Taurine Prevents Passive Avoidance Memory Impairment, Accumulation of Amyloid-β Plaques, and Neuronal Loss in the Hippocampus of Scopolamine-Treated Rats

Gorgani, Sattar; Jahanshahi, Mehrdad; Elyasi, Leila

doi:10.1007/s11062-019-09810-y

Cited by 10 publications

(6 citation statements)

References 35 publications

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“…To evaluate ischemic‐induced neuronal damage in the hippocampus of rats, brain sections were dyed using cresyl violet, as previously reported. [ 70 ] The brain sections were placed in xylene for deparaffinization and rehydrated in a series of graded ethanol until water is washed. Then, the brain sections were dyed in 0.02% cresyl violet (Sigma) solution for 10 min and washed in distilled water (twice).…”

Section: Methodsmentioning

confidence: 99%

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Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Noorgaldi,

Sarkala,

Enayati

et al. 2023

Archiv der Pharmazie

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Stroke is the most common cause of death among neurological diseases. The protective effects of Potentilla reptans L. include antioxidative, anti‐inflammatory, and antiapoptotic effects. In this study, the brain protection and beta‐amyloid effects of P. reptans root extract were investigated in the rat brain ischemia/reperfusion (IR) model. Forty male Wistar rats were randomly divided into five groups (n = 8), including IR, sham, and three groups receiving P. reptans with concentrations of 0.025, 0.05, and 0.1 (g/kg/b.w.), which were injected daily for 7 days. For the IR model, the common carotid artery was occluded bilaterally for 8 min. All injections were intraperitoneal (IP). The shuttle box test was used to measure passive avoidance memory. Then the brain tissue was extracted for the histological examination of neuron counts and β‐amyloid plaques using a morphometric technique, and finally, Statistical Package for the Social Sciences software was used for statistical analysis of the data. Pretreatment with P. reptans improved memory impairment. Also, by examining the tissues of the CA1, CA3, and dentate gyrus areas of the hippocampus, it was observed that the number of plaques in the groups receiving P. reptans extract was reduced compared to the IR group, especially at the concentration of 0.05 g/kg/b.w. Also, P. reptans improved the number of neurons at all concentrations, in which the concentration of 0.05 g/kg/b.w. showed more effective therapeutic results. Taken together, we found that P. reptans root extract has beneficial effects on memory impairment, neuronal loss, and β‐amyloid accumulation.

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Section: Methodsmentioning

confidence: 99%

“…The passive avoidance memory test was done in the same way as was done in our previous studies. [70,71] This apparatus has a box with two chambers: a light chamber and a dark chamber. Between the chambers, there is a guillotine door in the middle of the wall.…”

Section: Passive Avoidance Memory Testmentioning

confidence: 99%

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Noorgaldi,

Sarkala,

Enayati

et al. 2023

Archiv der Pharmazie

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“…After the 14-day intervention, the saline + SCO and 3 treatment groups were injected with a single dose of SCO (3 mg/kg, IP) (24) to induce an AD-like condition (Figure 1).…”

Section: Experimental Designmentioning

confidence: 99%

Naringin Reduced the Density and Total Number of Aβ Plaques and Restored Memory Function and Volume of Hippocampal CA1 Area in Alzheimer's Disease Model Rats: A Stereological Study

Yazdani,

Jahanshahi,

Elyasi

et al. 2024

Iran J Psychiatry Behav Sci

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Background: Alzheimer's disease (AD), the most prevalent form of dementia worldwide, is characterized by memory impairment and the accumulation of tau and beta-amyloid (Aβ) plaques. Naringin, a flavonoid, has exhibited strong anti-inflammatory, anti-oxidant, and anti-apoptotic properties. Objectives: In this study, we aimed to demonstrate the neuroprotective effects of naringin on memory function, the total number and density of Aβ plaques, and the volume of the hippocampal CA1 region in a scopolamine (SCO)-induced AD model in rats. Methods: Forty male Wistar rats were randomly divided into the following groups: a control group, a saline + SCO (3 mg/kg) group (pretreated with 200 µL saline), and 3 treatment groups receiving naringin at doses of 50 mg/kg/day + SCO, 100 mg/kg/day + SCO, and 200 mg/kg/day + SCO (pretreated with 50, 100, or 200 mg/kg of naringin) for 14 consecutive days via intraperitoneal (IP) injection. After the 14-day pretreatment period, the saline + SCO and 3 naringin treatment groups received SCO (3 mg/kg) to induce an AD-like condition. Memory function was assessed using the inhibitory passive avoidance test. Following brain harvesting, paraffin-embedded coronal brain slices were stained with Congo red, and the density and the total number of Aβ plaques and the volume of the hippocampal CA1 area were estimated using unbiased stereological techniques. Results: The results indicated that naringin significantly improved memory function, with the most pronounced effect observed in the naringin 200 mg/kg + SCO group. Stereological analysis revealed that SCO reduced the volume of the hippocampal CA1 area and increased the total number and density of Aβ plaques. Pretreatment with naringin significantly restored the hippocampal CA1 volume in the 200 mg/kg + SCO group compared to the saline + SCO group. Additionally, naringin reduced the total number and density of Aβ plaques, with the most significant decrease observed in the 200 mg/kg + SCO group. Conclusions: Naringin restored memory function and the volume of the hippocampal CA1 region while reducing the total number and density of Aβ plaques in a SCO-induced AD model in rats. This stereological study complements previous molecular research on naringin's neuroprotective effects in AD-like pathogenesis.

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“…Activated Bax translocates into the mitochondria to form protein-permeable channels/pores within the outer mitochondrial membrane in a process known as mitochondrial outer membrane permeabilization (MOMP). MOMP stimulates the release of pro-apoptotic factors (e.g., AIF, cyt-c, EndoG) from the mitochondrial intermembrane space into the cytoplasm to activate a caspase-dependent neuronal apoptosis in AD brains [ 189 , 190 ]. The investigations addressed by this review denote that the amelioration of apoptosis of cortical and hippocampal neurons in AD models is closely linked to the antioxidant and anti-inflammatory activities of RJ [ 28 , 70 , 119 , 120 ].…”

Section: Mechanisms Underlying Effects Of Rj On Cognition and Ad-rmentioning

confidence: 99%

Royal Jelly as an Intelligent Anti-Aging Agent—A Focus on Cognitive Aging and Alzheimer’s Disease: A Review

Ali

2020

Antioxidants

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The astronomical increase of the world’s aged population is associated with the increased prevalence of neurodegenerative diseases, heightened disability, and extremely high costs of care. Alzheimer’s Disease (AD) is a widespread, age-related, multifactorial neurodegenerative disease that has enormous social and financial drawbacks worldwide. The unsatisfactory outcomes of available AD pharmacotherapy necessitate the search for alternative natural resources that can target various the underlying mechanisms of AD pathology and reduce disease occurrence and/or progression. Royal jelly (RJ) is the main food of bee queens; it contributes to their fertility, long lifespan, and memory performance. It represents a potent nutraceutical with various pharmacological properties, and has been used in a number of preclinical studies to target AD and age-related cognitive deterioration. To understand the mechanisms through which RJ affects cognitive performance both in natural aging and AD, we reviewed the literature, elaborating on the metabolic, molecular, and cellular mechanisms that mediate its anti-AD effects. Preclinical findings revealed that RJ acts as a multidomain cognitive enhancer that can restore cognitive performance in aged and AD models. It promotes brain cell survival and function by targeting multiple adversities in the neuronal microenvironment such as inflammation, oxidative stress, mitochondrial alterations, impaired proteostasis, amyloid-β toxicity, Ca excitotoxicity, and bioenergetic challenges. Human trials using RJ in AD are limited in quantity and quality. Here, the limitations of RJ-based treatment strategies are discussed, and directions for future studies examining the effect of RJ in cognitively impaired subjects are noted.

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Taurine Prevents Passive Avoidance Memory Impairment, Accumulation of Amyloid-β Plaques, and Neuronal Loss in the Hippocampus of Scopolamine-Treated Rats

Cited by 10 publications

References 35 publications

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Neuroprotective effect of Potentilla reptans L. root in the rat brain global ischemia/reperfusion model

Naringin Reduced the Density and Total Number of Aβ Plaques and Restored Memory Function and Volume of Hippocampal CA1 Area in Alzheimer's Disease Model Rats: A Stereological Study

Royal Jelly as an Intelligent Anti-Aging Agent—A Focus on Cognitive Aging and Alzheimer’s Disease: A Review

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