Dexmedetomidine Protects the Brain: Exploring the α2AR/FAK Pathway in Post-Stroke Intestinal Barrier Repair

Frontiers in Bioscience-Landmark, Journal Year: 2025, Volume and Issue: 30(2)

Published: Feb. 20, 2025

Introduction: Globally, ischemic stroke is a major cause of mortality and disability, posing significant challenge in clinical practice public health. Recent studies have reported that leads to the impairment intestinal barrier migration bacteria multiple organs. This process exacerbates neurological damage by further impairing function leading bacterial translocation. Dexmedetomidine (Dex), an α2-adrenoceptor (α2AR) agonist, has proven anti-cerebral effects, yet its effects post-stroke dysfunction remain unclear. study aimed determine whether Dex mitigates brain injury following cerebral ischemia-reperfusion. Methods: A C57BL/6J mouse model middle artery occlusion (MCAO) was used for vivo experiments, while lipopolysaccharide (LPS)-induced Caco-2 monolayers served as vitro dysfunction. Neuronal apoptosis evaluated using neuronal nuclei (NeuN) terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) double labeling. Reverse transcription-quantitative PCR (RT-qPCR) performed measure pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6. Intestinal permeability assessed histological score, serum fluorescein isothiocyanate (FITC)-dextran fluorescence, endotoxin levels. The expression levels epithelial cadherin (E-cadherin), zonula occludens-1 (ZO-1), occludin were analyzed western blot immunofluorescence. Statistical analyses included analysis variance with Tukey’s post-hoc test. Results: treatment significantly reduced infarct volume (p < 0.001) improved scores compared MCAO controls. inhibited 0.01), evidenced TUNEL-positive cells Dex-treatment mice. TNF-α, IL-1β IL-6 markedly downregulated 0.05). While increased (elevated FITC-dextran levels, p restored integrity. upregulated E-cadherin 0.05) but did not restore decreased ZO-1 MCAO. promoted repair alleviated via α2AR/focal adhesion kinase (FAK) pathway Similarly, mitigated LPS-induced restoring FAK improving Conclusions: alleviates injury, possibly through activating α2AR/FAK pathway. These findings underscore potential therapeutic strategy addressing secondary complications patient outcomes.

Language: Английский

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Gastric-filling ultrasonography to evaluate gastric motor function in patients long-term bedridden undergoing stroke

Frontiers in Physiology, Journal Year: 2025, Volume and Issue: 16

Published: March 4, 2025

Objectives Gastric motor dysfunction is a common symptom in patients with stroke, yet lacks objective evaluation methods. This study aimed to assess the feasibility of using gastric filling ultrasonography evaluate function undergoing and explore relationship between ultrasound indicators clinical features. Methods We conducted case-control where all participants underwent 60-minute examination after consuming 300 mL test meal. The cross-sectional area (CSA) antrum was measured at four-time points: fasting for six eight hours (T0), immediately meal (T1), 30 (T30) 60 (T60) minutes. Using CSA, we calculated emptying rate (GER) T30 T60 (GER30, GER60). Additionally, frequency (ACF) amplitude (ACA) antral contractions, as well index (MI). compared these parameters two groups evaluated their correlation features such bed rest time, consciousness level, albumin or hemoglobin levels. Results recruited 37 stroke 31 healthy controls. Stroke exhibited lower GER controls, particularly evident T30. showed significantly reduced ACA, ACF, MI T1 T30, ACA being only measure showing statistical differences T60. Correlation analysis revealed negative associations GER30, GER60, time. For predicting anemia, GER30 had cut-off 31.52 (88% specificity, 50% sensitivity), while ’s 23.64 (76% 75% sensitivity). Conclusion Ultrasound measurement shows promise valuable screening tool detecting stroke.

Language: Английский

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Remote Organ Damage Induced by Stroke: Molecular Mechanisms and Comprehensive Interventions

Antioxidants and Redox Signaling, Journal Year: 2025, Volume and Issue: unknown

Published: April 2, 2025

Significance: Damage after stroke is not only limited to the brain but also often occurs in remote organs, including heart, lung, liver, kidney, digestive tract, and spleen, which are frequently affected by complex pathophysiological changes. The organs human body closely connected, signals transmitted through various molecular substances could regulate changes of organs. Recent Advances: latest studies have shown that inflammatory response plays an important role organ damage stroke, can aggravate activating oxidative stress, sympathetic axis, hypothalamic disturbing immunological homeostasis. Remote cause brain, aggravating damage. Critical Issues: Therefore, in-depth exploration mechanisms adopting corresponding comprehensive intervention strategies become necessary reduce promote protection. Future Directions: strategy involves multifaceted treatment methods such as inflammation regulation, antioxidants, neural stem cell differentiation. It provides a promising alternative for recovery patients inspiration future research treatment. interconnected at level. Only levels we save protect greatest extent. Antioxid. Redox Signal. 00, 000-000.

Language: Английский

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Indole lactic acid derived from Akkermansia muciniphila activates the aryl hydrocarbon receptor to inhibit ferroptosis in ischemic stroke

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

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The Role of Oxidative Stress in Ischaemic Stroke and the Influence of Gut Microbiota

Antioxidants, Journal Year: 2025, Volume and Issue: 14(5), P. 542 - 542

Published: April 30, 2025

Ischaemic stroke is the most prevalent subtype, accounting for 80–90% of all cases worldwide, and remains a leading cause morbidity mortality. Its pathophysiology involves complex molecular cascades, with oxidative stress playing central role. During cerebral ischaemia, reduced blood flow deprives neurons essential oxygen nutrients, triggering excitotoxicity, mitochondrial dysfunction, excessive production reactive nitrogen species (RONS). Not only do these damage cellular components, but they also activate inflammatory pathways, particularly those mediated by transcription factor nuclear kappa-B (NF-κB). The pro-inflammatory milieu intensifies neuronal damage, compromises blood–brain barrier integrity, exacerbates reperfusion-induced damage. Recent findings highlight importance gut microbiota in modulating outcomes, primarily through metabolic immunological interactions along gut–brain axis. Dysbiosis, characterised microbial diversity an imbalance between beneficial harmful strains, has been linked to increased systemic inflammation, stress, worse prognoses. Specific gut-derived metabolites, including short-chain fatty acids (SCFAs) trimethylamine N-oxide (TMAO), appear either mitigate or intensify injury. SCFAs may strengthen temper responses, whereas elevated TMAO levels increase thrombotic risk. This narrative review consolidates both experimental clinical data demonstrating role ischaemic explores microbiota’s ability modulate damaging processes. Therapeutic strategies targeting pathways rebalancing composition, such as antioxidant supplementation, dietary modulation, probiotics, faecal transplantation, present promising paradigms intervention. However, their widespread implementation hindered lack large-scale, randomised trials. Future efforts should employ multidisciplinary approach elucidate intricate mechanisms linking dysbiosis stroke, thereby paving way novel, mechanism-based therapies improved patient outcomes.

Language: Английский

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Risk factors for stroke-related pneumonia in patients with ischaemic stroke: a systematic evaluation and meta-analysis

Clinical Neurology and Neurosurgery, Journal Year: 2024, Volume and Issue: 246, P. 108593 - 108593

Published: Oct. 12, 2024

Language: Английский

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