Possible mechanisms involved in the protective effects of chrysin against lead-induced cognitive decline: An in vivo study in a rat model

Shahab Ghaderi; Alireza Komaki; Iraj Salehi; Zahra Basir; Masome Rashno

doi:10.1016/j.biopha.2022.114010

Possible mechanisms involved in the protective effects of chrysin against lead-induced cognitive decline: An in vivo study in a rat model

Biomed Pharmacother. 2023 Jan:157:114010. doi: 10.1016/j.biopha.2022.114010. Epub 2022 Nov 16.

Authors

Shahab Ghaderi¹, Alireza Komaki², Iraj Salehi³, Zahra Basir⁴, Masome Rashno⁵

Affiliations

¹ Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran; Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
² Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
³ Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran; Asadabad School of Medical Sciences, Asadabad, Iran.
⁴ Department of Basic Sciences, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
⁵ Asadabad School of Medical Sciences, Asadabad, Iran; Student Research Committee, Asadabad School of Medical Sciences, Asadabad, Iran. Electronic address: Masome.rashno@yahoo.com.

PMID: 36402029
DOI: 10.1016/j.biopha.2022.114010

Abstract

Lead (Pb) is a highly poisonous environmental pollutant that can induce cognitive decline. Chrysin, a natural flavonoid compound, has anti-oxidative, anti-inflammatory, and neuroprotective properties in different neurodegenerative disorders. The present study was designed to examine the putative effects of chrysin against Pb-induced cognitive impairment and the possible involved mechanisms. Adult male Wistar rats were exposed to Pb acetate (500 ppm in standard drinking water) either alone or in combination with daily oral administration of chrysin (30 mg/kg) for eight consecutive weeks. During the eight-week period of the study, the cognitive capacity of the rats was evaluated by employing both novel object recognition and passive avoidance tests. On day 56, hippocampal synaptic plasticity (long-term potentiation; LTP) was recorded in perforant path-dentate gyrus (PP-DG) synapses to assess field excitatory postsynaptic potentials (fEPSPs) slope and population spike (PS) amplitude. Subsequently, pro- and anti-inflammatory cytokines and histological changes were evaluated in the cerebral cortex and hippocampus of the rats. Moreover, Pb levels in blood and brain tissues were assessed. The results showed that Pb exposure causes cognitive decline, inhibition of hippocampal LTP induction, imbalance of pro- and anti-inflammatory cytokines, enhancement of Pb levels in blood and brain tissues, and neuronal loss. However, chrysin treatment improved cognitive dysfunction, ameliorated hippocampal LTP impairment, modulated inflammatory status, reduced Pb concentration, and prevented neuronal loss in the Pb-exposed rats. The results suggest that chrysin alleviates Pb-induced cognitive deficit, possibly through mitigation of hippocampal synaptic dysfunction, modulation of inflammatory status, reduction of Pb concentration, and prevention of neuronal loss.

Keywords: Chrysin; Cognitive decline; Inflammation; Lead acetate; Long-term potentiation; Neuronal loss.

Publication types

Retracted Publication

MeSH terms

Animals
Cognitive Dysfunction* / chemically induced
Cognitive Dysfunction* / drug therapy
Cognitive Dysfunction* / prevention & control
Dentate Gyrus* / physiology
Excitatory Postsynaptic Potentials
Hippocampus
Long-Term Potentiation
Male
Neuronal Plasticity
Rats
Rats, Wistar