open access

Vol 82, No 2 (2023)
Original article
Submitted: 2022-01-15
Accepted: 2022-02-09
Published online: 2022-03-22
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Propofol protects rats against intra-cerebroventricular streptozotocin-induced cognitive dysfunction and neuronal damage

L. Sun1, X. Dou1, W. Yang1
·
Pubmed: 35347698
·
Folia Morphol 2023;82(2):248-255.
Affiliations
  1. Department of Anaesthesiology, Weifang People’s Hospital, Weifang, Shandong, China

open access

Vol 82, No 2 (2023)
ORIGINAL ARTICLES
Submitted: 2022-01-15
Accepted: 2022-02-09
Published online: 2022-03-22

Abstract

Background: Cognitive dysfunction is a severe issue of Alzheimer’s disease. Thus,
the present study was conducted to enumerate the protective effect of propofol
(PPL) in rats against intra-cerebroventricular streptozotocin (STZ)-induced cognitive
dysfunction and neuronal damage.
Materials and methods: The effect of PPL was investigated to evaluate behavioural
changes in STZ-induced cognitive dysfunction in Wistar rats using Object
Recognition Task (ORT) for nonspatial, Morris Water Maze (MWM) for spatial and
locomotor activity. The effect of PPL was also investigated on acetylcholine (ACh)
esterase (AChE) activity and oxidative stress markers, e.g., nitrite, malonaldehyde
(MDA), superoxide dismutase (SOD), and glutathione (GSH). The level of pro-inflammatory
cytokines, e.g., tumour necrosis factor (TNF)-α, interleukin (IL)-1β,
and IL-6, was also studied in the PPL-treated group. The effect of PPL on the level
of neurotransmitters, e.g., dopamine (DA), serotonin (5-HT), and norepinephrine
(NE) and their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic
acid (5-HIAA), and homovanillic acid (HVA) levels were also estimated
in frozen hippocampal tissues by high-performance liquid chromatography.
Histopathology analysis of neurons in the hippocampus of rats was performed
using haematoxylin and eosin (H&E) staining.
Results: Propofol showed significant improvement in the spatial and nonspatial
memory deficit of rats in the MWM test and ORT in rats. It also causes improvement
in locomotor activity of rats by preserving ACh via inhibition of AChE. It also
potentiates the expression of DA, 5-HT, and NE with a simultaneous reduction in
the level of metabolites (DOPAC, HVA, and 5-HIAA). PPL showed a reduction of
oxidative stress in rats by restoring the level of nitrite, SOD, MDA, and GSH near
to normal. In the PPL-treated group, the level of TNF-α, IL-1β, and IL-6 was found
reduced in a dose-dependent manner. In histopathology analysis of neurons in the
hippocampus of the STZ rats, PPL causes dose-dependent reduction of pyknosis
in the nucleus, which confirmed the protective effect of PPL.
Conclusions: The present study demonstrated that PPL could significantly attenuate
cognitive dysfunction and neuronal damage in STZ-induced rats.

Abstract

Background: Cognitive dysfunction is a severe issue of Alzheimer’s disease. Thus,
the present study was conducted to enumerate the protective effect of propofol
(PPL) in rats against intra-cerebroventricular streptozotocin (STZ)-induced cognitive
dysfunction and neuronal damage.
Materials and methods: The effect of PPL was investigated to evaluate behavioural
changes in STZ-induced cognitive dysfunction in Wistar rats using Object
Recognition Task (ORT) for nonspatial, Morris Water Maze (MWM) for spatial and
locomotor activity. The effect of PPL was also investigated on acetylcholine (ACh)
esterase (AChE) activity and oxidative stress markers, e.g., nitrite, malonaldehyde
(MDA), superoxide dismutase (SOD), and glutathione (GSH). The level of pro-inflammatory
cytokines, e.g., tumour necrosis factor (TNF)-α, interleukin (IL)-1β,
and IL-6, was also studied in the PPL-treated group. The effect of PPL on the level
of neurotransmitters, e.g., dopamine (DA), serotonin (5-HT), and norepinephrine
(NE) and their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic
acid (5-HIAA), and homovanillic acid (HVA) levels were also estimated
in frozen hippocampal tissues by high-performance liquid chromatography.
Histopathology analysis of neurons in the hippocampus of rats was performed
using haematoxylin and eosin (H&E) staining.
Results: Propofol showed significant improvement in the spatial and nonspatial
memory deficit of rats in the MWM test and ORT in rats. It also causes improvement
in locomotor activity of rats by preserving ACh via inhibition of AChE. It also
potentiates the expression of DA, 5-HT, and NE with a simultaneous reduction in
the level of metabolites (DOPAC, HVA, and 5-HIAA). PPL showed a reduction of
oxidative stress in rats by restoring the level of nitrite, SOD, MDA, and GSH near
to normal. In the PPL-treated group, the level of TNF-α, IL-1β, and IL-6 was found
reduced in a dose-dependent manner. In histopathology analysis of neurons in the
hippocampus of the STZ rats, PPL causes dose-dependent reduction of pyknosis
in the nucleus, which confirmed the protective effect of PPL.
Conclusions: The present study demonstrated that PPL could significantly attenuate
cognitive dysfunction and neuronal damage in STZ-induced rats.

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Keywords

propofol, cognitive deficit, oxidative stress, inflammation

About this article
Title

Propofol protects rats against intra-cerebroventricular streptozotocin-induced cognitive dysfunction and neuronal damage

Journal

Folia Morphologica

Issue

Vol 82, No 2 (2023)

Article type

Original article

Pages

248-255

Published online

2022-03-22

Page views

2410

Article views/downloads

856

DOI

10.5603/FM.a2022.0027

Pubmed

35347698

Bibliographic record

Folia Morphol 2023;82(2):248-255.

Keywords

propofol
cognitive deficit
oxidative stress
inflammation

Authors

L. Sun
X. Dou
W. Yang

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