The possible role of miR-194-5p in brain and neurodegenerative diseases has been reported, but its role in intracerebral hemorrhage (ICH) has not been studied. This study estimated the mechanism of miR-194-5p in ICH. ICH rat model was established by injecting collagenase type VII. miR-194-5p expression in brain tissue of ICH rats was overexpressed by injection of miR-194-5p agomir. Then neurological function score and brain water content were measured. The morphological changes of brain tissue and neuronal apoptosis were evaluated by histological staining. Levels of NLRP3 inflammasomes, IL-1β and IL-18 were measured. The target relation between miR-194-5p and TRAF6 was verified and the binding of TRAF6 to NLRP3 was explored. miR-194-5p was decreased in ICH rats. After overexpression of miR-194-5p, the neuropathological injury in ICH rats was significantly reduced, and NLRP3-mediated inflammatory injury was inhibited. miR-194-5p targeted TRAF6. TRAF6 interacted with NLRP3 to promote the activation of NLRP3 inflammasomes. Overexpression of miR-194-5p reduced the interaction between TRAF6 and NLRP3, thereby alleviating the neuroinflammation. Collectively, overexpression of miR-194-5p reduced the TRAF6/NLRP3 interaction, thus inhibiting the activation of NLRP3 inflammasomes and reducing neuroinflammation during ICH. This study may shed new light on ICH treatment.
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http://dx.doi.org/10.1016/j.brainres.2020.147228 | DOI Listing |
EXCLI J
November 2024
Department of Life Sciences, Faculty of Science and Engineering, Manchester Metropolitan University, Manchester M1 5GD, UK.
Farnesol (FAR) is a sesquiterpene alcohol that exists in many fruits and vegetables and possesses promising anti-inflammatory and antioxidant activities. Cadmium (Cd) is an environmental pollutant known for its serious health effects. Liver injury associated with oxidative stress is a hazardous consequence of exposure to Cd.
View Article and Find Full Text PDFAs a key inflammatory factor, the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome plays a crucial role in neuroinflammation and the progression of neurodegenerative diseases. Dysregulation of NLRP3 signaling can trigger various inflammatory responses in the brain, contributing to the development of neurodegenerative diseases such as ischemic stroke, vascular dementia (VaD), Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Therefore, the NLRP3 signaling pathway is a promising therapeutic target for the treatment of neurodegenerative diseases, including VaD.
View Article and Find Full Text PDFCardiovasc Diabetol
January 2025
Department of Clinical Pharmacy, School of Preclinical Medicine and Clinical Pharmacy, China Pharmaceutical University, 24 Tong jia Lane, Nanjing, 210009, People's Republic of China.
Background: Inflammatory diseases impair the reparative properties of endothelial progenitor cells (EPC); however, the involvement of diabetes in EPC dysfunction associated with myocardial infarction (MI) remains unknown.
Methods: A model was established combining high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic mice with myocardial infarction. The therapeutic effects of transplanted wild-type EPC, Nlrp3 knockout EPC, and Nlrp3 overexpression EPC were evaluated.
Cell Commun Signal
January 2025
Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Background: Macrophages play a crucial role in chronic gastritis induced by the pathogenic Helicobacter pylori (H. pylori) infection. NLRP3 inflammasome has emerged as an important component of inflammatory processes.
View Article and Find Full Text PDFImmunopharmacol Immunotoxicol
January 2025
Tobacco and Health Research Center, Endocrinology and Metabolism Research Center, Molecular Medicine Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
Traumatic brain injury (TBI) precipitates a neuroinflammatory cascade, with the NLRP3 inflammasome emerging as a critical mediator. This review scrutinizes the complex activation pathways of the NLRP3 inflammasome by underscoring the intricate interplay between calcium signaling, mitochondrial disturbances, redox imbalances, lysosomal integrity, and autophagy. It is hypothesized that a combination therapy approach-integrating NF-κB pathway inhibitors with NLRP3 inflammasome antagonists-holds the potential to synergistically dampen the inflammatory storm associated with TBI.
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