Histopathological study on neuroapoptotic alterations induced by etomidate in rat hippocampus.

xlomafota13 shared this article with you from Inoreader Histopathological study on neuroapoptotic alterations induced by etomidate in rat hippocampus. Via histochem Related Articles Histopathological study on neuroapoptotic alterations induced by etomidate in rat hippocampus. Acta Histochem. 2021 Feb 16;123(3):151693 Authors: Alipour M, Asl MK, Khordad E, Alipour F, Raoofi A, Ebrahimzadeh-Bideskan A, Ebrahimi V Abstract In human, there is substantial neurogenesis in the hippocampus that is implicated in memory formation and learning. These new-born neurons can be affected by neuropathological conditions. Anesthesia and surgical procedures are associated with postoperative cognitive changes particularly, impaired memory and learning. Therefore, the aim of this study was to evaluate the possible neurodegenerative effects of etomidate in rat hippocampus. Thirty male Wistar rats weighing 250 ± 30 g were randomly divided into 3 groups: 1) Etomidate group; four times 20 mg intraperitoneal injection with 1-h intervals, 2) Control group; the equal volume of normal saline, and 3) Normal group; without any intervention. 6 h after the last injection, the brains were removed and processed according to routine histological methods. TUNEL assay and toluidine blue staining were performed to evaluate neuro-histopathological changes in different regions of hippocampus. Our results showed that the number of TUNEL positive cells and dark neurons (DNs) in etomidate group were significantly higher in the CA1, CA2, CA3, and dentate gyrus (DG) of hippocampus compared with the control and normal groups (p < 0.05). While, there was no significant difference between the various regions of hippocampus in control and normal groups. Our findings showed that etomidate can increase apoptotic cells and dark neurons induction in different regions of hippocampus mainly in DG. PMID: 33601320 [PubMed - as supplied by publisher] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.