Ampelopsin sodium induces mitochondrial-mediated apoptosis in human lung adenocarcinoma SPC-A-1 cell line.

Abstract

Ampelopsin is a well-known flavonoid which has variety of biological and pharmacological actions including anticancer effects and induction of apoptosis on the several cancer cell lines. The present study aimed to evaluate the role of ampelopsin sodium (Amp-Na) in the mitochondrial-mediated apoptosis of human lung adenocarcionma SPC-A-1 cells. The analysis of cell proliferation and ultrastructure were performed. Furthermore, to clarify its action mechanism by determining the mitochondrial membrane potential (Δψm), intracellular calcium (Ca2+) concentration, mitochondrial nitric oxide (NO) level and total ATPase activity. The results showed that Amp-Na markedly inhibited the SPC-A-1 cell proliferation and caused ultrastructural apoptosis feature in SPC-A-1 cells in a dose-dependent manner. Amp-Na led to a rapid and sustained Ca2+ elevation and Δψm reduction, and induced the mitochondrial NO production and decreased the total ATPase activity in SPC-A-1 cells. The results enhance the potential of Amp-Na as a therapeutic drug for treating lung cancer, and provide new information for mechanism of Amp-Na which induces mitochondrial-mediated apoptosis in tumor cells.

• Authors: Jun-Feng Jiang, Jing Zhai, Zhou-Ru-Jun Liu, Li Chao, Yun-Feng Zhao, Yong-Jie Wu, Ming-Xia Cui
• Journal: Die Pharmazie (Pharmazie) Vol. 71 Issue 8 Pg. 455-459 (08 01 2016) ISSN: 0031-7144 [Print] Germany
• PMID: 29442032 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antineoplastic Agents, Phytogenic
• Flavonoids
• ampelopsin
• Adenosine Triphosphatases
• Calcium

Topics

• Adenocarcinoma (drug therapy, pathology, ultrastructure)
• Adenocarcinoma of Lung
• Adenosine Triphosphatases (metabolism)
• Antineoplastic Agents, Phytogenic (pharmacology)
• Apoptosis (drug effects)
• Calcium (metabolism)
• Cell Line, Tumor
• Cell Proliferation
• Dose-Response Relationship, Drug
• Flavonoids (pharmacology)
• Humans
• Lung Neoplasms (drug therapy, pathology, ultrastructure)
• Membrane Potential, Mitochondrial (drug effects)
• Mitochondria (drug effects)