scholarly journals Early Toll-like receptor 4 inhibition improves immune dysfunction in the hippocampus after hypoxic-ischemic brain damage

2022 ◽  
Vol 19 (1) ◽  
pp. 142-151
Author(s):  
Zhu Xing ◽  
Tang Zhen ◽  
Fan Jie ◽  
Yu Jie ◽  
Liu Shiqi ◽  
...  
Keyword(s):  
Brain Damage ◽  
Immune Dysfunction ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

scholarly journals HMBG1 Mediates Ischemia—Reperfusion Injury by TRIF-Adaptor Independent Toll-Like Receptor 4 Signaling

2010 ◽  
Vol 31 (2) ◽  
pp. 593-605 ◽  
Author(s):  
Qing-Wu Yang ◽  
Feng-Lin Lu ◽  
Yu Zhou ◽  
Lin Wang ◽  
Qi Zhong ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Brain Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Hmgb1 Level ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

High-mobility group protein box-1 (HMGB1) has recently been recognized as a novel candidate in a specific upstream pathway promoting inflammation after brain ischemia. However, its downstream pathway and underlying mechanism have yet to be elucidated. The HMGB1 level in the acute cerebral infarct (ACI) group was significantly increased compared with that of control group, and correlated with the severity of neurologic impairment of ACI patients. Further, recombinant human HMGB1 (rhHMGB1) had no effect on microglia derived from mice lacking the Toll-like receptor 4 (TLR4−/–). Intracerebroventricular injection of rhHMGB1 in TLR4+/+ mice cause significantly more injury after cerebral ischemia–reperfusion than control group. But, TLR4−/– mice administered with rhHMGB1 showed moderate impairment after ischemia–reperfusion than TLR4+/+ mice. To determine the potential downstream signaling of HMGB1/TLR4 in cerebral ischemic injury, we used the ischemic–reperfusion model with Toll/interleukin-1 receptor domain-containing adaptor-inducing interferon-β knockout mice (TRIF−/–) and evaluated the activity and expression of TRIF pathway-related kinases. The results suggest that the TRIF pathway is not likely to be involved in TLR4-mediated ischemia brain injury. Finally, we found that TLR4 expressed by immigrant macrophages was involved in the development of ischemic brain damage. These results suggest that HMBG1 mediates ischemia–reperfusion injury by TRIF-adaptor independent Toll-like receptor 4 signaling. The TLR4 expressed by immigrant macrophages may be involved in the development of ischemic brain damage.

Blockade of central histaminergic H2 receptors facilitates catecholaminergic metabolism and aggravates ischemic brain damage in the rat telencephalon

2003 ◽  
Vol 974 (1-2) ◽  
pp. 117-126 ◽  
Author(s):  
Ryu Otsuka ◽  
Naoto Adachi ◽  
Gen Hamami ◽  
Keyue Liu ◽  
Toshihiro Yorozuya ◽  
...  
Keyword(s):  
Brain Damage ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
H2 Receptors

Ischemic neuronal damage after acute subdural hematoma in the rat: effects of pretreatment with a glutamate antagonist

1991 ◽  
Vol 74 (6) ◽  
pp. 944-950 ◽  
Author(s):  
Min-Hsiung Chen ◽  
Ross Bullock ◽  
David I. Graham ◽  
Jimmy D. Miller ◽  
James McCulloch
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Neuronal Damage ◽  
Nmda Receptor Antagonist ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Content Type ◽  
Irreversible Brain Damage ◽  
Slow Injection

✓ The ability of a competitive N-methyl-D-aspartate (NMDA) receptor antagonist (D-CPP-ene) to reduce irreversible brain damage has been examined in a rodent model of acute subdural hematoma. Acute subdural hematoma was produced by the slow injection of 400 µl homologous blood into the subdural space overlying the parietal cortex in halothane-anesthetized rats. Brain damage was assessed histologically in sections at multiple coronal planes in animals sacrificed 4 hours after induction of the subdural hematoma. Pretreatment with D-CPP-ene (15 mg/kg) significantly reduced the volume of ischemic brain damage produced by the subdural hematoma from 62 ± 8 cu mm (mean ± standard error of the mean) in vehicle-treated control rats to 29 ± 7 cu mm in drug-treated animals. These data demonstrate the anti-ischemic efficacy of NMDA antagonists in an animal model of intracranial hemorrhage in which intracranial pressure is elevated, and suggest that excitotoxic mechanisms (which are susceptible to antagonism by D-CPP-ene) may play a role in the ischemic brain damage which is observed in patients who die after acute subdural hematoma.

Sign in / Sign up

Export Citation Format

Share Document