Key result
Inhibiting the IRE1α/TRAF2/NF-κB pathway reduces neurological deficits, inflammation, and apoptosis after SAH in animal models.
Why the study?
The study was conducted to investigate the effect of the IRE1alpha/TRAF2/NF-kappaB pathway on early brain injury after subarachnoid hemorrhage.
Does inhibition of the IRE1α/TRAF2/NF-κB pathway reduce apoptosis and improve neurological deficits in an animal model of subarachnoid hemorrhage?
Does inhibition of the IRE1α/TRAF2/NF-κB pathway reduce apoptosis and improve neurological deficits in an animal model of subarachnoid hemorrhage?
Inhibition of the IRE1α/TRAF2/NF-κB pathway reduces inflammatory cytokines and neuronal apoptosis, improving neurological deficits in a preclinical model of subarachnoid hemorrhage.
Hypothesis-generating in rodent SAH; leaves open clinical translation of IRE1α inhibition.
OBJECTIVES: To investigate the effect of IRE1α/TRAF2/NF-κB pathway on early brain injury. METHODS: An endovascular puncture model of subarachnoid hemorrhage (SAH) was developed and SAH grading was performed. The following groups of experimental animals were randomly assigned: Blank group, Sham group, SAH+ DMSO group, SAH+STF-083010(IRE1α inhibitor) group, and SAH+BAY11-7082(NF-κB inhibitor) group. Neurological deficits were assessed in the animal models using a modified Garcia score. The expression of IRE1α, GRP78, TRAF2, NF-κB, and caspase3 was measured using western blot analysis. The concentrations of TNF-α, IL-1β and IL-6 were evaluated with ELISA kits. An analysis of neuronal apoptosis was performed using TUNEL staining. RESULTS: The neurological deficits, expression of IRE1α/TRAF2/NF-κB axis and its related proteins, inflammatory cytokines and apoptosis were increased after SAH, whereas their expressions were suppressed since the inhibition of the IRE1α/TRAF2/NF-κB signal pathway. Moreover, correlation analysis showed that TNF-α, IL-1β and IL-6 were positively correlated with apoptosis. CONCLUSIONS: The IRE1α/TRAF2/NF-κB signal pathway was activated and promoted apoptosis by promoting the expression of inflammatory cytokines after SAH.
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Liu et al. (2025) studied Subarachnoid hemorrhage (SAH). STF-083010 (IRE1α inhibitor) and BAY11-7082 (NF-κB inhibitor) vs. Blank, Sham, and SAH+DMSO groups was evaluated on Neurological deficits, expression of IRE1α/TRAF2/NF-κB axis, inflammatory cytokines, and apoptosis. Inhibition of the IRE1α/TRAF2/NF-κB signal pathway suppressed neurological deficits, inflammatory cytokines, and apoptosis after subarachnoid hemorrhage in an animal model.
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