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Propofol protects rats against intra-cerebroventricular streptozotocin-induced cognitive dysfunction and neuronal damage
, 1, 1
Affiliations- Department of Anaesthesiology, Weifang People’s Hospital, Weifang, Shandong, China
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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.
Keywords
propofol, cognitive deficit, oxidative stress, inflammation
About this articleTitle
Propofol protects rats against intra-cerebroventricular streptozotocin-induced cognitive dysfunction and neuronal damage
Journal
Issue
Article type
Original article
Pages
248-255
Published online
2022-03-22
Page views
2409
Article views/downloads
856
DOI
Pubmed
Bibliographic record
Folia Morphol 2023;82(2):248-255.
Keywords
propofol
cognitive deficit
oxidative stress
inflammation
Authors
L. Sun
X. Dou
W. Yang
References (25)- Bloom DE, Cafiero E, Jané-Llopis E, et al. The global economic burden of noncommunicable diseases. World Econ Forum. 2011: 1–46.
- Cai Z, Zhao B, Ratka A. Oxidative stress and β-amyloid protein in Alzheimer's disease. Neuromolecular Med. 2011; 13(4): 223–250.
- Chen Z, Trapp BD. Microglia and neuroprotection. J Neurochem. 2016; 136 Suppl 1: 10–17.
- De la Monte SM, Tong M. Brain metabolic dysfunction at the core of Alzheimer's disease. Biochem Pharmacol. 2014; 88(4): 548–559.
- Ellman GL, Courtney KD, Andres V, et al. A new and rapid colorimetric determination of acetylcholinesterase activity. Biochem Pharmacol. 1961; 7: 88–95.
- Farkas E, Luiten PG. Cerebral microvascular pathology in aging and Alzheimer's disease. Prog Neurobiol. 2001; 64(6): 575–611.
- Gallagher M, Colombo PJ. Ageing: the cholinergic hypothesis of cognitive decline. Curr Opin Neurobiol. 1995; 5(2): 161–168.
- Hyder A, Wunderlich C, Puvanachandra P, et al. The impact of traumatic brain injuries: A global perspective. NeuroRehabilitation. 2007; 22(5): 341–353.
- Kandimalla R, Reddy PH. Therapeutics of neurotransmitters in Alzheimer's disease. J Alzheimers Dis. 2017; 57(4): 1049–1069.
- Korczyn AD, Vakhapova V, Grinberg LT. Vascular dementia. J Neurol Sci. 2012; 322(1-2): 2–10.
- Kumaran D, Hassabis D, Spiers HJ, et al. Impaired spatial and non-spatial configural learning in patients with hippocampal pathology. Neuropsychologia. 2007; 45(12): 2699–2711.
- Lee CY, Landreth GE. The role of microglia in amyloid clearance from the AD brain. J Neural Transm (Vienna). 2010; 117(8): 949–960.
- Li WX, Luo RY, Chen C, et al. Effects of propofol, dexmedetomidine, and midazolam on postoperative cognitive dysfunction in elderly patients: a randomized controlled preliminary trial. Chin Med J (Engl). 2019; 132(4): 437–445.
- Liu H, Zhang J. Cerebral hypoperfusion and cognitive impairment: the pathogenic role of vascular oxidative stress. Int J Neurosci. 2012; 122(9): 494–499.
- O'Brien JT, Thomas A. Vascular dementia. Lancet. 2015; 386(10004): 1698–1706.
- Przedborski S. Neurodegeneration. Neuroimmune Pharmacology. 2016: 345–354.
- Razavi BM, Fazly Bazzaz BS. A review and new insights to antimicrobial action of local anesthetics. Eur J Clin Microbiol Infect Dis. 2019; 38(6): 991–1002.
- Schliebs R, Arendt T. The cholinergic system in aging and neuronal degeneration. Behav Brain Res. 2011; 221(2): 555–563.
- Tenner AJ. Complement in Alzheimer's disease: opportunities for modulating protective and pathogenic events. Neurobiol Aging. 2001; 22(6): 849–861.
- Threlkeld SW, Hill CA, Szalkowski CE, et al. Effects of test experience and neocortical microgyria on spatial and non-spatial learning in rats. Behav Brain Res. 2012; 235(2): 130–135.
- Truelsen T, Begg S, Mathers C. The global burden of cerebrovascular disease. Glob Burd Dis. 2000: 1–67.
- Van Beek AH, Claassen JA. The cerebrovascular role of the cholinergic neural system in Alzheimer's disease. Behav Brain Res. 2011; 221(2): 537–542.
- Wang B, Shravah J, Luo H, et al. Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation. Biochem Biophys Res Commun. 2009; 389(1): 105–111.
- Yuzer H, Yuzbasioglu MF, Ciralik H, et al. Effects of intravenous anesthetics on renal ischemia/reperfusion injury. Ren Fail. 2009; 31(4): 290–296.
- Zhao T, Ding Km, Zhang L, et al. Acetylcholinesterase and butyrylcholinesterase inhibitory activities of β-carboline and quinoline alkaloids derivatives from the plants of genuspeganum. J Chem. 2013; 2013: 1–6.
