Related Experiment Video

Updated: Sep 29, 2026

A Standardized Protocol for Inducing Stress-Induced Premature Senescence in Primary Human Melanocytes Using Tert-butyl Hydroperoxide
08:17

A Standardized Protocol for Inducing Stress-Induced Premature Senescence in Primary Human Melanocytes Using Tert-butyl Hydroperoxide

Published on: May 29, 2026

Melatonin suppresses NO-induced apoptosis via induction of Bcl-2 expression in PGT-beta immortalized pineal cells

Yeong-Min Yoo1, Sung-Vin Yim, Sung-Soo Kim

  • 1Department of Biology, College of Natural Science, Kangwon National University, Chunchon, South Korea.

Journal of Pineal Research
|September 11, 2002
PubMed

Insights

Melatonin prevents nitric oxide (NO)-induced cell death in pineal cells. This protective effect involves upregulating Bcl-2 expression, blocking caspase activation, and inhibiting cytochrome c release.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Neuroendocrinology

Background:

  • Nitric oxide (NO) is implicated in cellular apoptosis.
  • Melatonin is a hormone with known antioxidant and anti-apoptotic properties.
  • Understanding melatonin's protective mechanisms against NO-induced cell death is crucial.

Purpose of the Study:

  • To investigate the protective effect of melatonin against nitric oxide (NO)-induced apoptosis in PGT-beta immortalized pineal cells.
  • To elucidate the molecular mechanisms underlying melatonin's anti-apoptotic action.

Main Methods:

  • Cytotoxicity assays and DNA fragmentation analysis were used to assess cell viability and apoptosis.
  • Caspase-3 activity assays and Western blotting were performed to evaluate apoptosis markers.
  • Western blot analysis for Bcl-2 expression and cytochrome c release was conducted to explore protective pathways.

Main Results:

  • S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, induced dose-dependent apoptotic cell death.
  • Melatonin pretreatment (0.1 mm) attenuated NO-induced apoptosis, DNA fragmentation, and caspase-3 activity.
  • Melatonin suppressed the activation of caspase-3 and poly(ADP-ribose) polymerase (PARP).
  • Melatonin upregulated Bcl-2 expression and inhibited cytochrome c release into the cytosol.

Conclusions:

  • Melatonin exhibits a significant anti-apoptotic effect against NO-induced cell death in PGT-beta cells.
  • The protective mechanism involves the induction of Bcl-2 expression, which subsequently inhibits caspase-3 activation and cytochrome c release.

More Related Videos

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption12:02

Human Primary Trophoblast Cell Culture Model to Study the Protective Effects of Melatonin Against Hypoxia/reoxygenation-induced Disruption

Published on: July 30, 2016

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...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...