Silicon-Carbon Dots-Loaded Mesoporous Silica Nanocomposites (mSiO@SiCDs): An Efficient Dual Inhibitor of Cu-Mediated Oxidative Stress and Aβ Aggregation for Alzheimer's Disease.

The redox-active metal ions, especially Cu, are highly correlated to Alzheimer's disease (AD) by causing metal ion-mediated oxidative stress and toxic metal-bound β-amyloid (Aβ) aggregates. Numerous pieces of evidence have revealed that the regulation of metal homeostasis could be an effective therapeutic strategy for AD. Herein, in virtue of the interaction of both amino-containing silane and ethylenediaminetetraacetic acid disodium salt for Cu, the silicon-carbon dots (SiCDs) are deliberately prepared using these two raw materials as the cocarbon source; meanwhile, to realize the local enrichment of SiCDs and further maximize the chelating ability to Cu, the SiCDs are feasibly loaded to the biocompatible mesoporous silica nanoparticles (mSiO) with the interaction between residual silane groups on SiCDs and silanol groups of mSiO.

Roles of Eph/ephrin bidirectional signaling during injury and recovery of the central nervous system.

Multiple cellular components, including neuronal, glial and endothelial cells, are involved in the sophisticated pathological processes following central nervous system injury. The pathological process cannot reduce damage or improve functional recovery by merely targeting the molecular mechanisms of neuronal cell death after central nerve system injuries. Eph receptors and ephrin ligands have drawn wide attention since the discovery of their extensive distribution and unique bidirectional signaling between astrocytes and neurons.

The Rho-associated kinase inhibitors Y27632 and fasudil promote microglial migration in the spinal cord via the ERK signaling pathway.

Rho-associated kinase (ROCK) is a key regulatory protein involved in inflammatory secretion in microglia in the central nervous system. Our previous studies showed that ROCK inhibition enhances phagocytic activity in microglia through the extracellular signal-regulated kinase (ERK) signaling pathway, but its effect on microglial migration was unknown. Therefore, in this study, we investigated the effects of the ROCK inhibitors Y27632 and fasudil on the migratory activity of primary cultured microglia isolated from the spinal cord, and we examined the underlying mechanisms.

Elevated Homocysteine Level Related to Poor Outcome After Thrombolysis in Acute Ischemic Stroke.

BACKGROUND Hyperhomocysteinemia (HHcy) is a well-known risk factor for ischemic stroke. However, whether HHcy can influence the treatment outcome of acute ischemic stroke (AIS) patients has yet to be fully determined. In this study, we investigated the relationship between serum homocysteine (Hcy) level and prognosis in AIS patients who received tissue plasminogen activator (tPA) treatment.

Needle Sensation and Personality Factors Influence Therapeutic Effect of Acupuncture for Treating Bell's Palsy: A Secondary Analysis of a Multicenter Randomized Controlled Trial.

Background: It has not been solved what kind of needle sensation might influence outcomes of acupuncture treatment. Effects of personality factors on the therapeutic effect of acupuncture have not been investigated. This study aimed to find the effects of the traits of personality on the objective outcome when different acupuncture techniques were used in treating patients with Bell's palsy.

Rapidly activated epidermal growth factor receptor mediates lipopolysaccharide-triggered migration of microglia.

Previous reports have suggested that epidermal growth factor receptor (EGFR) is involved in microglia activation characterized by cell morphology changes, cytokine production and cell migration; and the biochemical regulation of the microglia migration is a potential therapeutic target following CNS inflammatory damages. However, the role of EGFR in microglia motility after inflammatory stimulation remains unknown. In the present study, lipopolysaccharide (LPS) was found to trigger rapid EGFR phosphorylation within 10 min, which was sustained during long-term stimulation in both primary microglial cells and the cultured BV2 microglial cells, furthermore, blocking EGFR phosphorylation by AG1478 significantly attenuated the LPS-induced chemotactic and chemokinetic migration of microglia.

Inhibitory effects of roscovitine on proliferation and migration of vascular smooth muscle cells in vitro.

Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are the major cause of in-stent restenosis (ISR). Intervention proliferation and migration of VSMCs is an important strategy for antirestenotic therapy. Roscovitine, a second-generation cyclin-dependent kinase inhibitor, can inhibit cell cycle of multiple cell types.

Cellular expression profile of RhoA in rats with spinal cord injury.

RhoA, a small GTPase, is involved in a wide array of cellular functions in the central nervous system, such as cell motility, cytoskeleton rearrangement, transcriptional regulation, phagocytosis and cell growth. It is not known how spinal cord injury (SCI) affects the expression of RhoA in different nerve cells. In the present study, we investigated the changes of RhoA expression in remote areas of the injury at the 3rd, 7th and 30th day after SCI, which was established by T10 contusion method.

Different responses of cell cycle between rat vascular smooth muscle cells and vascular endothelial cells to paclitaxel.

Although previous reports showed drug-eluting stent (DES) could effectively inhibit neointima formation, in-stent restenosis (ISR) remains an important obstacle. The purpose of this study was to investigate different effects of paclitaxel on proliferation and cell cycle regulators between vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs) of rats in vitro. The cultured VSMCs and VECs of rats from the same tissues were examined by using immunohistochemistry, flow cytometry and Western blotting in control and paclitaxel-treated groups.

Effectiveness of strengthened stimulation during acupuncture for the treatment of Bell palsy: a randomized controlled trial.

Background: The traditional Chinese theory of acupuncture emphasizes that the intensity of acupuncture must reach a threshold to generate de qi, which is necessary to achieve the best therapeutic effect. De qi is an internal compound sensation of soreness, tingling, fullness, aching, cool, warmth and heaviness, and a radiating sensation at and around the acupoints. However, the notion that de qi must be achieved for maximum benefit has not been confirmed by modern scientific evidence.

Bicarbonate efflux via GABA(A) receptors depolarizes membrane potential and inhibits two-pore domain potassium channels of astrocytes in rat hippocampal slices.

Increasing evidence indicates the functional expression of ionotropic γ-aminobutyric acid receptor (GABA(A) -R) in astrocytes. However, it remains controversial in regard to the intracellular Cl(-) concentration ([Cl(-) ](i) ) and the functional role of anion-selective GABA(A) -R in astrocytes. In gramicidin perforated-patch recordings from rat hippocampal CA1 astrocytes, GABA and GABA(A) -R-specific agonist THIP depolarized astrocyte membrane potential (V(m) ), and the THIP-induced currents reversed at the voltages between -75.

Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury.

Background: Emerging evidence indicates that reactive microglia-initiated inflammatory responses are responsible for secondary damage after primary traumatic spinal cord injury (SCI); epidermal growth factor receptor (EGFR) signaling may be involved in cell activation. In this report, we investigate the influence of EGFR signaling inhibition on microglia activation, proinflammatory cytokine production, and the neuronal microenvironment after SCI.

Methods: Lipopolysaccharide-treated primary microglia/BV2 line cells and SCI rats were used as model systems.

Stromal cell-derived factor 1α decreases β-amyloid deposition in Alzheimer's disease mouse model.

β-amyloid (Aβ) aggregates are known to induce neuronal and synaptic dysfunction, and thus are involved in learning and memory deficits in Alzheimer's disease (AD), making Aβ deposits a potential target for prevention or treatment. Microglia, especially bone marrow-derived microglia (BMDM), has been recently thought to play important roles in internalizing and phagocytozing Aβ. BMDM originate in the bone marrow, migrate into the blood as hematopoietic progenitor cells (HPCs) and enter the brain in a chemokine-dependent manner.

X-irradiation reduces the proliferation of astrocytes by cell cycle arrest.

Reactive astrogliosis is one of the key components of the cellular response to CNS injury and is considered a major impediment to axonal regeneration. Our previous study demonstrated that cell cycle inhibition treatment can reduce astrocyte activation and proliferation in vivo. In this study, we examined whether reactive astrogliosis can be suppressed by X-irradiation in vitro by modulating cell cycle progression.

Inhibiting epidermal growth factor receptor attenuates reactive astrogliosis and improves functional outcome after spinal cord injury in rats.

As a physical barrier to regenerating axons, reactive astrogliosis is also a biochemical barrier which can secrete inhibitory molecules, including chondroitin sulfate proteoglycans (CSPGs) in the pathological mechanism of spinal cord injury (SCI). Thus, inhibition of astroglial proliferation and CSPG production might facilitate axonal regeneration after SCI. Recent studies have demonstrated that epidermal growth factor receptor (EGFR) activation triggers quiescent astrocytes into becoming reactive astrocytes and forming glial scar after CNS injury.

Galectin-1 attenuates astrogliosis-associated injuries and improves recovery of rats following focal cerebral ischemia.

Astrogliosis occurs after brain ischemia, and excessive astrogliosis can devastate the neuronal recovery. Previous reports show that galectin-1 (Gal-1) regulates proliferation of several cell types and plays an important role after nervous system injuries. Here, we found that expression of Gal-1 was remarkably up-regulated in activated astrocytes around ischemic infarct.

Characteristics of depressive symptoms in essential tremor.

Depressive symptoms are common in essential tremor (ET) and may be a primary feature of the underlying disease. However, it is still unclear whether depression in ET and depression in primary affective disorders share common clinical manifestations. Sixty-one depressed ET patients and 112 depressed patients without ET were assessed using the Montgomery-Asberg Depression Rating Scale (MADRS).

Galectin-1 enhances astrocytic BDNF production and improves functional outcome in rats following ischemia.

Galectin-1, an endogenous mammalian lectin, has been implicated in a variety of CNS disorders. However, its role in cerebral ischemia is still elusive. In the present study, we investigated the effect of recombinant galectin-1 on production of astrocytic brain-derived neurotrophic factor (BDNF) and functional recovery following ischemia.

Tamoxifen alleviates irradiation-induced brain injury by attenuating microglial inflammatory response in vitro and in vivo.

Irradiation-induced brain injury, leading to cognitive impairment several months to years after whole brain irradiation (WBI) therapy, is a common health problem in patients with primary or metastatic brain tumor and greatly impairs quality of life for tumor survivors. Recently, it has been demonstrated that a rapid and sustained increase in activated microglia following WBI led to a chronic inflammatory response and a corresponding decrease in hippocampal neurogenesis. Tamoxifen, serving as a radiosensitizer and a useful agent in combination therapy of glioma, has been found to exert anti-inflammatory response both in cultured microglial cells and in a spinal cord injury model.

Tamoxifen attenuates inflammatory-mediated damage and improves functional outcome after spinal cord injury in rats.

Tamoxifen has been found to be neuroprotective in both transient and permanent experimental ischemic stroke. However, it remains unknown whether this agent shows a similar beneficial effect after spinal cord injury (SCI), and what are its underlying mechanisms. In this study, we investigated the efficacy of tamoxifen treatment in attenuating SCI-induced pathology.

Rat focal cerebral ischemia induced astrocyte proliferation and delayed neuronal death are attenuated by cyclin-dependent kinase inhibition.

Astroglial proliferation and delayed neuronal death are two common pathological processes in the ischemic brain. However, it is not clear if astrogliosis causes delayed neuronal death. In this study, we addressed this potential linkage by examining the relationship between attenuated astrocyte proliferation, induced by cyclin-dependent kinase (CDK) inhibition, and delayed neuronal death in rat ischemic hippocampus.

[Effects of cyclin dependent protein kinase inhibitor olomoucine on the neuronal apoptosis after status epilepticus: experiment with rats].

Objective: To investigate the effects of olomoucine, a cyclin dependent protein kinase (CDK) inhibitor, on the neuronal apoptosis after status epilepticus (SE).

Methods: Lithium chloride was injected intraperitoneally, and pilocarpine was injected intraperitoneally after 18 h to 24 SD rats so as to cause SE. Twenty-two of the 24 rats developed SE and 2 of them died.

Attenuation of astrogliosis by suppressing of microglial proliferation with the cell cycle inhibitor olomoucine in rat spinal cord injury model.

Microglial activation/proliferation and reactive astrogliosis are commonly observed and have been considered to be closely relevant pathological processes during spinal cord injury (SCI). However, the molecular mechanisms underlying this microglial-astroglial interaction are still poorly understood. We showed recently that the continuous injection of the cell cycle inhibitor olomoucine not only markedly suppressed microglial proliferation and associated release of pro-inflammatory cytokines, but also attenuated astroglial scar formation and the lesion cavity and mitigated the functional deficits in rat SCI animal model.