Related Experiment Video

Updated: Nov 17, 2025

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.4K

Apelin-36 Protects HT22 Cells Against Oxygen-Glucose Deprivation/Reperfusion-Induced Oxidative Stress and

Ziqi Shao1, Shanshan Dou2, Junge Zhu3

  • 1Cheeloo College of Medicine, Shandong University, Jinan, 250014, China.

Neurotoxicity Research
|February 13, 2021
PubMed

Insights

Apelin-36 protects against cerebral ischemia/reperfusion (I/R) injury by reducing oxidative stress and mitochondrial dysfunction. It activates SIRT1-mediated mitophagy, offering neuroprotection in neuronal apoptosis models.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Cerebral ischemia/reperfusion (I/R) injury involves oxidative stress, mitochondrial dysfunction, and neuronal apoptosis.
  • Mitophagy is crucial for clearing damaged mitochondria.
  • Apelin-36, a neuropeptide, shows potential in protecting against cerebral I/R injury, but its mechanisms require clarification.

Purpose of the Study:

  • To investigate the effects of Apelin-36 on oxidative stress and mitochondrial dysfunction in cerebral I/R injury.
  • To elucidate the role of mitophagy and the SIRT1 pathway in Apelin-36's neuroprotective effects.

Main Methods:

  • Established an oxygen-glucose deprivation/reperfusion (OGD/R) model in HT22 cells.
  • Assessed cell viability, apoptosis, reactive oxygen species (ROS), malondialdehyde (MDA), antioxidant enzymes (SOD, GSH), mitochondrial membrane potential (MMP), and apoptosis-related proteins (Bcl-2, Bax, Cytochrome c, Caspases).
  • Investigated mitophagy markers (p62, LC3B-II, Beclin1) and the involvement of SIRT1, PINK1, and Parkin, using specific inhibitors (EX527, CsA).

Main Results:

  • Apelin-36 improved cell viability, reduced apoptosis, and modulated Bcl-2/Bax ratio in OGD/R-injured cells.
  • Apelin-36 inhibited oxidative stress by decreasing ROS and MDA levels and iNOS expression, while increasing SOD and GSH.
  • Apelin-36 preserved mitochondrial function, evidenced by increased MMP and reduced levels of Cytochrome c, Cleaved caspase-9, and Cleaved caspase-3.
  • Apelin-36 activated SIRT1-mediated PINK1/Parkin-dependent mitophagy, indicated by altered p62, LC3B-II, and Beclin1 levels.
  • Inhibitors of SIRT1 (EX527) and mitophagy (CsA) reversed the protective effects of Apelin-36 on oxidative stress and mitochondrial dysfunction.

Conclusions:

  • Apelin-36 exerts neuroprotective effects against OGD/R-induced injury by mitigating oxidative stress and mitochondrial dysfunction.
  • The protective mechanism involves the activation of SIRT1-mediated PINK1/Parkin-dependent mitophagy.
  • Apelin-36 represents a potential therapeutic agent for cerebral I/R injury.
Keywords:
Apelin-36Mitochondrial dysfunctionMitophagyOxidative stressOxygen-glucose deprivation/reperfusion injury

More Related Videos

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease15:09

The Use of Primary Human Fibroblasts for Monitoring Mitochondrial Phenotypes in the Field of Parkinson's Disease

Published on: October 3, 2012

17.1K
Author Spotlight: Fluorescence-Based Quantification of Mitochondrial Membrane Potential and Superoxide Levels Using Live Imaging in HeLa Cells06:57

Author Spotlight: Fluorescence-Based Quantification of Mitochondrial Membrane Potential and Superoxide Levels Using Live Imaging in HeLa Cells

Published on: May 12, 2023

8.7K

Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
16.9K
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...
7.4K