Table 3.

Neuroprotective effects of honey supplementation on animal models.

Authors (Year)	Type of source	Purpose	Mechanism
Tang et al. (2017)	Animal study (rat)	To investigate the protective effects of honey against PQ-induced toxicity in the midbrain and lungs of rats.	Honey may act as an antioxidant defence mechanism to protect dopaminergic neurons from oxidative stress-related damage
Mohd Sairazi et al. (2017)	Animal study (rat)	To investigate the extent of the neuroprotective effect conferred by Malaysian honey, an antioxidant agent, in the cerebral cortex of rats against KA-induced oxidative stress and neurodegeneration in an animal model of KA-induced excitotoxicity.	The cerebral cortex’s decreased levels of thiobarbituric acid reactive chemicals and increased total antioxidant status level upon honey consumption.
Qaid et al. (2021)	Animal study (rat)	to investigate the role of honey on medial prefrontal cortical neuronal morphology and cholinergic markers such as acetylcholine (ACh) and acetylcholinesterase (AChE) following exposure to normobaric hypoxia in rats.	Honey improves brain cholinergic indicators, protecting against hypoxia-induced mPFC neuronal damage
Qaid et al. (2020b)	Animal study (rat)	To investigate the responses of antioxidant defences to normobaric hypoxia and the effects of honey on the brain oxidant/ antioxidant status of adult male rats.	Honey increases brain resistance to hypoxia and antioxidant enzymes might be upregulated in rats in both normoxic and hypoxic environments
Mohd Yusoff et al. (2018)	Animal study (rat)	To focus on its morphometric effect on cornuammonis1 (CA1) pyramidal neurons of the hippocampus	Honey was shown to have more substantial impacts on neuronal soma size for a bigger neural dendritic tree, more synaptic connections, and greater neuronal activity
Akouchekian et al. (2018)	Human study (Major neurocognitive disorder patients)	To investigate the efficacy of the herbal combination of sedge, saffron, and Astragalus honey on cognitive and depression score of patients with the major neurocognitive disorder (MCD)	In the brain tissue, honey reduces lipid peroxidation and simultaneously boosts the activities of glutathione reductase and superoxide dismutase
Muhammad et al. (2014)	Animal study (rat)	To investigate the effect of Acacia honey from north-west Nigeria on sodium arsenite-induced oxidative damage and clastogenicity in male Wistar rats	The honey from Nigeria may possess high hydrogen peroxide scavenging activity to mitigate oxidative stress and clastogenicity
Goes et al. (2018)	Animal study (mice)	To investigate the possible involvement of inflammatory cytokines, neurotrophic factors and neuronal recovery in the effect of chrysin in 6-hydroxy dopamine (6-OHDA), a well-established model of Parkinson’s disease, in the striatum of mice.	The neuroprotective effect of chrysin from honey in the treatment of Parkinson’s disease and, indicated the mechanism involved through the inflammatory cytokines, neurotrophic factors and recovery of dopaminergic neurons in the striatum.
Saad et al. (2015)	Animal study (rat)	To determine the possible mechanisms of neuroprotection elicited by pinocembrin with specific emphasis on chronic prophylactic use before the induction of global cerebral ischemia–reperfusion	Pinocembrin reduced oxidative stress, inflammatory, and apoptotic indicators as well as glutamate and lactate dehydrogenase activity to lessen the harm caused by cerebral ischemia–reperfusion
Campos et al. (2022)	Animal study (rat)	To evaluate the antioxidant and neuroprotective effects of chrysin against the neurotoxicity elicited by aluminium chloride (AlCl3).	In particular, chrysin reduced the cognitive impairment induced by AlCl3 as well as normalized the acetylcholinesterase and butyrylcholinesterase activities in the hippocampus. The chrysin counteracted the oxidative damage, in terms of lipid peroxidation, protein carbonylation, catalase, and superoxide dismutase impairment, in the brain cortex and hippocampus. Lastly, necrotic cells frequency in the same brain regions was also decreased by chrysin administration
Nassar et al. (2020)	Animal study (rat)	to examine the protective role of bee products: a mixture of honey, propolis, palm pollen, and royal jelly (HPPJ) against Sumithion-induced toxicity.	The protective role of bee products: a mixture of honey, propolis, palm pollen, and royal jelly (HPPJ) counteracted the hematological, renal, and hepatic toxicity of sumithion exposure.
Kadar et al. (2022)	Animal study (rat)	To investigate the effects of honey supplementation and to compare it with a pure form of antioxidant, caffeic acid (CA), on MetS parameters and inflammatory markers in the brains of MetS-induced rats.	Honey consumption significantly reduced rain TNF-α levels and increased brain BDNF levels.
Abdulmajeed et al. (2015)	Animal study (rat)	To investigate the possible neuroprotective effects of honey against lead (Pb)-induced neurotoxicity.	Honey has neuroprotective effects against lead-induced cognitive deficit probably by enhancing antioxidant activities.
Adeniyi et al. (2022)	Animal study (rat)	To evaluate the ameliorative potential of honey in lipopolysaccharides-induced neuroinflammation.	Honey reduces TNF- α, IL6, nitrite and malondialdehyde levels and increases glutathione. Then, the positive restoration of neuronal structure and Nissl body distribution in the hippocampus, prefrontal cortex, and striatum.