4.2 Article

Role of RGS2 in sevoflurane-induced cognitive dysfunction in aged rats

Journal

PAKISTAN JOURNAL OF PHARMACEUTICAL SCIENCES
Volume 35, Issue 1, Pages 58-66

Publisher

UNIV KARACHI
DOI: 10.36721/PJPS.2022.35.1.REG.059-067.1

Keywords

Sevoflurane; cognitive dysfunction; RGS2; hippocampus

Funding

  1. Project of Natural Science Foundation of Inner Mongolia Autonomous Region [2020MS08095]

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This study found that inhalation anesthesia may lead to postoperative cognitive dysfunction in some patients. Through experiments on aged rats, it was found that sevoflurane inhalation can cause changes in cognitive function, as well as down-regulation of RGS2 expression in the hippocampus, increased neuronal apoptosis, and decreased expression of NGF and BDNF. Therefore, sevoflurane inhalation may be one of the important factors leading to cognitive dysfunction.
After undergoing inhalation anesthesia, some patients, especially elderly patients, experience postoperative cognitive dysfunction, such as personality changes and memory impairment. In the present study, 20-month-old rats were randomly allocated to sevoflurane (Sevo group) and control groups (Con group), and they inhaled 3% sevoflurane or 40% oxygen for 8 hours, respectively. The Morris water maze test found that the cognitive function of rats in the Sevo group were significantly different on 1d and 3d after anesthesia than that of rats in the Con group. The expression of RGS2 mRNA and protein in hippocampus of Sevo group was lower compared to the Con group, while Ca2+ was higher than con group. The expression of CaM and CaMK II in Sevo group was higher compared to the Con group. We found that Bcl-2 reduced, but the expression of Bax and Caspase-3 increased, indicating that apoptosis of hippocampal neurons was increased after sevoflurane inhalation. Both the expression of NGF and BDNF was depressed in the Sevo group. After continuous inhalation of 3% sevoflurane for 8h, the expression of RGS2 in the hippocampi of aged rats is down regulated. RGS2 may be an important factor that leads to cognitive dysfunction in rats.

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