Vol. 37 Issue 1 Pg. 95-9 (Jan 2014) ISSN: 1001-4454 [Print] China
• PMID: 25090714 (Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents
• Reactive Oxygen Species
• Tumor Suppressor Protein p53
• Xanthenes
• neo-gambogic acid

Topics

• Antineoplastic Agents (pharmacology)
• Apoptosis (drug effects)
• Blotting, Western
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cell Survival (drug effects)
• Dose-Response Relationship, Drug
• Flow Cytometry
• Garcinia (chemistry)
• Humans
• Membrane Potential, Mitochondrial (drug effects)
• Mitochondria (drug effects, metabolism)
• Reactive Oxygen Species (metabolism)
• Signal Transduction (drug effects)
• Stomach Neoplasms (metabolism, pathology)
• Tumor Suppressor Protein p53 (metabolism)
• Xanthenes (pharmacology)