Effect of dexmedetomidine on sevoflurane-induced endoplasmic reticulum stress in hippocampus of neonatal rats

Pengzu BAI; Liliang ZHANG; Haisheng ZHANG; Zeyu YAO

doi:10.16016/j.1000-5404.202011228

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Effect of dexmedetomidine on sevoflurane-induced endoplasmic reticulum stress in hippocampus of neonatal rats

更新时间：2026-01-09

- Effect of dexmedetomidine on sevoflurane-induced endoplasmic reticulum stress in hippocampus of neonatal rats
- Journal of Third Military Medical University Vol. 43, Issue 10, Pages: 964-969(2021)
- 作者机构：
- 作者简介：
- 基金信息：
  
  the Natural Science Foundation of Qinghai Province(2019-ZJ-7085)
- DOI：10.16016/j.1000-5404.202011228
  CLC：
- Received：24 November 2020，
  
  Published：30 May 2021
- 稿件说明：
移动端阅览
Pengzu BAI, Liliang ZHANG, Haisheng ZHANG, et al. Effect of dexmedetomidine on sevoflurane-induced endoplasmic reticulum stress in hippocampus of neonatal rats[J]. Journal of Third Military Medical University, 2021, 43(10): 964-969.
DOI：

Pengzu BAI, Liliang ZHANG, Haisheng ZHANG, et al. Effect of dexmedetomidine on sevoflurane-induced endoplasmic reticulum stress in hippocampus of neonatal rats[J]. Journal of Third Military Medical University, 2021, 43(10): 964-969. DOI： 10.16016/j.1000-5404.202011228.

摘要

Abstract

Objective

To investigate the mechanism of dexmedetomidine (DEX) in sevoflurane (SEVO) induced hippocampal neuron injury in neonatal rats.

Methods

Forty male Sprague-Dawley (SD) rats (7-day-old

10~15 g) were given i.p. injections of saline or DEX (μg·kg

-1

)

and then exposed for 6 h to 2.5% SEVO. After rat hippocampal tissue was collected and separated

flow cytometry

immunofluorescence staining and Western blotting were used respectively to detect cell apoptosis

expression of endoplasmic reticulum(ER) stress markers PERK and Caspase-12

and expression of MAPK signal pathway-related proteins (ERK

JNK and P38).

Results

The apoptotic rate of hippocampal cells was significantly lower (24.27±4.52

43.90±10.94

0.05)

and the expression of PERK and Caspase-12 was also obviously decreased in the rats after co-administration of SEVO and DEX than those exposed to SEVO alone (

0.05). The expression levels of p-ERK

p-JNK and p-P38 were significantly increased in the rats after SEVO exposure than the control rats (

0.05)

and the levels were lowest in the rats after co-administration (

0.05).

Conclusion

DEX alleviates ER stress probably by inhibiting the MAPK signaling pathway

and then improves neurotoxicity induced by SEVO.

关键词

Keywords

references

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