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Apigenin induces the apoptosis and regulates MAPK signaling pathways in mouse macrophage ANA-1 cells

Yuexia Liao1, Weigan Shen2, Guimei Kong1

  • 1Department of Chinese Medicine Integrated with Western Medicine, Yangzhou University School of Medicine, Yangzhou, P.R. China.

Plos One
|March 21, 2014
PubMed

Insights

Apigenin, a plant flavonoid, triggers apoptosis in mouse macrophages by increasing reactive oxygen species (ROS) and modulating the MAPK pathway. This research highlights apigenin

Area of Science:

  • Cell Biology
  • Biochemistry
  • Immunology

Background:

  • Apigenin is a natural flavonoid with known antioxidant, anti-cancer, and anti-inflammatory effects.
  • Limited research exists on apigenin's capacity to induce apoptosis specifically in macrophages.

Purpose of the Study:

  • To investigate the effect of apigenin on apoptosis induction in mouse macrophage ANA-1 cells.
  • To elucidate the underlying mechanisms, including reactive oxygen species (ROS) generation and MAPK pathway involvement.

Main Methods:

  • Cell viability assessed using MTT assay.
  • Apoptosis analyzed via flow cytometry, TUNEL assay, and DNA laddering.
  • Intracellular ROS levels measured with a dichlorofluorescein-diacetate probe.
  • Apoptosis-related protein expression (Bcl-2, caspases, MAPK pathway proteins) determined by western blot.

Main Results:

  • Apigenin reduced ANA-1 cell viability and induced apoptosis in a dose- and time-dependent manner.
  • Apigenin increased intracellular ROS, downregulated Bcl-2, and upregulated caspase-3 and caspase-8 expression.
  • Apigenin modulated MAPK signaling by downregulating phospho-ERK/JNK and upregulating phospho-p38.

Conclusions:

  • Apigenin induces apoptosis in mouse macrophages.
  • The mechanism involves increased intracellular ROS and MAPK pathway regulation.
  • Apigenin's effects are linked to Bcl-2 inhibition, suggesting a role in programmed cell death.

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