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A serious neurosurgical emergency, subarachnoid hemorrhage (SAH) is characterized by vascular and neuropathy, as well as complex pathological mechanisms like vascular lesions, inflammatory responses, and nerve cell damage. The inflammatory response is an essential aspect of SAH's pathophysiology, causing the release of a number of inflammatory mediators and oxidative stress products like TNF-α, MCP-1, MMPs, and so on, which either directly or indirectly contribute to the development of SAH.It has recently been discovered that some antibodies against inflammatory mediators, antioxidant stress, botanicals, and traditional Chinese medicine decrease the inflammatory response of SAH. Additionally, certain biomarkers linked to inflammation may serve as a foundation for clinical diagnosis.Although these mechanisms are still not completely understood, we can explore potential therapeutic targets by studying the role of inflammatory responses and bioactive molecules in the formation of SAH. [Display omitted] •Neuroinflammatory response triggers release of mediators, oxidative stress products, and vasoactive substances post-SAH.•Targeting inflammatory signaling pathways mitigates neuroinflammation in SAH.•Vascular regulation improves cerebral hemodynamics and neuroprotection after SAH.•Inflammation-derived bioactive molecules serve as diagnostic biomarkers for SAH.

[This corrects the article DOI: 10.3389/fphar.2024.1466953.].

Aim: This systematic review aims to evaluate the effectiveness of microbiota-modulating interventions (such as probiotics, prebiotics, and fecal microbiota transplantation) in reducing cognitive symptoms, pain, and neuroinflammation in human studies relevant to fibromyalgia (FM). The review will investigate the role of gut–brain axis modulation through these interventions and explore the potential therapeutic benefits for FM management. Materials and Methods: A comprehensive search was conducted in electronic databases including PubMed, Scopus, and the Cochrane Library for studies published from 1 January 2015 to 30 April 2025. Studies were eligible if they were randomized controlled trials (RCTs), pilot studies, or observational studies assessing the impact of microbiota-targeted interventions (probiotics, prebiotics, fecal microbiota transplantation) on cognitive function, pain, or neuroinflammation in patients with FM. Studies were excluded if they involved animal models, lacked relevant outcome measures, or were not peer-reviewed. Although only a subset of the included studies directly involved FM patients, all were selected for their relevance to symptom domains (e.g., pain, cognition, mood) and mechanisms (e.g., neuroinflammation, gut–brain axis dysfunction) that are central to FM. A total of 11 human studies were included in the final qualitative synthesis. Results: Preliminary findings from the included studies suggest that microbiota-targeted interventions, particularly probiotics and prebiotics, show promise in reducing cognitive symptoms, pain, and neuroinflammation in FM patients. Improvements in mood and quality of life were also reported, indicating potential benefits for overall well-being. However, heterogeneity in study designs, sample sizes, and outcome measures limit the ability to draw definitive conclusions. Conclusions: This systematic review highlights the potential of microbiota modulation as a therapeutic strategy for managing FM symptoms, particularly cognitive dysfunction and neuroinflammation.

Traumatic brain injury is a leading cause of neuroinflammation and anxiety disorders in young adults. Immune-targeted therapies have garnered attention for the amelioration of TBI-induced anxiety. A previous study has indicated that voluntary exercise intervention following TBI could reduce neuroinflammation. It is essential to determine the effects of voluntary exercise after TBI on anxiety via inhibiting neuroinflammatory response. Mice were randomly divided into four groups (sham, TBI, sham + voluntary wheel running (VWR), and TBI + VWR). One-week VWR was carried out on the 2nd day after trauma. The neurofunction of TBI mice was assessed. Following VWR, anxiety behavior was evaluated, and neuroinflammatory responses in the perilesional cortex were investigated. Results showed that after one week of VWR, neurofunctional recovery was enhanced, while the anxiety behavior of TBI mice was significantly alleviated. The level of pro-inflammatory factors decreased, and the level of anti-inflammatory factors elevated. Activation of nucleotide oligomerization domain-like thermal receptor protein domain associated protein 3 (NLRP3) inflammasome was inhibited significantly. All these alterations were consistent with reduced microglial activation at the perilesional site and positively correlated with the amelioration of anxiety behavior. This suggested that timely rehabilitative exercise could be a useful therapeutic strategy for anxiety resulting from TBI by targeting neuroinflammation.

Background Cognitive dysfunction is a frequent complication to open-heart surgery. Cerebral inflammation caused by blood-brain barrier (BBB) dysfunction due to a systemic inflammatory response is considered a possible etiology. The effects of the glucocorticoid, methylprednisolone, on cerebrospinal fluid (CSF) markers of BBB function, neuroinflammation, and brain injury in patients undergoing cardiac surgery with cardiopulmonary bypass were studied. Methods In this prospective, randomized, blinded study, 30 patients scheduled for elective surgical aortic valve replacement were randomized to methylprednisolone 15 mg/kg ( n  = 15) or placebo ( n  = 15) as a bolus dose administered after induction of anesthesia. CSF and blood samples were obtained the day before and 24 h after surgery for assessment of systemic and brain inflammation (interleukin-6, interleukin-8, tumor necrosis factor-alpha), axonal injury (total-tau, neurofilament light chain protein), neuronal injury (neuron-specific enolase), astroglial injury (S-100B, glial fibrillary acidic protein), and the BBB integrity (CSF/serum albumin ratio). Results In the control group, there was a 54-fold and 17-fold increase in serum interleukin-6 and interleukin-8, respectively. This systemic activation of the inflammatory cytokines was clearly attenuated by methylprednisolone ( p  < 0.001). The increase of the CSF levels of the astroglial markers was not affected. A postoperative BBB dysfunction was seen in both groups as the CSF/serum albumin ratio increased from 6.4 ± 8.0 to 8.0 in the placebo group ( p  < 0.01) and from 5.6 ± 2.3 to 7.2 in the methylprednisolone group ( p  < 0.01) with no difference between groups ( p  = 0.98). In the CSF, methylprednisolone attenuated the interleukin-6 release ( p  < 0.001), which could be explained by the fall in systemic interleukin-6, and the serum to CSF gradient of IL-6 seen both at baseline and after surgery. In the CSF, methylprednisolone enhanced the interleukin-8 release ( p  < 0.001) but did not affect postoperative changes in CSF levels of tumor necrosis factor alpha. Serum levels of S-100B and neuron-specific enolase increased in both groups with no difference between groups. CSF levels of total tau, neurofilament light chain protein, and neuron-specific enolase were not affected in any of the groups. Conclusions Preventive treatment with high-dose methylprednisolone attenuated the systemic inflammatory response to open-heart surgery with cardiopulmonary bypass, but did not prevent or attenuate the increase in BBB permeability or the neuroinflammatory response. Trial registration Clinical Trials, Identifier: NCT01755338 , registered 24 December 2012

Background Cerebral ischemia / reperfusion injury can induce nerve cell apoptosis and ferroptosis and activation of the neuroinflammatory cascade plays a critical role in ischemic stroke progression. Mesenchymal stem cells (MSCs) can aid in repairing nerve injuries and regulating inflammatory responses, but their roles in ischemic stroke are unknown. Methods Here, we investigate the impact of microglial susceptibility to ferroptosis on neuronal apoptosis using an oxygen-glucose deprivation/reperfusion (OGD/R) model. Furthermore, we examined the effects of hypoxia-preconditioned olfactory mucosa mesenchymal stem cells (hOM-MSCs) on attenuating microglial ferroptosis and improving neuroinflammatory response in models of OGD/R and middle cerebral artery occlusion (MCAO). Results Firstly, it has been confirmed that the susceptibility of microglial to ferroptosis significantly amplifies their neuroinflammatory response, thereby accelerating neuronal apoptosis in the OGD/R model. A functional assay identified that the core functional factor, peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α), secreted from hOM-MSCs has a critical role in the hOM-MSC-modulated recovery of cellular activity in neurons. This discovery was accomplished through inhibiting microglia ferroptosis and the enhancement of immune regulation in the area affected by an infarct, all of which are closely linked to neuroinflammatory reactions. Mechanistically, exposure to hOM-MSCs partially mediates the amelioration of neuroinflammatory response and restoration of neural function in ischemic stroke by means of PGC-1α activation within the infarct region, via initiation of the PPARα-GPX4/ACSL4-NFκB signaling cascades in microglia. Conclusions These findings provide convincing proof that PGC-1α plays a crucial role in facilitating the advantageous impacts of hOM-MSCs on the enhancement of neural functionality following an ischemic stroke. The treatment of hOM-MSC could be a promising and effective neuroprotective candidate to ischemic stroke, and PGC-1α may be used in isolation or in combination with hOM-MSCs for ischemic stroke treatment. Highlights The susceptibility of microglial to ferroptosis significantly amplifies their neuroinflammatory response, thereby accelerating neuronal apoptosis in the OGD/R model. The hOM-MSC enhances neural functionality following an ischemic stroke through attenuating microglial ferroptosis and improving neuroinflammatory response. The hOM-MSCs are partially mediated by PGC-1α through initiation of the PPARα-GPX4/ACSL4-NFκB signaling cascades in microglia. The treatment of hOM-MSC could be a promising and effective neuroprotective candidate to ischemic stroke, and PGC-1α may be used in isolation or in combination with hOM-MSCs for ischemic stroke treatment.

Riluzole exhibits neuroprotective and therapeutic effects in several neurological disease models associated with excessive synaptic glutamate (Glu) release. We recently showed riluzole prevents acute excitotoxic hippocampal neural injury at 3 days in the kainic acid (KA) model of temporal lobe epilepsy (TLE). Currently, it is unknown if preventing acute neural injury and the neuroinflammatory response is sufficient to suppress epileptogenesis. The KA rat model of TLE was used to determine if riluzole attenuates acute hippocampal neural injury and reactive gliosis. KA was administered to adult male Sprague-Dawley (250 g) rats at 5 mg/kg/hr until status epilepticus (SE) was observed, and riluzole was administered at 10 mg/kg 1 h and 4 h after SE and once day for the next 2 days. Immunostaining was used to assess neural injury (FJC and NeuN), microglial activation (Iba1 and ED-1/CD68) and astrogliosis (GFAP and vimentin) at day 7 and day 14 after KA-induced SE. Learning and memory tests (Y-maze, Novel object recognition test, Barnes maze), behavioral hyperexcitability tests, and spontaneous generalized recurrent seizure (SRS) activity (24-hour video monitoring) were assessed at 11-15 weeks. Here we show that KA-induced hippocampal neural injury precedes the neuroimmune response and that riluzole attenuates acute neural injury, microglial activation, and astrogliosis at 7 and 14 days. We find that reducing acute hippocampal injury and the associated neuroimmune response following KA-induced SE by riluzole attenuates hippocampal-dependent cognitive impairment, behavioral hyperexcitability, and tonic/clonic generalized SRS activity after 3 months. We also show that riluzole attenuates SE-associated body weight loss during the first week after KA-induced SE. Riluzole acts on multiple targets that are involved to prevent excessive synaptic Glu transmission and excitotoxic neuronal injury. Attenuating KA-induced neural injury and subsequent microglia/astrocyte activation in the hippocampus and extralimbic regions with riluzole reduces TLE-associated cognitive deficits and generalized SRS and suggests that riluzole could be a potential antiepileptogenic drug.

Spinal cord injury (SCI) is a global medical problem with high disability and mortality rates. At present, the diagnosis and treatment of SCI are still lacking. Spinal cord injury has a complex etiology, lack of diagnostic methods, poor treatment effect and other problems, which lead to the difficulty of spinal cord regeneration and repair, and poor functional recovery. Recent studies have shown that gene expression plays an important role in the regulation of SCI repair. MicroRNAs (miRNAs) are non-coding RNA molecules that target mRNA expression in order to silence, translate, or interfere with protein synthesis. Secondary damage, such as oxidative stress, apoptosis, autophagy, and inflammation, occurs after SCI, and differentially expressed miRNAs contribute to these events. This article reviews the pathophysiological mechanism of miRNAs in secondary injury after SCI, focusing on the mechanism of miRNAs in secondary neuroinflammation after SCI, so as to provide new ideas and basis for the clinical diagnosis and treatment of miRNAs in SCI. The mechanisms of miRNAs in neurological diseases may also make them potential biomarkers and therapeutic targets for spinal cord injuries.

Autism spectrum disorder (ASD) is a developmental disorder of the brain characterized by shortfall in the social portfolio of an individual and abbreviated interactive and communication aspects rendering stereotypical behavior and pitfalls in a child’s memory, thinking, and learning capabilities. The incidence of ASD has accelerated since the past decade, portraying environment as one of the primary assets, comprising of metallic components aiming to curb the neurodevelopmental pathways in an individual. Many regulations like Clean Air Act and critical steps taken by countries all over the globe, like Sweden and the USA, have rendered the necessity to study the effects of environmental metallic components on ASD progression. The review focuses on the primary metallic components present in the environment (aluminum, lead, mercury, and arsenic), responsible for accelerating ASD symptoms by a set of general mechanisms like oxidative stress reduction, glycolysis suppression, microglial activation, and metalloprotein disruption, resulting in apoptotic signaling, neurotoxic effects, and neuroinflammatory responses. The effect of these metals can be retarded by certain protective strategies like chelation, dietary correction, certain agents (curcumin, mangiferin, selenium), and detoxification enhancement, which can necessarily halt the neurodegenerative effects. Graphical abstract

Hypoxia and ischemia are the main underlying pathogenesis of stroke and other neurological disorders. Cerebral hypoxia and/or ischemia (e.g., stroke) can lead to neuronal injury/death and eventually cause serious neurological disorders or even death in the patients. Despite knowing these serious consequences, there are limited neuroprotective strategies against hypoxic and ischemic insults in clinical settings. Recent studies indicate that microRNAs (miRNAs) are of great importance in regulating cerebral responses to hypoxic/ischemic stress in addition to the neuroprotective effect of the δ-opioid receptor (DOR). Moreover, new discovery shows that DOR can regulate miRNA expression and inhibit inflammatory responses to hypoxia/ischemia. We, therefore, summarize available data in current literature regarding the role of DOR and miRNAs in regulating the neuroinflammatory responses in this article. In particular, we focus on microglia activation, cytokine production, and the relevant signaling pathways triggered by cerebral hypoxia/ischemia. The intent of this review article is to provide a novel clue for developing new strategies against neuroinflammatory injury resulting from cerebral hypoxia/ischemia.