Enriched environment may improve secondary brain injury after traumatic brain injury by regulating the TLR2/NF-κB signaling pathway.

Background: Traumatic brain injury (TBI) can cause damage to the blood-brain barrier, resulting in neuroinflammatory reactions and brain edema that seriously affect the recovery of neurological function. We hypothesize that an enriched environment (EE) regulates the TLR2/NF-κB signaling pathway and thereby modulates the integrity of the blood-brain barrier to achieve neuroprotective effects.

Objective: This study evaluated the expression of toll-like receptor (TLR)-2 after TBI in a rat model, with the aim of determining whether TLR2/NF-κB improves secondary brain injury by inhibiting the release of inflammatory factors and reducing brain edema.

Up-regulation of BMAL1 by epigallocatechin-3-gallate improves neurological damage in SBI rats.

Brain Muscle ARNT-Like Protein 1 (BMAL1) suppresses oxidative stress in brain injury during surgery. Epigallocatechin-3-gallate (EGCG), a monomer in green tea, has been identified as an antioxidant and a potential agonist for BMAL1. In this work, the mechanism by which BMAL1 is regulated was investigated, as well as the therapeutic effect of EGCG on surgically injured rats.

Possible role of Sox11 in a rat model of surgical brain injury.

Objectives: Sox11, one of the SoxC family members, is an important transcription factor during neural development and neurogenesis. However, there is no report about its function in neural apoptosis. This research aims to examine the function of Sox11 in surgical brain injury (SBI).

Tetramethylpyrazine protects mitochondrial function by up-regulation of TFAM and inhibition of neuronal apoptosis in a rat model of surgical brain injury.

Objectives: Mitochondrial dysfunction caused by mitochondrial DNA (mtDNA) damage and mutation is widely accepted as one of the pathological processes of neurodegenerative diseases. As an mtDNA binding protein, mitochondrial transcription factor A (TFAM) maintains the integrity of mtDNA through transcription, replication, nucleoid formation, damage perception, and DNA repair. In recent works, the overexpression of TFAM increased the mtDNA copy count, promoted mitochondrial function, and improved the neurological dysfunction of neurodegenerative diseases.

Potential mechanism of TMEM2/CD44 in endoplasmic reticulum stress‑induced neuronal apoptosis in a rat model of traumatic brain injury.

Traumatic brain injury (TBI) can lead to the disruption of endoplasmic reticulum (ER) homeostasis in neurons and induce ER stress. Transmembrane protein 2 (TMEM2) may regulate ER stress through the p38/ERK signaling pathway, independent of the classic unfolded protein response (UPR) pathway. The present study examined the expression of TMEM2 following TBI in a rat model, in an aim to determine whether the mitogen‑activated protein kinase (MAPK) signaling pathway is controlled by TMEM2/CD44 to mitigate secondary brain injury.

Rosiglitazone inhibits acyl-CoA synthetase long-chain family number 4 and improves secondary brain injury in a rat model of surgical brain injury.

Ferroptosis is a recently discovered non-apoptotic form of cellular death. Acyl-CoA synthetase long-chain family number 4 (ACSL4) is necessary for iron-dependent cellular death, and reactive oxygen species (ROS) produced by ACSL4 are the executioners of ferroptosis. Rosiglitazone improves ferroptosis by inhibiting ACSL4.

RGFP966 exerts neuroprotective effect via HDAC3/Nrf2 pathway after surgical brain injury in rats.

Unlabelled: Histone deacetylase 3 (HDAC3) restores chromatin nucleosomes to a transcriptional repression state, thereby inhibiting gene expression. Studies have found that HDAC3 expression is upregulated in a variety of pathological states of the central nervous system and related to its neurotoxicity. However, the role of HDAC3 in surgical brain injury (SBI) has not been thoroughly explored.

VEGF regulates the blood‑brain barrier through MMP‑9 in a rat model of traumatic brain injury.

Blood-brain barrier (BBB) damage is closely related to morbidity and mortality in patients with traumatic brain injury (TBI). Inhibition of VEGF effectively protects BBB integrity in clinical ischemic stroke. Protecting BBB integrity, reducing brain edema and alleviating post-TBI secondary brain injury are key to a favorable patient prognosis.

Downregulation of TREM2/NF-кB signaling may damage the blood-brain barrier and aggravate neuronal apoptosis in experimental rats with surgically injured brain.

Surgical brain injury (SBI) is unavoidable in neurosurgery, and could aggravate secondary brain injury. Post-brain injury, multiple inflammatory factors are released, resulting in neuroinflammation and cell apoptosis, with subsequent brain edema and nerve function injury. TREM2, an immune protein mainly expressed in microglia, is an important link for nerve cells to participate in the inflammatory response.

Inhibition of LRRK2-Rab10 Pathway Improves Secondary Brain Injury After Surgical Brain Injury in Rats.

Leucine-rich repeat kinase 2 (LRRK2) is considered as a potential target for the treatment of Parkinson's disease. This protein is expressed in the brain and has been associated with various diseases and lysosomal maintenance. Rab10 is a member of the Rab protein GTPase family that has been recently shown to be a kinase substrate of LRRK2.

Inhibition of the p‑SPAK/p‑NKCC1 signaling pathway protects the blood‑brain barrier and reduces neuronal apoptosis in a rat model of surgical brain injury.

Surgical brain injury (SBI) can disrupt the function of the blood‑brain barrier (BBB), leading to brain edema and neurological dysfunction. Thus, protecting the BBB and mitigating cerebral edema are key factors in improving the neurological function and prognosis of patients with SBI. The inhibition of WNK lysine deficient protein kinase/STE20/SPS1‑related proline/alanine‑rich kinase (SPAK) signaling ameliorates cerebral edema, and this signaling pathway regulates the phosphorylation of the downstream Na‑K‑Cl cotransporter 1 (NKCC1).

Inhibition of the NKCC1/NF-κB Signaling Pathway Decreases Inflammation and Improves Brain Edema and Nerve Cell Apoptosis in an SBI Rat Model.

Surgical brain injury (SBI) triggers microglia to release numerous inflammatory factors, leading to brain edema and neurological dysfunction. Reducing neuroinflammation and protecting the blood-brain barrier (BBB) are key factors to improve the neurological function and prognosis after SBI. Na-K-Cl cotransporter 1 (NKCC1) and nuclear factor κB (NF-κB) have been implicated in the secretion of inflammatory cytokines by microglia in brain injury.

Advances in the study of the role and molecular mechanism of with‑no‑lysine kinase 3 in nervous system diseases (Review).

With‑no‑lysine kinase 3 (WNK3) is a serine/threonine kinase that functions by regulating downstream signaling molecules. WNK3 mainly regulates intracellular and extracellular Na+, Cl‑ and K+ levels by regulating downstream ion transporters, the disruption of which has been associated with cerebral ischemia, epilepsy, glioma and other diseases. In addition, WNK3 was demonstrated to regulate neuronal splicing factor RNA binding fox‑1 homolog‑1 to influence autism.

Possible mechanisms of the PERK pathway on neuronal apoptosis in a rat model of surgical brain injury.

Protein kinase R-like endoplasmic reticulum kinase (PERK) is an important transmembrane protein in the endoplasmic reticulum (ER). PERK signaling has a critical function in neuronal apoptosis. This work aimed to assess PERK signaling for its function in surgical brain injury (SBI) and to explore the underlying mechanisms.

The Blood Component Iron Causes Neuronal Apoptosis Following Intracerebral Hemorrhage via the PERK Pathway.

PERK signaling pathway plays an important role in neuronal apoptosis after Intracerebral hemorrhage (ICH). ICH can cause the release of blood components into the brain. However, which component in the blood plays a major role still unclear.

Matrix metalloproteinase-9 regulates the blood brain barrier via the hedgehog pathway in a rat model of traumatic brain injury.

The mechanisms of secondary brain injury after traumatic brain injury (TBI) are complex and are the result of multiple factors. Protecting the blood-brain barrier (BBB) and ameliorating cerebral edema are two key factors for improving the prognosis of TBI patients. The BBB is regulated by the hedgehog pathway through Scube2 and Shh protein.

The PERK Pathway Plays a Neuroprotective Role During the Early Phase of Secondary Brain Injury Induced by Experimental Intracerebral Hemorrhage.

The protein kinase RNA-like endoplasmic reticulum kinase (PERK) pathway, which is a branch of the unfolded protein response, participates in a range of pathophysiological processes of neurological diseases. However, few studies have investigated the role of the PERK in intracerebral hemorrhage (ICH). The present study evaluated the role of the PERK pathway during the early phase of ICH-induced secondary brain injury (SBI) and its potential mechanisms.

Annexin A7 Levels Increase in Rats With Traumatic Brain Injury and Promote Secondary Brain Injury.

The incidence of traumatic brain injury (TBI) has been increasing annually. Annexin A7 is a calcium-dependent phospholipid binding protein. It can promote melting of the cell membrane.

LRRK2 Contributes to Secondary Brain Injury Through a p38/Drosha Signaling Pathway After Traumatic Brain Injury in Rats.

Leucine-rich repeat kinase 2 (LRRK2) is widely expressed in the brain and exerts neurotoxicity in Parkinson's disease. The p38/Drosha signaling activation has been reported to increase cell death under stress. This study was designed to investigate the potential role and mechanism of LRRK2 in secondary brain injury after traumatic brain injury (TBI).

PERK Pathway Activation Promotes Intracerebral Hemorrhage Induced Secondary Brain Injury by Inducing Neuronal Apoptosis Both and .

The protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) signaling pathway was reported to exert an important role in neuronal apoptosis. The present study was designed to investigate the roles of the PERK signaling pathway in the secondary brain injury (SBI) induced by intracerebral hemorrhage (ICH) and its potential mechanisms. Sprague-Dawley rats were used to establish ICH models by injecting autologous blood (100 μl), and cultured primary rat cortical neurons were exposed to oxyhemoglobin (10 μM) to mimic ICH .

RACK1 upregulation induces neuroprotection by activating the IRE1-XBP1 signaling pathway following traumatic brain injury in rats.

Receptor for activated protein kinase C 1 (RACK1) is a multifaceted scaffolding protein known to be involved in the regulation of signaling events required for neuronal protection. In the present study, we investigated the role of RACK1 in secondary brain injury in a rat traumatic brain injury (TBI) model. A weight-drop TBI model was established in Sprague Dawley rats, and RACK1 in vivo knockdown and overexpression were performed 24 h before TBI insult.

Rehabilitation Treatment and Progress of Traumatic Brain Injury Dysfunction.

Traumatic brain injury (TBI) is a major cause of chronic disability. Worldwide, it is the leading cause of disability in the under 40s. Behavioral problems, mood, cognition, particularly memory, attention, and executive function are commonly impaired by TBI.

A Therapeutic Target of Cerebral Hemorrhagic Stroke: Matrix Metalloproteinase- 9.

Background: Cerebral hemorrhagic stroke, including intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), and hemorrhagic transformation after cerebral infarction, is a major medical emergency in the neurology, neurosurgery, emergency and other clinical departments. The pathophysiological mechanisms of these cerebral hemorrhagic diseases have not been fully elucidated, and there are no effective pharmacological and molecular treatments against these diseases. Matrix metalloproteinase-9 (MMP-9), also known as collagenase B, is one of the most important members of the matrix metalloproteinases (MMPs) family.

Matrix metalloproteinase 9 may be involved in contraction of vascular smooth muscle cells in an in vitro rat model of subarachnoid hemorrhage.

Our previous study determined that prominent cerebral vasospasm (CVS) may occur in an in vivo model of subarachnoid hemorrhage (SAH) in rats. Matrix metalloproteinase 9 (MMP‑9) expression levels in basilar arteries were upregulated in a similar manner to the development of CVS following SAH. To identify the changes that occur in the contractility of cerebrovascular smooth muscle cells and the expression levels of MMP‑9 in an in vitro model of SAH, rat cerebrovascular smooth muscle cells were isolated, cultured, and then stimulated with hemolysate.