A5050295259- Neuroinflammation and Neurodegeneration Mechanisms
- Intracranial Aneurysms: Treatment and Complications
- Traumatic Brain Injury and Neurovascular Disturbances
- Intracerebral and Subarachnoid Hemorrhage Research
- Cancer-related molecular mechanisms research
- S100 Proteins and Annexins
- Acute Ischemic Stroke Management
- Mitochondrial Function and Pathology
- Immune cells in cancer
- Neurological Disease Mechanisms and Treatments
- RNA modifications and cancer
- Circular RNAs in diseases
- Histone Deacetylase Inhibitors Research
- Hearing, Cochlea, Tinnitus, Genetics
- MicroRNA in disease regulation
- Adipose Tissue and Metabolism
- Hearing Loss and Rehabilitation
- Neurological Disorders and Treatments
- Neurosurgical Procedures and Complications
- Vestibular and auditory disorders
- Cancer Cells and Metastasis
- Autophagy in Disease and Therapy
- Ferroptosis and cancer prognosis
- Facial Trauma and Fracture Management
- Cerebrospinal fluid and hydrocephalus
Affiliated Hospital of Southwest Medical University
2016-2025
Southwest Medical University
2020-2025
Beijing University of Technology
2025
Loma Linda University
2018-2024
Wenzhou Medical University
2010-2024
First Affiliated Hospital of Wenzhou Medical University
2010-2024
Shantou University
2023-2024
First Affiliated Hospital of Shantou University Medical College
2023-2024
Affiliated Hospital of Nantong University
2024
Nantong University
2024
Neuroinflammation is an important host defense response to secondary brain injury after intracerebral hemorrhage (ICH). Triggering receptor expressed on myeloid cells 2 (TREM2) confers strong neuroprotective effects by attenuating neuroinflammation in experimental ischemic stroke. Recent studies suggest that apolipoprotein E (apoE) a novel, high-affinity ligand of TREM2. This study aimed investigate the TREM2 activation and neuronal apoptosis mouse model ICH.
Background and Purpose— Mitoquinone has been reported as a mitochondria-targeting antioxidant to promote mitophagy in various chronic diseases. Here, our aim was study the role of mitoquinone activation oxidative stress–induced neuronal death reduction after subarachnoid hemorrhage (SAH) rats. Methods— Endovascular perforation used for SAH model male Sprague-Dawley Exogenous injected intraperitoneally 1 hour SAH. ML385, an inhibitor Nrf2 (nuclear factor-E2-related factor 2), given...
Oxidative stress and neuronal apoptosis have been demonstrated to be key features in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Previous studies indicated that Mas receptor activation initiates an anti-oxidative anti-apoptotic role the brain. However, whether can attenuate oxidative SAH remains unknown. To investigate beneficial effect of on induced by SAH, a total 196 rats were subjected endovascular perforation model SAH. AVE 0991 (AVE), selective agonist Mas, was...
White matter injury (WMI) is associated with motor deficits and cognitive dysfunctions in subarachnoid hemorrhage (SAH) patients. Therapeutic strategy targeting WMI would likely improve the neurological outcomes after SAH. Low-density lipoprotein receptor-related protein-1 (LRP1), a scavenger receptor of apolipoprotein E (apoE), able to modulate microglia polarization towards anti-inflammatory M2 phenotypes during inflammatory oxidative insult. In present study, we investigated effects LRP1...
Abstract Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality. The mechanisms underlying its pathological complications have not been fully identified. Here, we investigate the potential involvement of glymphatic system in neuropathology SAH. We demonstrate that blood components rapidly enter paravascular space following SAH and penetrate into perivascular parenchyma throughout brain, causing disastrous events such as cerebral vasospasm, delayed ischemia,...
Neuronal injury is the primary cause of poor outcome after subarachnoid hemorrhage (SAH). The apolipoprotein E (APOE) gene has been suggested to be involved in prognosis SAH patients. However, role APOE neuronal not well studied. In this study, was induced APOE-knockout (APOE-/-) and wild-type (WT) mice investigate impact deficiency on early phase SAH. experiments study were performed murine models vivo cultured microglia neurons vitro. model by endovascular perforation APOE-/- WT mice....
Under subarachnoid hemorrhage (SAH) conditions, astrocytes undergo a marked intensification of glycolytic activity, resulting in the generation substantial amounts lactate to maintain energy demand for neurons and other brain cells. Lactate has garnered increasing attention recent years because its emerging role critical biological processes such as inflammation regulation neuroprotection, particularly through histone lactylation. Bromodomain-containing protein 4 (BRD4) plays crucial...
Abstract Micro/nanoscale 3D bioelectrodes gain increasing interest for electrophysiological recording of electroactive cells. Although printing has shown promise to flexibly fabricate bioelectronics compared with conventional microfabrication, relatively‐low resolution limits the printed bioelectrode high‐quality signal monitoring. Here, a novel multi‐material electrohydrodynamic (EHDP) strategy is proposed sub‐microscale gold pillars in vitro recordings. EHDP employed conductive circuits...
BACKGROUND: Subarachnoid hemorrhage (SAH) is a critical condition that has far-reaching implications for public health systems globally due to its severe consequences and long-term disabilities. This study aims provide comprehensive analysis of SAH trends from 1990 2021 project future up 2041, aiding in better understanding management global burden. METHODS: We utilized data the GBD (Global Burden Disease) database, using joinpoint regression, frontier, decomposition analyses assess changes...
To investigate the effects of personal listening device use on hearing in young listeners.Conventional frequency audiometry (0.5-8 kHz) and extended high-frequency (10-20 were performed 120 users 30 normal-hearing adults.The thresholds 3 to 8 kHz range significantly increased listeners. The became broad as exposure duration was increased. Impaired detected 14.1% (34 240 ears) ears (> 25 dB HL one or more frequencies 0.5-8 kHz). could also be even if their conventional normal.Our results...
Background and Purpose Inflammasome‐mediated pyroptosis is an important neuronal cell death mechanism. Previous studies reported that activation of melanocortin MC 4 receptor exerted neuroprotection in several neurological diseases. Here, we have investigated the role with RO27‐3225 suppressing after experimental intracerebral haemorrhage (ICH) underlying Experimental Approach One hundred sixty‐nine male CD1 mice were used. ICH was induced by injection bacterial collagenase into right‐side...
β-Caryophyllene (BCP) mediates neuroprotection in cerebral ischemic animals. The neurovascular unit (NVU) acts as an intricate network to maintain the neuronal homeostatic microenvironment. However, effects exerted by BCP on NVU remain unclear. Therefore, we established vitro model investigate of oxygen-glucose deprivation and re-oxygenation (OGD/R)-induced injury. This involved co-culture brain microvascular endothelial cells, neurons, astrocytes. (10 μmol/L) was applied for 24 h prior...
As an important initiator and responder of brain inflammation in the central nervous system (CNS), astrocytes transform into two new reactive phenotypes with changed morphology, altered gene expression secretion profiles, termed detrimental A1 beneficial A2. Inflammatory events have been shown to occur during phase early injury (EBI) after subarachnoid hemorrhage (SAH). However, phenotype transformation as well its potential contribution inflammatory status EBI SAH has yet be determined. In...
Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is closely associated with neuroinflammation. Microglial activation an early event that leads to neuroinflammation after SAH. Peli1 E3 ubiquitin ligase mediates the induction of pro-inflammatory cytokines in microglia. Here we report contributions SAH mediated pathology. An model was induced by endovascular perforation adult male C57BL/6J mice. markedly mice brains a time-dependent manner and predominantly expressed...
Subarachnoid haemorrhage (SAH) is a fatal neurovascular disease following cerebral aneurysm rupture with high morbidity and mortality rates. Long non-coding RNAs (lncRNAs) are type of mammalian genome transcript, abundantly expressed in the brain involved many nervous system diseases. However, little currently known regarding influence lncRNAs early injury (EBI) after SAH. This study analysed expression profiles mRNAs SAH tissues mice using high-throughput sequencing. The results showed...