Current neurovascular research最新文献

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.

Objective: The aim of this study was to explore the primary changes in corneal nerve fiber structure and its influencing factors in patients with primary glaucoma.

Method: A retrospective analysis was conducted in this study. A total of 51 patients with primary glaucoma who were diagnosed and treated in our hospital from March 2020 to March 2022 were selected as the research objects and designated as the glaucoma group. In addition, 51 patients with normal eyes were chosen as the control group. The characteristic changes of corneal nerve fibers, the thickness of the nerve fiber layer, and the number of ganglion cell complexes and dendritic cells were measured. Multivariate logistic regression analysis was performed to analyze the influencing factors of ganglion fiber structure change.

Result: Compared with the control group, the length of corneal nerve fibers and the density of corneal nerve fibers in the glaucoma group were significantly shortened, the number of branches was significantly reduced, the curvature was significantly increased, and the number of dendritic cells was significantly increased (P <0.05). Compared with the control group, the thickness of the upper, lower, nasal, temporal, and peripheral nerve fiber layers in the glaucoma group was obviously reduced (P <0.05). Compared with the control group, the thickness of the above inferior, nasal, temporal, and peripheral nerve fiber layers in the glaucoma group was significantly reduced (P <0.05). Compared with the control group, the above, below, and mean ganglion cell complex thickness in the glaucoma group was significantly reduced (P <0.05). Logistic regression analysis showed that intraocular pressure and the number of dendritic cells were risk factors for ganglion fiber structure change. In contrast, nerve fiber layer thickness and ganglion cell complex were protective factors for ganglion fiber structure change (P <0.05).

Conclusion: There were primary changes in the structure of corneal nerve fibers in patients with primary glaucoma, which were more slender, tortuous, and sparse, and the primary changes in nerve fiber structure could be affected by intraocular pressure, the number of dendritic cells, the thickness of the nerve fiber layer, and the ganglion cell complex.

Background: Ischemic stroke due to Large Vessel Occlusion (LVO) represents a critical and time-sensitive neurological emergency. Advancements in imaging technology and endovascular therapies have transformed the management of LVO. Nonetheless, thrombectomy failure diminishes the chances of patients achieving a favorable clinical outcome.

Objective: We aimed to determine the factors influencing recanalization failure in order to optimize thrombectomy therapy along with enhancing patient outcomes.

Methods: A retrospective analysis was performed employing consecutive LVO patients who underwent Endovascular Thrombectomy (EVT) in a tertiary comprehensive stroke center between January 2020 and June 2024. Recanalization failure (mTICI 0-2a) following thrombectomy was assessed using the Kolmogorov-Smirnov test, χ2 test, Fisher's exact test, and multivariable logistic regression to identify the related factors.

Results: A total of 82 EVT patients were analyzed. The mean age was 58.20 years and 70.73% of the patients were male. The rate of recanalization failure was 61%. Multivariable logistic regression analysis with age-sex adjusted factors has revealed hypertension [aOR: 5.31 (95% CI: 1.23-22.77); p =0.025] and no IVT [aOR: 2.75 (95% CI: 1.06-7.14); p =0.037] to be independent predictors of recanalization failure in this study.

Conclusion: Hypertension and the absence of prior intravenous thrombolysis have been found to be significant contributing factors to the high rate of thrombectomy failure in large-vessel occlusion.

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 immunohistochemistry 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.

Objective: To explore the effect of baseline Systemic Inflammatory Response reflected by platelet-to-lymphocyte ratio (PLR) and pre-thrombectomy cerebral edema reflected by Net Water Uptake (NWU) on futile recanalization in patients with Acute Ischemic Stroke (AIS) after successful thrombectomy, and to investigate the potential mediating role of baseline cerebral edema.

Methods: 134 Patients with anterior circulation ischemic stroke receiving successful thrombectomy were retrospectively studied. Their demographic and clinical characteristics were collected at admission, and the NWU was quantitatively calculated based on baseline computed tomography (CT). The predictive value of PLR for futile recanalization and the relationship between PLR, NWU, and futile recanalization using mediation analysis were explored. Patients were followed up for 90 days and were divided into a futile recanalization group and a favorable prognosis group [90-day modified Rankin Scale score of 0-2].

Results: High baseline PLR, NWU, no first-pass reperfusion, and large baseline ischemic core volume were independent predictors of futile recanalization after successful thrombectomy in patients with AIS. Mediation analysis results indicate that PLR may partially mediate the occurrence of futile recanalization through NWU.

Conclusion: Baseline PLR and NWU were independent predictors of futile recanalization, and higher PLR and NWU values were associated with a higher likelihood of futile recanalization. The findings suggest that early cerebral edema reflected by a high NWU value may be a mediator of PLR-affecting prognosis.

The close connection between the brain microvascular endothelial cells (BMECs) that are enclosed within this barrier is the result of an intracellular junction, which is responsible for the constricted connection. The regulation and control of drug delivery systems both require nanoparticles, which are extremely small particles made up of a variety of materials, including polymers, metals, and other chemicals. Nanoparticles are a crucial component of the regulation and control of drug delivery systems. There is a possibility that nanomaterials composed of inorganic chemicals, such as gold nanoparticles, could be utilized in the treatment of neurodegenerative illnesses like Parkinson's disease. In addition to this, they are used as nano-carriers for the aim of distributing drugs to the region of the brain that is being targeted. There are a number of advantages that are easily apparent when compared to other methods of administering drugs for neurological diseases. The current review demonstrates both the advantages and disadvantages of utilizing a wide variety of nanomaterials for brain delivery, as well as the potential impact that this will have in the future on the safety and effectiveness of patient care.

Background: Aloe-emodin (AE), a monomer derived from traditional Chinese medicine, has demonstrated remarkable efficacy in the clinical management of cognitive disorders. Ferroptosis (FPT), a specialized form of programmed cell death, plays a critical role in the pathological progression of various cognitive diseases.

Methods: This study explored the therapeutic potential of AE in a rat model of Wilson's disease cognitive impairments (WDCI) and examined whether these effects are mediated through the silencing information regulator 1 (SIRT1)-regulated FPT signaling pathway. Employing techniques, such as the Morris water maze (MWM), Hematoxylin & eosin (H&E) staining, Transmission electron microscopy (TEM), Immunofluorescence (IF), assessments of oxidative stress markers, and measurements of FPT-related protein levels, we evaluated the extent of SIRT1-mediated FPT and the therapeutic efficacy of AE.

Results: The findings from the WD copper-loaded rat model experiments revealed that MWM, H&E, TEM, and IF outcomes indicated AE's potential to promote the restoration of learning and memory functions, ameliorate hippocampal neuronal morphological damage, and preserve cell membrane integrity. Results from western blot (WB) and ELISA analyses demonstrated that AE markedly upregulated the expression of SIRT1, nuclear factor erythroid-2-related factor 2 (Nrf2), solute carrier family 7 member 11 (SCL7A11), and glutathione peroxidase 4 (GPX4) proteins while simultaneously reversing the expression of oxidative stress markers such as malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD), and reactive oxygen species (ROS). Consequently, we posit that AE may attenuate WD copper-loaded rat model hippocampal neuronal FPT by activating the SIRT1-mediated signaling pathway.

Conclusion: These findings suggested that AE mitigates WD copper-loaded rat model hippocampal neuronal damage through the activation of SIRT1-mediated FPT, thereby presenting a valuable candidate Chinese herbal monomer for the clinical treatment of WDCI.

Objective: Nearly half of Acute Ischemic Stroke (AIS) patients failed to achieve favorable outcomes despite successful reperfusion treatment. This phenomenon is referred to as Futile Recanalization (FR). Screening patients at risk of FR is vital for stroke management. Previous studies reported the diagnostic value of alkaline phosphatase (ALP) levels in certain aspects of stroke prognosis. However, the association between serum ALP level and FR among AIS patients treated with thrombectomy remained unclear.

Methods: We screened stroke patients who underwent thrombectomy at our center from January 2017 to June 2021, and those who achieved successful reperfusion (modified Thrombolysis in Cerebral Infarction score=3) were ultimately analyzed. Demographic information, vascular risk factors, and laboratory test results were collected at admission. The 3-month unfavorable outcome was defined as a modified Rankin Scale score of 3 to 6. The effect of ALP levels on FR was investigated with a logistic regression model.

Results: Of 788 patients who underwent thrombectomy, 277 achieved successful reperfusion. Among them, 142 patients (51.3%) failed to realize favorable outcomes at 3 months. After adjusting for confounding variables, higher ALP levels (p =0.002) at admission were independently associated with unfavorable outcomes at three months. Adding ALP values to conventional risk factors improved the performance of prediction models for FR.

Conclusion: The current study found that the serum ALP levels at admission emerged as a potential biomarker for futile reperfusion in stroke patients undergoing thrombectomy. Further studies are warranted to confirm the clinical applicability of ALP level for futile recanalization prediction.