Roles of TRAF6 in Central Nervous System.

Tumor necrosis factor receptor-associated factor (TRAF) is an important binding protein of tumor necrosis factor (TNF) superfamily and the toll/IL-1 receptor (TIR) superfamily, which play an important role in innate immunity and acquired immunity. TRAFs family have 7 members (TRAF1-7), and TRAF6 has its special facture and biological function. TRAF6 has two special domains: C-terminal domain and N-terminal domain, which could integrate with multiple kinases and regulate signaling pathway function as an E3 ubiquitin ligase.

Melatonin Alleviates Intracerebral Hemorrhage-Induced Secondary Brain Injury in Rats via Suppressing Apoptosis, Inflammation, Oxidative Stress, DNA Damage, and Mitochondria Injury.

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking. We designed this study to investigate the therapeutic effects and mechanisms of melatonin on the secondary brain injury (SBI) after ICH. An in vivo ICH model was induced via autologous whole blood injection into the right basal ganglia in Sprague-Dawley (SD) rats.

HMGB1 promotes neurovascular remodeling via Rage in the late phase of subarachnoid hemorrhage.

High-mobility group box1 (HMGB1) is a nuclear protein widely expressed in the central nervous system. Extracellular HMGB1 serves as a proinflammatory cytokine and contributes to brain injury during the acute stage post-stroke. Recently, increasing evidence has demonstrated beneficial effects of HMGB1 in some types of brain injury, but little is known about its effects during the late phase of subarachnoid hemorrhage (SAH).

Tumor necrosis factor receptor-associated factor 6 participates in early brain injury after subarachnoid hemorrhage in rats through inhibiting autophagy and promoting oxidative stress.

Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a member of the TRAF family and an important multifunctional intracellular adaptin of the tumor necrosis factor superfamily and toll/IL-1 receptor (TIR) superfamily. TRAF6 has been studied in several central nervous system diseases, including ischemic stroke, traumatic brain injury, and neurodegenerative diseases, but its role in subarachnoid hemorrhage (SAH) has not been fully illustrated. This study was designed to explore changes of expression level and potential roles and mechanisms of TRAF6 in early brain injury (EBI) after SAH using a Sprague-Dawley rat model of SAH induced in 0.

P2X7 Participates in Intracerebral Hemorrhage-Induced Secondary Brain Injury in Rats via MAPKs Signaling Pathways.

This study aimed to study the role of P2X7 in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI) and the underlying mechanisms. An autologous blood injection was used to induce ICH model in Sprague-Dawley rats, and cultured primary rat cortical neurons were exposed to oxyhemoglobin to mimic ICH in vitro. siRNA interference and over-expression of P2X7, agonists and antagonists of P2X7, p38 MAPK and ERK were exploited.

Involvement of Nox2 and Nox4 NADPH oxidases in early brain injury after subarachnoid hemorrhage.

Oxidative stress is responsible for a poor prognosis of subarachnoid hemorrhage (SAH) patients. Nox2 has been shown to participate in SAH-induced early brain injury (EBI). Nox4 is another major subtype of Nox family widely expressed in central nervous system (CNS).

Potential dual role of nuclear factor-kappa B in experimental subarachnoid hemorrhage-induced early brain injury in rabbits.

Objective And Design: Nuclear factor-kappa B (NF-κB) has multiple physiological and pathological functions. The role of NF-κB can be protective or destructive. We aim to investigate the biphasic activation of NF-κB in brain after subarachnoid hemorrhage (SAH).

Transient receptor potential channel 1/4 reduces subarachnoid hemorrhage-induced early brain injury in rats via calcineurin-mediated NMDAR and NFAT dephosphorylation.

Transient receptor potential channel 1/4 (TRPC1/4) are considered to be related to subarachnoid hemorrhage (SAH)-induced cerebral vasospasm. In this study, a SAH rat model was employed to study the roles of TRPC1/4 in the early brain injury (EBI) after SAH. Primary cultured hippocampal neurons were exposed to oxyhemoglobin to mimic SAH in vitro.

Review: Therapeutic Targeting of HMGB1 in Stroke.

High mobility group box-1 (HMGB1) is a nuclear protein that is expressed in almost all eukaryotic cells. In the nucleus, it maintains nuclear homeostasis and promotes gene transcription. HMGB1 can be passively released into the extracellular milieu after cell necrosis or actively secreted by activated immune cells.

The Role of Omega-3 Polyunsaturated Fatty Acids in Stroke.

Stroke is the third commonest cause of death following cardiovascular diseases and cancer. In particular, in recent years, the morbidity and mortality of stroke keep remarkable growing. However, stroke still captures people attention far less than cardiovascular diseases and cancer.

NADPH Oxidase: A Potential Target for Treatment of Stroke.

Stroke is the third leading cause of death in industrialized nations. Oxidative stress is involved in the pathogenesis of stroke, and excessive generation of reactive oxygen species (ROS) by mitochondria is thought to be the main cause of oxidative stress. NADPH oxidase (NOX) enzymes have recently been identified and studied as important producers of ROS in brain tissues after stroke.