ArticleJournal of neuroinflammation2020
Farnesoid X receptor knockout protects brain against ischemic injury through reducing neuronal apoptosis in mice.
Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- GFH312 Reduces Neuronal Death by Inhibiting RIPK1-Mediated Apoptosis and Necroptosis After Ischemic Stroke.CNS neuroscience & therapeutics · 2026Article
- Microbiota-gut-brain axis and bile acids-driven neuromodulation.Neural regeneration research · 2026Article
- Discovery of sulfonyl benzoic acid derivatives with joint TGR5-agonist and FXR-antagonist activity for myocardial ischemia/reperfusion injury protection.Acta pharmaceutica Sinica. B · 2026Article
- Sortilin is Associated with PGRN-Mediated Endoplasmic Reticulum Stress and Activation of Microglia in a Rat Model of Degenerative Cervical Myelopathy.Neuromolecular medicine · 2026Article
- Bile acid signaling, metabolism, and aging.Liver research (Beijing, China) · 2026Review
- Gut-Brain Axis and Bile Acid Signaling: Linking Microbial Metabolism to Brain Function and Metabolic Regulation.International journal of molecular sciences · 2025Review
- Dietary cholesterol impairs cognition via gut microbiota-derived deoxycholic acid in obese mice.Gut microbes · 2025Article
- Emerging Roles of Bile Acids in Neuroinflammation.International journal of molecular sciences · 2025Review
- Review
- Piezo1 disrupts blood-brain barrier via CaMKII/Nrf2 in ischemic stroke.Cellular and molecular life sciences : CMLS · 2025Article
- The gut microbiota-bile acid axis: a crucial regulator of immune function and metabolic health.World journal of microbiology & biotechnology · 2025Review
- The role of the farnesoid X receptor in diabetes and its complications.Molecular and cellular biochemistry · 2025Review
- Sulfated chitosan directs the recovery of ischemic stroke by attenuating the inflammatory cascade.Theranostics · 2025Article
- Inhibition of OGFOD1 by FG4592 confers neuroprotection by activating unfolded protein response and autophagy after ischemic stroke.Journal of translational medicine · 2024Article
- Dapoxetine prevents neuronal damage and improves functional outcomes in a model of ischemic stroke through the modulation of inflammation and oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The contributions of bacteria metabolites to the development of hepatic encephalopathy.Liver research (Beijing, China) · 2023Article
- Four-parameter analysis in modified Rotarod test for detecting minor motor deficits in mice.BMC biology · 2023Article
- Liver's influence on the brain through the action of bile acids.Frontiers in neuroscience · 2023Review
- Linking Nonalcoholic Fatty Liver Disease and Brain Disease: Focusing on Bile Acid Signaling.International journal of molecular sciences · 2022Review
- Blocking C3dAging and disease · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFarnesoid X receptor (FXR) is a nuclear receptor that plays a critical role in controlling cell apoptosis in diverse diseases. Previous studies have shown that knocking out FXR improved cardiac function by reducing cardiomyocyte apoptosis in myocardial ischemic mice. However, the role of FXR after cerebral ischemia remains unknown. In this study, we explored the effects and mechanisms of FXR knockout (KO) on the functional recovery of mice post cerebral ischemia-reperfusion.
methodsAdult male C57BL/6 wild type and FXR KO mice were subjected to 90-min transient middle cerebral artery occlusion (tMCAO). The mice were divided into five groups: sham, wild-type tMCAO, FXR KO tMCAO, wild-type tMCAO treated with calcium agonist Bayk8644, and FXR KO tMCAO treated with Bayk8644. FXR expression was examined using immunohistochemistry and Western blot. Brain infarct and brain atrophy volume were examined at 3 and 14 days after stroke respectively. Neurobehavioral tests were conducted up to 14 days after stroke. The protein levels of apoptotic factors (Bcl-2, Bax, and Cleaved caspase-3) and mRNA levels of pro-inflammatory factors (TNF-α, IL-6, IL-1β, IL-17, and IL-18) were examined using Western blot and RT-PCR. TUNEL staining and calcium imaging were obtained using confocal and two-photon microscopy.
resultsThe expression of FXR was upregulated after ischemic stroke, which is located in the nucleus of the neurons. FXR KO was found to reduce infarct volume and promote neurobehavioral recovery following tMCAO compared to the vehicle. The expression of apoptotic and pro-inflammatory factors decreased in FXR KO mice compared to the control. The number of NeuN
conclusionsFXR KO can promote neurobehavioral recovery and attenuate ischemic brain injury, inflammatory release, and neuronal apoptosis via reducing calcium influx, suggesting its role as a therapeutic target for stroke treatments.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.