Related Experiment Video

Updated: May 22, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Apamin inhibits THP-1-derived macrophage apoptosis via mitochondria-related apoptotic pathway

Soo-Jung Kim1, Ji-Hyun Park, Kyung-Hyun Kim

  • 1Department of Pathology, College of Medicine, Catholic University of Daegu, 3056-6, Daemyung 4-Dong, Nam-gu, Daegu 705-718, South Korea.

Experimental and Molecular Pathology
|April 28, 2012
PubMed

Insights

Apamin, a bee venom component, reduces macrophage death and lipid buildup, offering a potential treatment for atherosclerosis. This study shows apamin

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pharmacology

Background:

  • Atherosclerotic lesion development is primarily driven by macrophage death.
  • Oxidative stress in monocytes/macrophages is crucial for atherosclerosis initiation and progression.
  • Apamin, from bee venom, has anti-inflammatory properties and inhibits Ca(2+)-activated K(+) channels.

Purpose of the Study:

  • To investigate the effects of apamin on macrophage apoptosis and lipid deposition.
  • To elucidate the mechanisms by which apamin influences the mitochondria-related apoptotic pathway in macrophages.

Main Methods:

  • THP-1 derived macrophages were treated with oxidized low-density lipoprotein (oxLDL) and apamin.
  • Oil-red O staining was used to assess intracellular lipid deposition.
  • Gene and protein expression of apoptosis-related factors (Bax, caspase-3, PARP, Bcl-2, Bcl-xL) were analyzed.
  • In vivo studies utilized TUNEL staining to evaluate apoptotic cell death.

Main Results:

  • Apamin significantly inhibited intracellular lipid deposition in macrophages.
  • Apamin treatment decreased the number of apoptotic macrophages by modulating pro-apoptotic (Bax, caspase-3, PARP) and anti-apoptotic (Bcl-2, Bcl-xL) gene/protein expression.
  • In vivo TUNEL staining confirmed reduced apoptotic cell death with apamin treatment.

Conclusions:

  • Apamin plays a significant role in regulating monocyte/macrophage apoptosis.
  • Apamin demonstrates potential as a therapeutic agent for preventing atherosclerosis by reducing macrophage apoptosis and lipid accumulation.

More Related Videos

Highly Efficient Transfection of Human THP-1 Macrophages by Nucleofection07:54

Highly Efficient Transfection of Human THP-1 Macrophages by Nucleofection

Published on: September 2, 2014

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...