Current neurovascular research最新文献

Introduction: Post-stroke dysphagia (PSD) is a common complication after acute stroke. It can be effectively alleviated by electroacupuncture (EA) stimulation at the Baihui acupoint; however, the underlying mechanism remains unclear.

Methods: Male ICR mice were used, and the suture occlusion method was employed to establish the middle cerebral artery occlusion (MCAO) mouse model. EA stimulation was applied to the Baihui acupoint for intervention. After treatment, the survival rate of the mice was assessed. Subsequently, a water swallow test was conducted to evaluate the degree of dysphagia in the mice. Additionally, neurological function was assessed through Garcia scoring and measurement of serum Ca2+-Mg2+-ATPase activity. Fur-thermore, MRI was utilized to evaluate the therapeutic effects of EA on cerebral infarction and edema rates. Then, the antioxidant activity of the EA intervention was assessed by measuring indicators of oxida-tive damage. Finally, the expressions of gamma- aminobutyric acid type B receptor subunit 1 (GAB-ABR1), N-methyl-D-aspartate receptor 1 (NMDAR1) were detected through WB, RT-qPCR, and immu-nofluorescence.

Results: EA intervention effectively increased the survival rate of MCAO mice and alleviated their dysphagia. Additionally, the impaired neurological function of the mice was improved, and cerebral infarction and edema rates were reduced. Furthermore, EA alleviated oxidative stress in mice, reduced damage to neurons in the nucleus ambiguus, and upregulated GABABR1 while downregulating NMDAR1.

Discussion: Although we suggested that EA may exert therapeutic activity for PSD by maintaining the balance of NMDAR1 and GABABR1, this conclusion still requires further experimental validation.

Conclusion: EA stimulation of the Baihui acupoint was effective in treating PSD, which was related to its ability to improve damaged neurons, upregulate GABABR1, and downregulate NMDAR1. These findings provided a new insight into the mechanisms of EA treatment for PSD and serve as a theoretical basis for future clinical research.

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Background: Stroke, primarily known as ischemic stroke, is a leading cause of mortality and disability worldwide. Reperfusion after the ischemia stroke resolves is necessary for maintaining the health of brain tissues; however, it also induces inflammation and oxidative stress, resulting in brain injury. This study aimed to investigate the role of circ0001679 in the pathology of I/R (Ischemia/Reperfusion)-induced brain injury and explore its therapeutic potential for I/R injury.

Methods: The Oxygen-Glucose Deprivation/Re-oxygenation (OGD/R) model was employed in primary mouse astrocytes, and the Middle Cerebral Artery Occlusion (MCAO) model was established in mice to mimic ischemia-reperfusion-induced injury. Si-circ0001679, anti-miR- 216, and TLR4 ORF-clone were transfected either in cells or mice to study the molecular mechanisms during I/R-induced injury. Inflammation and oxidative stress were monitored after treatment.

Results: Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress.

Conclusion: This study unveiled a novel regulatory axis of circ0001679-miR-216-TLR4 in I/Rinduced brain injury. Targeting circ0001679 may represent a promising therapeutic strategy for I/R-induced brain injury.

Background: Electroacupuncture (EA) exerts a protective role in Blood-brain Barrier (BBB) damage after ischemic stroke, but whether this effect involves the regulation of the pericytes in vitro is unclear.

Methods: The in vitro BBB models were established with brain microvascular endothelial cells (BMECs) and pericytes, and the co-cultured cells were randomly divided into three groups: the control group, oxygen-glucose deprivation/reoxygenation (OGD/R) group and EA group. OGD/R was performed to simulate cerebral ischemia-reperfusion in vitro. EA serum was prepared by EA treatment at the "Renzhong" (GV26) and "Baihui" (GV20) acupoints in middle cerebral artery occlusion/ reperfusion rats. Furthermore, the characteristics of BMECs and pericytes were identified with immunological staining. The cell morphology of the BBB model was observed using an inverted microscope. The function of BBB was measured with transendothelial electrical resistance (TEER) and sodium fluorescein, and the viability, apoptosis, and migration of pericytes were detected by cell counting kit-8, flow cytometry, and Transwell migration assay.

Results: BMECs were positive staining for Factor-VIII, and pericytes were positive staining for the α-SMA and NG2. EA serum improved cell morphology of the BBB model, increased TEER and decreased sodium fluorescein in OGD/R condition. Besides, EA serum alleviated pericytes apoptosis rate and migration number, and enhanced pericytes viability rate in OGD/R condition.

Conclusion: EA serum protects against BBB damage induced by OGD/R in vitro, and this protection might be achieved by attenuating pericytes apoptosis and migration, as well as enhancing pericytes viability. The findings provided new evidence for EA as a medical therapy for ischemic stroke.

Introduction: Early Brain Injury (EBI) significantly contributes to poor neurological outcomes and death following subarachnoid hemorrhage (SAH). The mechanisms underlying EBI post-SAH remain unclear. This study explores the relationship between serial cerebral blood flow (CBF) changes and neurological symptoms, as well as the mechanisms driving CBF changes in the ultra-early stages after experimental SAH in mice.

Methods: SAH was induced by endovascular perforation in male ddY mice. Mice were sacrificed at 6, 12, 24, and 48 h after behavioral tests using the modified neurological score and grid walking test, and CBF was measured via Laser Speckle Flow Imaging (LSFI). Neurofunctional evaluation, CBF analysis, and Western blotting were used to assess SAH-induced damage.

Results: Neurological symptoms were significantly worse at 12 h post-SAH compared to sham (9.5 ± 1.7 vs. 25.6 ± 0.63, respectively; p < 0.0001). CBF was significantly reduced at 12 h post- SAH compared to sham (35.34 ± 8.611 vs. 91.06 ± 12.45, respectively; p < 0.0001). Western blotting revealed significantly elevated thrombin and matrix metalloproteinase 9 levels 12 h post-SAH (p < 0.05).

Conclusion: Our results suggest that microthrombus formation peaked at 12 h post-SAH, potentially causing EBI and worsening neurological symptoms. Microthrombus formation in the ultraearly stages may represent a novel therapeutic target for managing EBI.

Aim: The aim of this study was to explore etiologies and risk factors by age and sex in young adult patients with ischemic stroke.

Methods: We recruited patients with ischemic stroke aged between 18 and 49 years. We assessed pathological etiologies by the Trial of Org 10,172 in Acute Stroke Treatment (TOAST) classification and risk factors by the International Pediatric Stroke Study (IPSS) classification. We explored the distribution of etiologies and risk factors by age and sex and investigated baseline features associated with functional outcomes at 3 months.

Results: Of 8521 stroke patients consecutively admitted, 1017 patients (11.9%) aged between 18-49 years, of whom large artery atherosclerosis was the most common etiology (n=375, 36.9%), followed by other determined cause (n=194, 19.1%) and undetermined cause (n=184, 18.1%). Compared to male patients, female patients had more cardioembolism (16.34% vs 8.42%) and less small artery occlusion (8.56% vs 17.76%). As age increased, the proportions of large artery atherosclerosis (P <0.001) and small artery occlusion (P <0.001) increased, and the proportion of other determined causes decreased (P <0.001). Of 184 patients with undetermined causes, 173 (94.0%) had at least one IPSS risk factor. A higher serum level of D-dimer at baseline was associated with an increased risk of unfavorable outcome (OR 1.118, 95% CI 1.052- 1.189), adjusting for the effect of age and stroke severity.

Conclusion: Approximately one-fifth of young patients with ischemic stroke had undetermined etiology, for whom the IPSS classification helps to explore risk factors. A higher level of Ddimer was associated with a higher risk of unfavorable outcomes at 3 months.

Objective: Regenerative therapy using stem cells to treat cerebral infarction is currently in the research phase. However, this method is costly. It also faces other significant challenges, including optimization of timing, delivery methods, and dosage. Therefore, more practical and effective therapies are required. Bioabsorbable artificial dura mater made from nonwoven Polyglycolic Acid (PGA) fabric is used clinically to treat cerebral infarction. Basic Fibroblast Growth Factor (bFGF) has attracted considerable attention as a potential therapeutic candidate for the treatment of cerebral infarctions. In this study, we aimed to prepare a bFGF-releasing PGA dura mater and investigate its therapeutic efficacy for the recovery of neurological function in a mouse model of focal cerebral infarction.

Methods: An artificial dura mater (Durawave) made from nonwoven PGA fabric was subjected to oxygen plasma treatment, followed by bFGF adsorption. The release of bFGF from the resulting PGA dura mater was evaluated in vitro using enzyme-linked immunosorbent assays. bFGF-releasing PGA dura mater was placed at the site of induced cerebral infarctions in mice. Neurological function was assessed 14 days after insertion, followed by a histological assessment.

Results: The prepared PGA dura mater released bFGF in a dose-dependent manner. Neurological function in the bFGF-treated groups was significantly better than that in the control group. bFGFreleasing PGA dura mater also significantly increased the number of neural progenitor cells in the peri-infarct cortex and striatum and showed a trend toward promoting angiogenesis.

Conclusion: bFGF-releasing PGA dura mater improved neurological function in a mouse model of focal cerebral infarction.

Objective: We aimed to investigate the prognostic factors associated with lobar intracerebral hemorrhage (ICH) and to construct convenient models to predict 3-month unfavorable functional outcomes or all-cause death.

Methods: Our study included 322 patients with spontaneous lobar ICH from 13 hospitals in Beijing as a derivation cohort. The clinical outcomes were unfavorable functional prognosis, defined as a modified Rankin Scale (mRS) score of 4-6, or all-cause death. Variable selection was performed using the Least Absolute Shrinkage and Selection Operator (LASSO) analysis, and two nomogram models were constructed. Additionally, multivariable logistic regression analysis was conducted to identify the factors associated with unfavorable prognosis. Finally, the Area Under The Receiver Operating Characteristic Curve (AUROC), calibration curve, and decision curve analyses (DCA) were performed to evaluate the models in both the derivation and external validation cohorts.

Results: Predictive factors for unfavorable functional outcomes in lobar ICH included age, dyslipidemia, ICH volume, NIHSS score, Stroke-Associated Pneumonia (SAP), and lipidlowering therapy. The model included age, GCS score, NIHSS score, antihypertensive therapy, in-hospital rehabilitation training, and ICH volume to predict all-cause mortality. Our models exhibited good discriminative ability, with an AUC of 0.897 (95% CI: 0.862-0.933) for unfavorable functional outcomes and 0.894 (95% CI: 0.870-0.918) for death. DCA and calibration curves confirmed the models' excellent clinical decision-making and calibration capabilities.

Conclusion: Nomogram models for predicting 3-month unfavorable outcomes or death in patients with lobar ICH were developed and independently validated in this study, providing valuable prognostic information for clinical decision-making.