Study on the Alleviation of Sevoflurane Induced
Nerve Injury in Developing Rats by Dexmedetomidine through the RasGRF1-NR2B-ERK
Pathway

doi:10.1009-0959.2025.120002

Abstract

Abstract:

Objective： To explore the mechanism by which dexmedetomidine （DEX） alleviates sevoflurane induced nerve injury during the developmental period through the Ras guanine nucleotide releasing factor 1 （RasGRF1）-N-methyl-D-aspartate receptor 2B subunit （NR2B） -ERK signaling pathway.Methods： Twenty 7-day-old male SD rats were randomly divided into the CTL group and the SEV group， with 10 rats in each group. The results of the Morris water maze test and the protein expressions of NR2B and ERK in the brain tissue of the hippocampus were compared. The AAV-RasGRF1 and AAV-RasGRF1 shRNAi were constructed. Another 30 rats were randomly divided into the Control group， Sevo group， Sevo+NS group， Sevo+DEX25 group， Sevo+DEX50 group， and Sevo+DEX75 group （n=5）. Except for the Control group， AAV-RasGRF1 and AAV-RasGRF1 shRNAi were injected into the bilateral hippocampus of rats by stereotactic brain injection. After 2 weeks， 2% sevoflurane was exposed for 3 consecutive days. DEX or sodium chloride solution was intraperitoneally injected 30 minutes before exposure. Detect the protein expressions of NR2B， ERK and phosphorylated ERK （pERK）， as well as the rates of ERK/pERK and apoptosis of nerve cells.Results： When SD rats were exposed to sevoflurane for 6 hours， the expression quantity of NR2B receptors in the brain tissue of the hippocampus reached the peak （P<0.05）. The swimming time of the SEV group in the quadrant where the platform is located was shorter than that of the CTL group （P<0.05）. On the 4th day， the localization navigation latency of rats in the SEV group was longer than that in the CTL group （P<0.05）. On the 5th day， the localization latency in the SEV group was longer than that in the CTL group， while the residence time in the original quadrant was shorter than that in the CTL group， and the neurological function score was higher than that in the CTL group （P<0.05）. On the 4th day， the localization latency was the shortest in the Sevo+DEX75 group （P<0.05）. On the 5th day， among the sevoflurane treatment groups， the Sevo+DEX75 group had the shortest localization latency， the longest stay time in the original quadrant， and the lowest neurological function score （P<0.05）. The apoptosis rate of nerve cells and NR2B level in the Sevo+DEX75 group were the lowest， and the p-ERK/ERK was the highest in the Sevo+DEX75 group （P<0.05）.Conclusion： DEX may play a protective role against sevoflurane induced nerve injury during developmental period by acting on the RasGRF1-NR2B-ERK signaling pathway.

Key words: Dexmedetomidine； , RasGRF1-NR2B-ERK signaling pathway； , Sevoflurane； , Developmental period； , Neural injury； , Mechanism of action

CLC Number:

R614

MA Huijie, JIN Yanwu, ZHANG Boya, LI Linyan, WANG Guizhi, SUN Yingui.

Study on the Alleviation of Sevoflurane Induced Nerve Injury in Developing Rats by Dexmedetomidine through the RasGRF1-NR2B-ERK Pathway [J]. CHINESE JOURNAL OF MEDICINAL GUIDE, 2025, 27(12): 1304-1304-1311.

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Study on the Alleviation of Sevoflurane Induced Nerve Injury in Developing Rats by Dexmedetomidine through the RasGRF1-NR2B-ERK Pathway

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