Brain research bulletin · 2026
Trigeminal nerve electrical stimulation attenuates hypoxic-ischemic brain injury by regulating GLT-1-mediated endoplasmic reticulum stress.
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Yu Daihua
Аннотация
OBJECTIVE: Neonatal hypoxic-ischemic encephalopathy (HIBD) remains a major cause of neonatal mortality and long-term neurological disability. This study investigated the neuroprotective effects of trigeminal nerve stimulation (TNS) and the underlying mechanisms, with a particular focus on glutamate transporter-1 (GLT-1)-mediated endoplasmic reticulum stress (ERS).
METHODS: Seven-day-old Sprague-Dawley rats were subjected to hypoxic-ischemic brain injury and randomly assigned to Sham, HIBD, HIBD + TNS, HIBD + TNS + DHK (GLT-1 inhibitor), and HIBD + TNS + GSK2606414 (PERK inhibitor) groups. Cerebral infarct volume and histopathological injury were evaluated by TTC and hematoxylin-eosin staining. Hippocampal GLT-1 expression was determined by quantitative real-time PCR and Western blotting, whereas ERS-related proteins were analyzed by Western blotting.
RESULTS: TNS markedly reduced cerebral infarct volume and histopathological injury, increased hippocampal GLT-1 expression, and decreased the expression of the ERS-related proteins GRP78, ATF4, and CHOP in HIBD rats. Pharmacological inhibition of GLT-1 or PERK signaling partially abolished the neuroprotective effects of TNS, indicating that GLT-1-mediated regulation of ERS contributes to TNS-induced neuroprotection.
CONCLUSION: TNS protects against neonatal hypoxic-ischemic brain injury by enhancing hippocampal GLT-1 expression and suppressing ERS-mediated neuronal injury. These findings identify TNS as a promising neuromodulatory strategy for neonatal HIBD and provide new mechanistic insights into its neuroprotective effects.
METHODS: Seven-day-old Sprague-Dawley rats were subjected to hypoxic-ischemic brain injury and randomly assigned to Sham, HIBD, HIBD + TNS, HIBD + TNS + DHK (GLT-1 inhibitor), and HIBD + TNS + GSK2606414 (PERK inhibitor) groups. Cerebral infarct volume and histopathological injury were evaluated by TTC and hematoxylin-eosin staining. Hippocampal GLT-1 expression was determined by quantitative real-time PCR and Western blotting, whereas ERS-related proteins were analyzed by Western blotting.
RESULTS: TNS markedly reduced cerebral infarct volume and histopathological injury, increased hippocampal GLT-1 expression, and decreased the expression of the ERS-related proteins GRP78, ATF4, and CHOP in HIBD rats. Pharmacological inhibition of GLT-1 or PERK signaling partially abolished the neuroprotective effects of TNS, indicating that GLT-1-mediated regulation of ERS contributes to TNS-induced neuroprotection.
CONCLUSION: TNS protects against neonatal hypoxic-ischemic brain injury by enhancing hippocampal GLT-1 expression and suppressing ERS-mediated neuronal injury. These findings identify TNS as a promising neuromodulatory strategy for neonatal HIBD and provide new mechanistic insights into its neuroprotective effects.