Combined VEGF and bFGF loaded nanofiber membrane protects against neuronal injury and hypomyelination in a rat model of chronic cerebral hypoperfusion.

Currently, there are no effective therapeutic targets for the treatment of chronic cerebral hypoperfusion(CCH)-induced cerebral ischemic injury. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are discovered as the inducers of neurogenesis and angiogenesis. We previously made a nanofiber membrane (NFM), maintaining a long-term release of VEGF and bFGF up to 35 days, which might make VEGF and bFGF NFM as the potential protective agents against cerebral ischemic insult.

Fecal microbiota transplantation and short-chain fatty acids protected against cognitive dysfunction in a rat model of chronic cerebral hypoperfusion.

Aims: Clear roles and mechanisms in explaining gut microbial dysbiosis and microbial metabolites short-chain fatty acids (SCFAs) alterations in chronic cerebral ischemic pathogenesis have yet to be explored. In this study, we investigated chronic cerebral hypoperfusion (CCH)-induced gut microbiota and metabolic profiles of SCFAs as well as the effects and mechanisms of fecal microbiota transplantation (FMT) and SCFAs treatment on CCH-induced hippocampal neuronal injury.

Methods: Bilateral common carotid artery occlusion (BCCAo) was used to establish the CCH model.

Fecal microbiota transplantation and replenishment of short-chain fatty acids protect against chronic cerebral hypoperfusion-induced colonic dysfunction by regulating gut microbiota, differentiation of Th17 cells, and mitochondrial energy metabolism.

Background: Little is known about the association between gut microbiota and intestinal injury under a state of chronic cerebral hypoperfusion (CCH). Here, the effects of gut microbiota and short-chain fatty acids (SCFAs), as important metabolic products, on intestinal function and potential mechanisms after CCH were investigated.

Methods: Rats were subjected to bilateral common carotid artery occlusion (BCCAo) to induce CCH.

VEGF loaded nanofiber membranes inhibit chronic cerebral hypoperfusion-induced cognitive dysfunction by promoting HIF-1a/VEGF mediated angiogenesis.

We investigated the potential effects and mechanisms of vascular endothelial growth factor (VEGF)-nanofiber membranes (NFMs) treatment in a rat model of chronic cerebral hypoperfusion (CCH). VEGF-NFMs treatment promoted angiogenesis in surgical temporal cortex and hippocampus, alleviating decreased CBF in these two cerebral regions. VEGF-NFMs application improved reduced NAA/Cr ratio, preventing neuronal loss.

Preservation of spatial memory and neuroprotection by the fatty acid amide hydrolase inhibitor URB597 in a rat model of vascular dementia.

Background: Chronic cerebral hypoperfusion (CCH) is a major risk factor for vascular dementia (VaD). There are currently no broadly effective prevention or treatment strategies for VaD, but recent studies have reported promising results following vascular bypass surgery and pharmacomodulation of the brain endocannabinoid system (ECS). In this study, early effects of encephalomyosynangiosis (EMS) bypass surgery and augmented endocannabinoid signaling on CCH-induced cognitive dysfunction and neuronal damage were investigated.

Neuroprotective effects of andrographolide on chronic cerebral hypoperfusion-induced hippocampal neuronal damage in rats possibly via PTEN/AKT signaling pathway.

To explore the potential effects of andrographolide on chronic cerebral hypoperfusion (CCH)-induced neuronal damage as well as the underlying mechanisms. Rat CCH model was established by 2-vessel occlusion (2VO). The CCH rats received andrographolide treatment for 4 weeks.

URB597 protects against NLRP3 inflammasome activation by inhibiting autophagy dysfunction in a rat model of chronic cerebral hypoperfusion.

Background: Previous studies reported that URB597 (URB) had therapeutic potential for treating chronic cerebral hypoperfusion (CCH)-induced neuroinflammation and autophagy dysfunction. However, the interaction mechanisms underlying the CCH-induced abnormal excessive autophagy and neuroinflammation remain unknown. In this study, we investigated the roles of impaired autophagy in nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing (NLRP) 3 inflammasome activation in the rat hippocampus and the underlying mechanisms under the condition of induced CCH as well as the effect of URB treatment.

Andrographolide enhances hippocampal BDNF signaling and suppresses neuronal apoptosis, astroglial activation, neuroinflammation, and spatial memory deficits in a rat model of chronic cerebral hypoperfusion.

Andrographolide is a medical herbal compound with documented anti-inflammatory activity and therapeutic efficacy in animal models of Alzheimer's disease, traumatic brain injury, and ischemic stroke. The present study examined the potential therapeutic effects of andrographolide on chronic cerebral hypoperfusion (CCH)-induced hippocampal neuronal damage and cognitive dysfunction. A CCH model was established in male Sprague Dawley (SD) rats using 2-vessel occlusion (2VO).

Inhibition of excessive autophagy and mitophagy mediates neuroprotective effects of URB597 against chronic cerebral hypoperfusion.

URB597 (URB) has therapeutic potential for treating chronic cerebral hypoperfusion (CCH)-induced neuronal death. The present study investigated the protective effects of URB on autopahgy and mitophagy in a CCH model as well as the underlying mechanisms. The ultrastructural changes were examined by electron microscopy.

The potential protective effects of cannabinoid receptor agonist WIN55,212-2 on cognitive dysfunction is associated with the suppression of autophagy and inflammation in an experimental model of vascular dementia.

Vascular dementia (VaD) is characteristic of chronic brain ischemia and progressive memory decline, which has a high incidence in the elderly. However, there are no effective treatments for VaD, and the underlying mechanism of its pathogenesis remains unclear. This study investigated the effects of a synthetic cannabinoid receptor agonist WIN55,212-2 (WIN) on VaD, and molecular mechanisms of the effects.

Cannabinoid receptor agonist WIN55,212-2 and fatty acid amide hydrolase inhibitor URB597 ameliorate neuroinflammatory responses in chronic cerebral hypoperfusion model by blocking NF-κB pathways.

The present study explored the protective effects of cannabinoid receptor agonist WIN55,212-2 (WIN) and fatty acid amide hydrolase inhibitor URB597 (URB) against neuroinflammation in rats with chronic cerebral hypoperfusion (CCH). Activated microglia, astrocytes, and nuclear factor kappa B (NF-κB) p65-positive cells were measured by immunofluorescence. Reactive oxygen species (ROS) was assessed by dihydroethidium staining.

URB597 improves cognitive impairment induced by chronic cerebral hypoperfusion by inhibiting mTOR-dependent autophagy.

Chronic cerebral hypoperfusion (CCH) is associated with various ischemic cerebrovascular diseases that are characterized by cognitive impairment. The role of autophagy in cognitive dysfunction under conditions of CCH is poorly understood. To address this issue, the present study investigated the effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597 on autophagy and cognition in a CCH model as well as the underlying mechanisms.

Cannabinoid receptor agonist WIN55,212-2 and fatty acid amide hydrolase inhibitor URB597 may protect against cognitive impairment in rats of chronic cerebral hypoperfusion via PI3K/AKT signaling.

The present study further investigated the protective effects of cannabinoid receptor agonist WIN55,212-2 (WIN) and fatty acid amide hydrolase (FAAH) inhibitor URB597 (URB) on chronic cerebral hypoperfusion (CCH)-induced cognitive impairment in rats. Spatial learning and memory were assessed with the Morris water maze and by measuring Long-term potentiation. The expression of microtubule-associated protein-2 (MAP)-2, growth-associated protein-43 (GAP)-43, synaptophysin, cannabinoid receptor 1 (CB1), brain-derived neurotrophic factor (BDNF), FAAH, N-acylphosphatidylethanolamine phospholipase D(NAPE-PLD) and monoacyl glycerol lipase (MGL) as well as phosphoinositide 3-kinase (PI3K)/AKT signaling pathway molecules and downstream targets including AKT, phosphorylated (p-)AKT, cyclic AMP response element- binding protein (CREB), p-CREB, Bcl-2-associated death protein (BAD), p-BAD, glycogen synthase kinase (GSK)-3β, p-GSK-3β, forkhead box protein (FOXO) 3A and p-FOXO3A was determined by western blotting.

Cognitive function, depression, anxiety and quality of life in Chinese patients with untreated unruptured intracranial aneurysms.

Detected unruptured intracranial aneurysms (UIA) are becoming more common with the increased utilization of CT angiography, MR angiography and digital subtraction angiography. A proportion of patients with UIA remain untreated. We investigated to assess cognitive function, depression, anxiety and quality of life (QoL) in Chinese patients with untreated UIA.

Effects of statins-use for patients with aneurysmal subarachnoid hemorrhage: a meta-analysis of randomized controlled trials.

Aneurysmal subarachnoid hemorrhage (aSAH)-induced cerebral vasospasm and delayed ischemic neurological deficit (DIND) are the major causes of morbidity and mortality in patients with aSAH. The effects of statins-use for patients with aSAH remain controversial. Here,a total of 249 patients from six randomized controlled trials(RCTs) were subjected to meta-analysis.

The effects of intracranial pressure monitoring in patients with traumatic brain injury.

Background: Although international guideline recommended routine intracranial pressure (ICP) monitoring for patients with severe traumatic brain injury(TBI), there were conflicting outcomes attributable to ICP monitoring according to the published studies. Hence, we conducted a meta-analysis to evaluate the efficacy and safety of ICP monitoring in patients with TBI.

Methods: Based on previous reviews, PubMed and two Chinese databases (Wangfang and VIP) were further searched to identify eligible studies.

Elevated C-reactive protein levels may be a predictor of persistent unfavourable symptoms in patients with mild traumatic brain injury: a preliminary study.

The pathogenesis of persistent unfavourable outcomes following mild traumatic brain injury (mTBI) are not fully understood. Low-grade systemic inflammation might contribute to the development of persistent unfavourable outcomes in patients with mTBI. We used plasma high-sensitivity C-reactive protein (CRP) levels as the biomarker of systemic inflammation to investigate whether elevated CRP levels were associated with persistent adverse outcomes in these patients.

Quality of life and psychological impact in adult patients with hemorrhagic moyamoya disease who received no surgical revascularization.

Objectives: Surgical treatment for adult hemorrhagic moyamoya disease (MMD) remains controversial. A large proportion of Chinese adult patients with hemorrhagic MMD still choose conservative treatment. In this study, we investigated to assess psychological function and quality of life (QoL) in adult patients with hemorrhagic MMD who received no surgical revascularization.

The changes of signal transduction pathways in hippocampal regions and postsynaptic densities after chronic cerebral hypoperfusion in rats.

The mechanisms underlying the cognitive impairment after chronic cerebral hypoperfusion (CCH) are not fully clarified. In the present study, we investigated the molecular basis for the cognitive deficits under the condition of CCH in rats. The ultrastructural changes of postsynaptic densities (PSDs) were examined by ethanolic phosphotungstic acid (EPTA) electron microscopy.

A dural arteriovenous fistula in cavernous sinus developed from viral meningitis.

Although hormonal influences, inflammation, trauma, sinus thrombosis, venous hypertension, and congenital origin have been proposed as sources of dural arteriovenous fistulas (DAVFs) in cavernous and sigmoid sinuses, the etiology of these lesions remains controversial. We present a case with a cavernous sinus DAVF developed from viral meningitis which has not been previously described. A 24-year-old male was admitted to our institute because of periorbital pain, decreased vision, pulsatile tinnitus, chemosis, and exophthalmos on the right side after he had suffered viral meningitis four months before.

Chronic cerebral hypoperfusion in rats causes proteasome dysfunction and aggregation of ubiquitinated proteins.

The deposition of abnormal protein aggregates is a feature of several neurodegenerative diseases. We have employed a rat model to investigate whether chronic cerebral hypoperfusion (CCH) induces proteasome dysfunction and the accumulation of ubiquitinated proteins and aggregates in the CNS. Protein aggregation was analyzed by ethanolic phosphotungstic acid (EPTA) electron microscopy (EM), immunogold EM, laser-scanning confocal microscopy, and Western blotting.

Cognitive impairment and changes of neuronal plasticity in rats of chronic cerebral hypoperfusion associated with cerebral arteriovenous malformations.

A new rat model associated with cerebral arteriovenous malformations (AVMs) was developed to study the effect of chronic cerebral hypoperfusion on cognitive function and neuronal plasticity in rats. Aged-matched animals comprised a control group. Three months after surgery, Morris water waze test was performed to evaluate the cognitive function in rats.