Deans' stroke musings: Targeting the NLRP3-ROS Axis: Disrupting the Oxidative-Inflammatory Vicious Cycle in Intracerebral Hemorrhage

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, October 31, 2025

Targeting the NLRP3-ROS Axis: Disrupting the Oxidative-Inflammatory Vicious Cycle in Intracerebral Hemorrhage

Didn't your competent? doctor create a solution for this problem years ago?

oxidative stress (8 posts to November 2013)

Targeting the NLRP3-ROS Axis: Disrupting the Oxidative-Inflammatory Vicious Cycle in Intracerebral Hemorrhage

Authors Cao L , Pi W, Zhang Y, Zheng C, Yong VW, Xue M

Received 22 March 2025

Accepted for publication 13 July 2025

Published 24 July 2025 Volume 2025:18 Pages 9849—9870

DOI https://doi.org/10.2147/JIR.S529884

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Dr Adam Bachstetter

Liang Cao Journal of Inflammation Research downloaded from https://www.dovepress.com/ For personal use only. 1,2, Wenjun Pi3, Yi Zhang4, Chunfu Zheng5, Voon Wee Yong6, Mengzhou Xue1,2

1 Department of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People’s Republic of China;

2 Henan International Joint Laboratory of Intracerebral Hemorrhage and Brain Injury, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, People’s Republic of China;

3 Department of Traumatic Orthopedics, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, People’s Republic of China;

4 Office of Research, Shunyi Maternal and Children’s Hospital of Beijing Children’s Hospital, Beijing, People’s Republic of China;

5 Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada;

6 Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada Correspondence: Voon Wee Yong; Mengzhou Xue,

Email vyong@ucalgary.ca; xuemengzhou@zzu.edu.cn

Abstract:

Intracerebral hemorrhage (ICH) is a highly fatal disease that currently lacks effective treatment options. However, secondary brain injury has become a key focus in translational research, with oxidative stress (OS) identified as a central factor in ICH pathophysiology. Following ICH, hematoma components and inflammatory factors overwhelm the antioxidant defense system, triggering OS. Concurrently, neuroinflammation arises, driven by activated microglia that adopt a pro-inflammatory phenotype and release cytokines and chemokines. While neuroinflammation may support repair, it can also cause harmful secondary damage. Recent evidence indicates that NLRP3 is an important inflammasome considered a key player in OS and neuroinflammation. OS can activate the NLRP3 inflammasome by producing reactive oxygen species (ROS), further exacerbating the inflammatory response. Additionally, NLRP3 also plays an important role in regulating neuroinflammation. The activation of the NLRP3 inflammasome promotes the release of pro-inflammatory cytokines, further intensifying the neuroinflammatory response. The activation of NLRP3 is closely related to the polarization of microglia, potentially driving microglia to polarize towards the M1 type (pro-inflammatory), thereby exacerbating neuroinflammation. Therefore, we hypothesize that NLRP3 plays a critical regulatory role in OS and neuroinflammation following ICH. This review summarizes the regulatory role of the NLRP3 inflammasome in the interplay between OS and neuroinflammation, as well as its potential therapeutic targets related to ICH.