A5011842437- Intracerebral and Subarachnoid Hemorrhage Research
- Cerebrospinal fluid and hydrocephalus
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disease Mechanisms and Treatments
- Heme Oxygenase-1 and Carbon Monoxide
- Traumatic Brain Injury and Neurovascular Disturbances
- Hemoglobinopathies and Related Disorders
- Inflammation biomarkers and pathways
- Kruppel-like factors research
- Spinal Hematomas and Complications
- Glioma Diagnosis and Treatment
- Phagocytosis and Immune Regulation
- Alzheimer's disease research and treatments
- Immune cells in cancer
- Neurosurgical Procedures and Complications
- Acute Ischemic Stroke Management
- Neurogenesis and neuroplasticity mechanisms
- Neuroscience of respiration and sleep
- Cerebrovascular and Carotid Artery Diseases
- Barrier Structure and Function Studies
- Heavy Metal Exposure and Toxicity
- Iron Metabolism and Disorders
- Plant Stress Responses and Tolerance
- Peripheral Neuropathies and Disorders
- Cellular transport and secretion
Sanya Central Hospital
2020-2024
Hainan Medical University
2022-2024
Second Hospital of Shanxi Medical University
2007-2024
Shanxi Medical University
2015-2024
Longgang Central Hospital
2022
Northwest A&F University
2019-2020
Loma Linda University
2016-2018
Central South University
2008-2010
Xiangya Hospital Central South University
2008
Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related erythrocyte lysis and hemoglobin release. An increase of brain water content was associated with an iron, which is degradation product. Expression AQP4 highly modified in several disorders, it can play a key role cerebral formation. However, the question whether regulated by drugs lacks reliable evidence, interacting roles iron overload after ICH are unknown. The goal this study clarify relationship...
Activated microglia are divided into pro-inflammatory and anti-inflammatory functional states. In state, activated contribute to phagocytosis, neural repair anti-inflammation. Nrf2 as a major endogenous regulator in hematoma clearance after intracerebral hemorrhage (ICH) has received much attention. This study aims investigate the mechanism underlying Nrf2-mediated regulation of microglial phenotype phagocytosis ICH. vitro experiments, BV-2 cells were assigned normal group administration...
Heme-degradation after erythrocyte lysis plays an important role in the pathophysiology of intracerebral hemorrhage. Low-density lipoprotein receptor-related protein-1 is a receptor expressed predominately at neurovascular interface, which facilitates clearance hemopexin and heme complex. In present study, we investigated low-density removal neuroprotection mouse model Endogenous were increased ipsilateral brain hemorrhage, accompanied by hemoglobin levels, water content, blood-brain barrier...
Background and Purpose- Heme iron are considered to be key factors responsible for secondary insults after intracerebral hemorrhage (ICH). Our previous study showed that LRP1 (low-density lipoprotein receptor-related protein-1)-Hx (hemopexin) facilitates removal of heme. The TLR7 (Toll-like receptor 7)-BTK (Bruton tyrosine kinase)-CRT (calreticulin) pathway regulates the expression LRP1-Hx. This is designed clarify whether activation heme scavenging establish potential role BTK-CRT-LRP1-Hx...
Abstract Efficient clearance of hematomas is crucial for improving clinical outcomes in patients with intracerebral hemorrhage (ICH). The glymphatic system, facilitated by aquaporin‐4 (AQP4), plays a role cerebrospinal fluid (CSF) entry and metabolic waste clearance. This study examined the system ICH pathology, focus on AQP4. Collagenase‐induced models were established, AQP4 expression regulated through mifepristone as an agonist, TGN‐020 inhibitor, Aqp4 gene knockout. Fluorescence tracing...
Background and Purpose . PPAR- γ is a transcriptional factor which associated with promoting hematoma clearance reducing neurological dysfunction after intracerebral hemorrhage (ICH). Haptoglobin- (Hp-) hemoglobin- (Hb-) CD163 acts as main pathway to Hb scavenging ICH. The effect of on the Hp-Hb-CD163 signaling has not been reported. We hypothesized that might protect against ICH-induced neuronal injury via activating in rat ICH model. Methods. 107 Sprague-Dawley rats were used this...
The role of vitamin D3 (VitD3) in the upregulation osteopontin (OPN) and eNOS endothelium cerebral arteries after subarachnoid hemorrhage (SAH) is investigated. endovascular perforation SAH model Sprague-Dawley rats ( n = 103) was used. VitD3 pretreatment (30 ng/kg) increased endogenous OPN expression compared with naïve 5 per group). Neurobehavioral scores were significantly improved Pre-SAH+VitD3 group group. effects attenuated by intracerebroventricular (i.c.v) injections siRNA for D...
Hematoma is the chief culprit in brain injury following intracranial cerebral hemorrhage (ICH). Noninvasive hematoma clearance could be an option to prevent and alleviate early after ICH. Peroxisome proliferator-activated receptor γ (PPAR-γ) nuclear factor-erythroid 2 related factor-2 (Nrf2) facilitate removal of Monascin acts as natural Nrf2 activator with PPAR-γ agonist, long-term effects monascin ICH have not been elucidated.ICH rats was induced by stereotactic, intrastriatal injection...