|
Seizures
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
HMGB1 and TLR4 levels were both elevated in patients with an average seizure duration >5 min compared to patients with a seizure duration ≤5 min (P=0.001 and P=0.014, respectively).
|
31241711 |
2019 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Neutralization of HMGB1 with an anti-HMGB1 monoclonal antibody decreased the incidence of SE and alleviated the severity of seizure activity in DZP-refractory SE, which was mediated by a Toll-like receptor 4 (TLR4)-dependent pathway.
|
31802434 |
2019 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
HMGB1 as an initiator and amplifier of neuroinflammation, and its activation is implicated in the propagation of seizures in animal models.
|
30644560 |
2019 |
|
Seizures
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Serum IL-1β, IL-6, and HMGB1 levels were analyzed within 2 hours after seizure attacks using the ELISA in only 68 patients (38 FS, 10 GEFS+, and 20 controls).
|
31591845 |
2019 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Receiver operating characteristic curve analysis revealed that HMGB1 could more accurately predict seizure frequency than IL-1β; when the serum concentration of HMGB1 was >9.625 ng/mL, there was 80.6% sensitivity and 92.5% specificity for predicting seizure frequency reduction.
|
30303442 |
2018 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
HMGB1 isoforms reflect different pathophysiological processes, and the disulfide isoform, which is generated in the brain during oxidative stress, is implicated in seizures, cell loss and cognitive dysfunctions.
|
29031614 |
2018 |
|
Seizures
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
The objective of the present study was to investigate the role of high‑mobility group box‑1 (HMGB1) in mediating the activation of glial cells through the toll‑like receptor 4 (TLR4)/nuclear factor (NF)‑κB signaling pathway in seizure, and the underlying mechanism.
|
29393419 |
2018 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
High mobility group box 1 enhances hyperthermia-induced seizures and secondary epilepsy associated with prolonged hyperthermia-induced seizures in developing rats.
|
28879430 |
2017 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
High-mobility group box 1 (HMGB1), an inflammatory cytokine, significantly increases following seizures and may be involved in upregulation of P‑gp.
|
28627626 |
2017 |
|
Seizures
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Consistent with animal data, we observed early expression of disulfide HMGB1 in patients with newly diagnosed epilepsy, and its persistence was associated with subsequent seizures.
|
28504645 |
2017 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Here, we investigated the therapeutic potential of an anti-HMGB1 monoclonal antibody (mAb) in epilepsy. anti-HMGB1 mAb attenuated both acute seizure models (maximal electroshock seizure, pentylenetetrazole-induced and kindling-induced), and chronic epilepsy model (kainic acid-induced) in a dose-dependent manner.
|
28167116 |
2017 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In the present study, we focused on whether anti-HMGB1 antibody treatment could relieve status epilepticus- triggered BBB breakdown and inflammation response in addition to the seizure behavior itself.
|
28446773 |
2017 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
That a surge in extracellular HMGB1 approximated seizure initiation suggests a key pathophysiological contribution of HMGB1 to the onset of epilepsy-related hyperexcitability.
|
28222432 |
2017 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
HMGB1 also activates the Receptor for Advanced Glycation Endproducts (RAGE), but it was unknown whether RAGE activation contributes to seizures or to HMGB1 proictogenic effects.
|
23523633 |
2013 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Recent evidence in experimental models of seizures and in temporal lobe epilepsy support an important role of high-mobility group box 1 and toll-like receptor 4 signalling in the mechanisms of hyperexcitability leading to the development and perpetuation of seizures.
|
21414994 |
2011 |
|
Seizures
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Pharmacological targeting of these proinflammatory pathways using selective receptor antagonists, or the use of transgenic mice with perturbed cell signaling, demostrated that the activation of IL-1R type 1 and TLR4 by their respective endogenous ligands, i.e., interleukin (IL)-1b and High Mobility Group Box 1, is implicated in the precipitation and recurrence of experimentally induced seizures in rodents.
|
21967368 |
2011 |