rTMS Regulates the Balance Between Proliferation and Apoptosis of Spinal Cord Derived Neural Stem/Progenitor Cells.

Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive technique that uses electromagnetic fields to stimulate the brain. rTMS can restore an impaired central nervous system and promote proliferation of neural stem/progenitor cells (NSPCs), but optimal stimulus parameters and mechanisms underlying these effects remain elusive. The purpose of this study is to investigate the effect of different rTMS stimulus parameters on proliferation and apoptosis of spinal cord-derived NSPCs, the expression of brain-derived neurotrophic factor (BDNF) after rTMS, and the potentially underlying pathways.

Inhibiting endogenous tissue plasminogen activator enhanced neuronal apoptosis and axonal injury after traumatic brain injury.

Tissue plasminogen activator is usually used for the treatment of acute ischemic stroke, but the role of endogenous tissue plasminogen activator in traumatic brain injury has been rarely reported. A rat model of traumatic brain injury was established by weight-drop method. The tissue plasminogen activator inhibitor neuroserpin (5 μL, 0.

AG490 ameliorates early brain injury via inhibition of JAK2/STAT3-mediated regulation of HMGB1 in subarachnoid hemorrhage.

High mobility group box 1 (HMGB1) is a classic damage-associated molecular pattern that has an important role in the pathological inflammatory response. studies have demonstrated that the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway is involved in the regulation of HMGB1 expression, mediating the inflammatory response. Therefore, the purpose of the present study was to evaluate JAK2/STAT3 pathway involvement in the subarachnoid hemorrhage (SAH)-dependent regulation of HMGB1, using an rat model.

Protection of FK506 against neuronal apoptosis and axonal injury following experimental diffuse axonal injury.

Diffuse axonal injury (DAI) is the most common and significant pathological features of traumatic brain injury (TBI). However, there are still no effective drugs to combat the formation and progression of DAI in affected individuals. FK506, also known as tacrolimus, is an immunosuppressive drug, which is widely used in transplantation medicine for the reduction of allograft rejection.

Dynamic expression of nerve growth factor and its receptor TrkA after subarachnoid hemorrhage in rat brain.

Delayed ischemic neurologic deficit after subarachnoid hemorrhage results from loss of neural cells. Nerve growth factor and its receptor TrkA may promote regeneration of neural cells, but their expression after subarachnoid hemorrhage remains unclear. In the present study, a rat model of subarachnoid hemorrhage was established using two injections of autologous blood into the cistern magna.

Rosiglitazone ameliorates diffuse axonal injury by reducing loss of tau and up-regulating caveolin-1 expression.

Rosiglitazone up-regulates caveolin-1 levels and has neuroprotective effects in both chronic and acute brain injury. Therefore, we postulated that rosiglitazone may ameliorate diffuse axonal injury via its ability to up-regulate caveolin-1, inhibit expression of amyloid-beta precursor protein, and reduce the loss and abnormal phosphorylation of tau. In the present study, intraperitoneal injection of rosiglitazone significantly reduced the levels of amyloid-beta precursor protein and hyperphosphorylated tau (phosphorylated at Ser(404)(p-tau (S(404))), and it increased the expression of total tau and caveolin-1 in the rat cortex.

Rapidly increased vasopressin promotes acute platelet aggregation and early brain injury after experimental subarachnoid hemorrhage in a rat model.

Objective: To investigate the dynamic expression of vasopressin and its potential role in rat brain tissue after experimental subarachnoid hemorrhage (SAH).

Methods: Male Sprague-Dawley rats were divided into 10min, 1h, 6h, 24h, 48h and 72h groups. The SAH model was established by endovascular puncture.

Effect of Statins on Aneurysmal Subarachnoid Hemorrhage: A Meta-Analysis of Randomized Controlled Trials.

Aim: The role of statins for treating aneurysmal subarachnoid hemorrhage (aSAH) remains uncertain. In this study, the relevance of different end points was evaluated in order to clarify the action and efficacy of statins.

Material And Methods: A systematic literature retrieval was carried out to obtain randomized controlled trials (RCTs) from before March 2013 on the use of statins for aSAH.

Receptor-associated protein promotes t-PA expression, reduces PAI-1 expression and improves neurorecovery after acute ischemic stroke.

Receptor-associated protein (RAP) is a receptor antagonist that inhibits ligand interactions with the receptors that belong to the low density lipoprotein receptor gene family. The low-density lipoprotein receptor-related protein 1 (LRP1) has a crucial role in regulating tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) expression. Furthermore, the functional balance of these two proteins is directly associated with the initiation and development of cerebral ischemic stroke.

The rapid lipopolysaccharide-induced release of matrix metalloproteinases 9 is suppressed by simvastatin.

A rapid increase in matrix metalloproteinase-9 (MMP-9) expression by stimulated leukocytes is common in many diseases. Recent evidence suggests that the beneficial effects of statins are mediated in part by the suppression of MMP-9 release. In this study, we investigated the effect of statin on MMP-9 expression and its antagonist, tissue inhibitor of metalloproteinase-1 (TIMP-1) in LPS-stimulated leukocytes.

Etanercept alleviates early brain injury following experimental subarachnoid hemorrhage and the possible role of tumor necrosis factor-α and c-Jun N-terminal kinase pathway.

Cerebral inflammation plays a crucial role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). This study investigated the effects of c-Jun N-terminal kinase (JNK) inhibitor SP600125, acetylcholine (Ach), etanercept, and anti-TNF-α on cellular apoptosis in the cerebral cortex and the hippocampus, in order to establish the role of JNK and TNF-α in EBI. The SAH model was established using an endovascular puncture protocol.

Meta-analysis of the efficacy and safety of therapeutic hypothermia in children with acute traumatic brain injury.

Objective: To evaluate the efficacy and safety of therapeutic hypothermia in children with acute traumatic brain injury (TBI).

Methods: A systematic literature review using PubMed, Embase, Cochrane Library, Chinese National Knowledge Infrastructure, Wanfang, VIP, and Chinese Biomedical Database was performed to retrieve studies of randomized controlled trials (RCTs) on therapeutic hypothermia for children with TBI published before March 2014. Data extraction and quality evaluation of RCTs were performed by 2 investigators independently.

The role of rosiglitazone in the proliferation of vascular smooth muscle cells after experimental subarachnoid hemorrhage.

Background: Recent evidence has demonstrated that rosiglitazone can attenuate cerebral vasospasm following subarachnoid hemorrhage (SAH). Some studies have shown that rosiglitazone can suppress inflammation and immune responses after SAH. However, the precise molecular mechanisms by which cerebral vasospasm is attenuated is not clear.

Advances in research of the neuroprotective mechanisms of cerebral ischemic postconditioning.

Ischemic postconditioning refers to controlling reperfusion blood flow during reperfusion after ischemia, which can induce an endogenous neuroprotective effect and reduce ischemia-reperfusion injury. Activation of endogenous neuroprotective mechanisms plays a key role in protecting against brain ischemia-reperfusion injury. The mechanisms of cerebral ischemic postconditioning are not completely clear, and the following aspects may be involved: downregulation of oxidative stress, attenuating mitochondrial dysfunction, attenuating endoplasmic reticulum stress, accelerating the elimination of glutamate, increasing rCBF, inhibiting apoptosis, inhibiting autophagy, and regulating signal transduction.

Suppression of STIM1 in the early stage after global ischemia attenuates the injury of delayed neuronal death by inhibiting store-operated calcium entry-induced apoptosis in rats.

Ca²⁺ overload is considered to be the most important ion imbalance in the neuronal injury. Store-operated Ca²⁺ entry has been suggested to be a significant mechanism of excessive Ca²⁺ influx in many cells. The role of store-operated Ca²⁺ entry in neuronal ischemic injury has yet to be elucidated.

Role of caveolin-1 in the biology of the blood-brain barrier.

Caveolin-1 is the principal marker of caveolae in endothelial cells. It plays an important role in physiological and pathological conditions of the blood-brain barrier and serves as a mediator in drug delivery through the blood-brain barrier. Caveolin-1 is related to the diminished expression of tight junction-associated proteins and metabolic pinocytosis vesicles when the blood-brain barrier is destroyed by outside invaders or malignant stimulus.

The roles of MMP-9/TIMP-1 in cerebral edema following experimental acute cerebral infarction in rats.

Matrix metalloproteinases 9 (MMP-9) and its endogenous inhibitor, tissue inhibitor of metalloproteinases 1 (TIMP-1), regulate homeostasis and turnover of the extra cellular matrix (ECM). They play important roles in acute cerebral infarction (ACI). The contributions of MMP-9 and TIMP-1 to the early stages of ACI are not completely understood.

Dynamic change in cerebral microcirculation and focal cerebral metabolism in experimental subarachnoid hemorrhage in rabbits.

Regional cerebral blood flow (rCBF) in the cerebral metabolism and energy metabolism measurements can be used to assess blood flow of brain cells and to detect cell activity. Changes of rCBF in the cerebral microcirculation and energy metabolism were determined in an experimental model of subarachnoid hemorrhage (SAH) model in 56 large-eared Japanese rabbits about 12 to 16-month old. Laser Doppler flowmetry was used to detect the blood supply to brain cells.