Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...

Neurogenesis and Regeneration of Nervous Tissue

Neurogenesis and Regeneration of Nervous Tissue

In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Plasma exosome-derived miRNA-887-5p alleviates high glucose- and lipid-induced endothelial cell dysfunction.

Nutrition & diabetes·2026

Same author

Reliability-aware modality completion with cross-modal distillation for federated learning with missing modalities.

Neural networks : the official journal of the International Neural Network Society·2026

Same author

The Role of Nuclear Factor Erythroid 2-Related Factor 2 in the Crosstalk Between Oxidative Stress and M1/M2 Microglial Polarization Following Ischemic Stroke.

Molecular neurobiology·2026

Same author

Mechanistic insights into aroma aging of ripened Pu-erh tea during long-term storage.

Food chemistry·2026

Same author

Total flavones of Rhododendron protect against BBB injury following cerebral ischemia/reperfusion via promoting astrocytic polarization towards A2 subtype.

Apoptosis : an international journal on programmed cell death·2026

Same author

Nox4 mediates chondrocyte senescence and cartilage degradation in post-traumatic osteoarthritis via the ROS/p38MAPK signaling pathway.

International immunopharmacology·2026

Same journal

Inflammation Impairs Poststroke Recovery by Disrupting Iron Homeostasis in Brain.

Antioxidants & redox signaling·2026

Same journal

Histone Lactylation Links Glycolysis to Ferroptosis in Diabetic Cataract.

Antioxidants & redox signaling·2026

Same journal

Insights into the Multifaceted Roles of 3-Mercaptopyruvate Sulfurtransferase in Liver Diseases.

Antioxidants & redox signaling·2026

Same journal

NINJ1 Aggravates Doxorubicin-Induced Cardiotoxicity by Suppressing AMPK-Mediated HIF-1α Deubiquitination.

Antioxidants & redox signaling·2026

Same journal

<i>Corrigendum to:</i> Suppression of Cardiac Autophagy by Hyperinsulinemia in Insulin Receptor-Deficient Hearts Is Mediated by Insulin-Like Growth Factor Receptor Signaling.

Antioxidants & redox signaling·2026

Same journal

Sleeve Gastrectomy Is Associated with Improved Systemic Redox Homeostasis in T2DM Through Ghrelin-GHSR Attenuation, POMC Neuronal Modulation, and CD4<sup>+</sup> T Cell Metabolic Reprogramming.

Antioxidants & redox signaling·2026

See all related articles

Search research articles

Related Experiment Video

Updated: May 8, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

ROCK Inhibition Reprograms Microglial Polarization to Promote Neuroprotection via NOX2/ROS/TXNIP Suppression.

Ziyu Wang¹, Xin Xu¹, Leshu Wang¹

¹Department of Pharmacology, School of Pharmacy, Anhui Medical University, Hefei, China.

Antioxidants & Redox Signaling

|May 6, 2026

Summary

This summary is machine-generated.

Rho-associated protein kinase (ROCK) inhibition shifts harmful M1 microglia to beneficial M2 types, reducing brain injury. This occurs by suppressing the NF-κB/NOX2/ROS/TXNIP pathway, offering a novel therapeutic target for stroke.

Keywords:

M2 microglia NOX2 ROCK inhibition TXNIP cerebral I/R

More Related Videos

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

Related Experiment Videos

Last Updated: May 8, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

Area of Science:

Neuroscience
Cell Biology
Biochemistry

Background:

Cerebral ischemia/reperfusion (I/R) injury is a major complication of stroke treatment.
Microglial polarization (M1/M2 balance) critically influences neuroinflammation and I/R injury.
Rho-associated protein kinase (ROCK) inhibition shows promise in mitigating I/R injury, but its effect on microglial polarization is unclear.

Purpose of the Study:

To investigate the role and mechanism of ROCK inhibition in regulating M1 and M2 microglial polarization.
To elucidate how ROCK inhibition influences neuroinflammation and cerebral I/R injury.
To utilize fluoxetine as a positive control for ROCK inhibition effects.

Main Methods:

In vivo and in vitro models of cerebral I/R injury.
Assessment of microglial polarization markers (M1/M2 phenotypes).
Analysis of key signaling pathway components: ROCK2, NF-κB, NOX2, ROS, and TXNIP.
Pharmacological inhibition and knockdown strategies were employed.

Main Results:

ROCK inhibition (fasudil) and fluoxetine alleviated cerebral I/R injury and promoted M2 microglial polarization.
ROCK2 knockdown suppressed M1 markers, reduced NOX2 and TXNIP expression, and inhibited NF-κB activation.
Inhibition of NF-κB, NOX2, or ROS production led to decreased NOX2, TXNIP expression, and ROS generation.

Conclusions:

ROCK inhibition promotes a shift from M1 to M2 microglial polarization.
This shift is mediated by the suppression of the NF-κB/NOX2/ROS/TXNIP signaling pathway.
This study reveals a novel mechanism for ROCK inhibition in neuroprotection and microglial regulation.