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Updated: Feb 14, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
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Ampelopsin sodium induces mitochondrial-mediated apoptosis in human lung adenocarcinoma SPC-A-1 cell line

Jun-Feng Jiang, Jing Zhai, Zhou-Ru-Jun Liu

    Die Pharmazie
    |February 15, 2018
    PubMed

    Insights

    Ampelopsin sodium effectively inhibits lung cancer cell growth by inducing apoptosis. This compound alters mitochondrial function, including calcium levels and membrane potential, suggesting its therapeutic potential for lung cancer treatment.

    Area of Science:

    • Biochemistry
    • Molecular Biology
    • Pharmacology

    Background:

    • Ampelopsin is a flavonoid with known anticancer properties, including apoptosis induction.
    • Lung adenocarcinoma is a significant cause of cancer mortality worldwide.

    Purpose of the Study:

    • To investigate the role of ampelopsin sodium (Amp-Na) in mitochondrial-mediated apoptosis of human lung adenocarcinoma SPC-A-1 cells.
    • To elucidate the mechanism of action of Amp-Na in inducing apoptosis.

    Main Methods:

    • Cell proliferation assays and ultrastructural analysis were performed.
    • Mitochondrial membrane potential (Δψm), intracellular calcium (Ca2+) concentration, mitochondrial nitric oxide (NO) levels, and total ATPase activity were measured.

    Main Results:

    • Amp-Na significantly inhibited SPC-A-1 cell proliferation in a dose-dependent manner.
    • Amp-Na induced apoptosis characterized by ultrastructural changes.
    • Amp-Na caused increased Ca2+ levels, reduced Δψm, elevated mitochondrial NO production, and decreased total ATPase activity.

    Conclusions:

    • Amp-Na demonstrates potential as a therapeutic agent for lung cancer.
    • The findings provide new insights into the mechanism by which Amp-Na induces mitochondrial-mediated apoptosis in tumor cells.

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