Enhancement of cognitive functions by rice bran extract in a neuroinflammatory mouse model via regulation of PPARγ

Mostafa, Aya; Abdel‐Kader, Reham M.; Heikal, Ola A.

doi:10.1016/j.jff.2018.07.023

Cited by 16 publications

(9 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, they proved that this treatment regimen resulted in increased beta-and gamma-secretase activities accompanied with the increased expression of amyloid precursor protein (APP) leading to the accumulation of Aβ1-42 in the hippocampus and cerebral cortex of mice brains [15]. This model was further confirmed in our research group where we were able to show accumulation of Aβ1-42 protein in the cerebral cortex of the mice and decline in memory and cognition [16,17].…”

Section: Animals' Treatmentsupporting

confidence: 53%

Pyrroloquinoline Quinone Enhances Cognition of Neuroinflammatory Alzheimer’s Disease Mouse Model via Mitochondrial Biogenesis Regulation

Fadel¹,

Abdel‐Kader²

2021

NNB

View full text Add to dashboard Cite

Background: Mitochondrial biogenesis has been recently implicated to play an important role in Alzheimer’s disease (AD). Recently it has been reported that brains of AD patients show reduced expression in major genes and proteins such as PGC-1α involved in mitochondrial biogenesis. This led to the idea that enhancing mitochondrial biogenesis in AD, might represent a plausible strategy for AD treatment. Pyrroloquinoline quinone (PQQ) has been recently implicated in enhancing cognitive functions during aging; however, its effect on mitochondrial biogenesis in neuroinflammatory AD mouse model was not previously examined. Objective: The aim of this project was to test the cognitive enhancement effect of PQQ in a neuroinflammatory mouse model mimicking AD, and whether PQQ is able to activate mitochondrial biogenesis in brains of our AD mouse model. Methods: Neuroinflammatory AD mouse model was developed by Lipopolysaccharide (250 g kg-1 body weight, i.p) injection for 7 days, followed by daily PQQ treatment (10 mg kg-1 body weight) on days 4-7. Cognitive functions were assessed using Y-Maze, Water-Maze and object recognition tests. Neurodegeneration was evaluated using H&E. Finally, mitochondrial proteins were measured using immunohistochemistry. Results: PQQ treatment improved spatial recognition and working memory. PQQ treated mice brains showed decreased levels of neurodegeneration. Moreover, their brains showed greater amounts of both PGC-1α and the mitochondrial-membrane-bound protein cytochrome-c, indicating enhancement of mitochondrial biogenesis. Conclusion: This study demonstrates the ability of PQQ to improve memory in neuroinflammatory AD model via enhancing mitochondrial biogenesis, which may represent an alternative mechanistic approach for treating AD.

show abstract

Section: Animals' Treatmentsupporting

confidence: 53%

Pyrroloquinoline Quinone Enhances Cognition of Neuroinflammatory Alzheimer’s Disease Mouse Model via Mitochondrial Biogenesis Regulation

Fadel¹,

Abdel‐Kader²

2021

NNB

View full text Add to dashboard Cite

show abstract

“…Finally in 2018, our team reported that the Egyptian RBE enhances cognitive and behavioral functions in LPS-induced neuroinflammatory mouse model and the nuclear fractions extracted from the brains of mice treated with the RBE showed an increase in PPAR-γ binding to its response element [20]. Those data collectively support the hypothesis that RBE may have an anti-inflammatory effect which is mediated through activation of PPAR-γ receptor.…”

Section: Introductionmentioning

confidence: 69%

“…The current study provides further evidence for the possible agonistic effect of RBE on PPAR-γ nuclear receptor and the involvement of PPAR-γ activation in the neuroprotective effect of RBE in LPS-induced neuroinflammatory mouse model. In 2018, RBE was reported to increase the binding of PPAR-γ receptor to its DNA response element and that PPAR-γ plays a role in the cognition enhancing the effect of RBE [20]. Previously it was thought that PPAR-γ ligands exert their anti-inflammatory effect through increasing PPAR-γ sumoylation which is a post translational modification for PPAR-γ receptor [27,28].…”

Section: Discussionmentioning

confidence: 99%

“…Heat-stabilized Egyptian RBE was obtained from International Trade and Marketing Company, Egypt. It was dissolved in 0.6% DMSO and given orally in a dose of 100 mg/kg [20]. PG was obtained from Al-Andalous Pharmaceutical, Egypt, dissolved in 0.6% DMSO, and given orally in a dose of 30 mg/kg [21].…”

Section: Methodsmentioning

confidence: 99%

“…Then, the extract was evaporated under vacuum at a temperature not more than 50°C. The phytochemical profile of RBE was determined and reported before [20]. The bioactive compounds of RBE, γ-oryzanol, were determined using HPLC (Agilent 1100).…”

Section: Preparation Of Stabilized Rbementioning

confidence: 99%

See 2 more Smart Citations

Rice Bran Extract Protected against LPS-Induced Neuroinflammation in Mice through Targeting PPAR-γ Nuclear Receptor

et al. 2020

View full text Add to dashboard Cite

PPAR-γ anti-inflammatory functions have received significant attention since its agonists have been shown to exert a wide range of protective effects in many experimental models of neurologic diseases. Rice bran is very rich in polyunsaturated fatty acids, which are reported to act as PPAR-γ partial agonists. Herein, the anti-inflammatory effect of rice bran extract (RBE) through PPAR-γ activation was evaluated in LPS-induced neuroinflammatory mouse model in comparison to pioglitazone (PG) using 80 Swiss albino mice. RBE (100 mg/kg) and PG (30 mg/kg) were given orally for 21 days and LPS (0.25 mg/kg) was injected intraperitoneally for the last 7 days. TNF-α and COX-2 brain contents were evaluated by real-time PCR and immunohistochemical analysis. In addition, NFκB binding to its response element was evaluated alongside with the effect of treatments on IκB gene expression. Furthermore, PPAR-γ sumoylation was also studied. Finally, histopathological examination was performed for different brain areas. RBE administration was found to protect against the LPS-induced inflammatory effects by decreasing the inflammatory mediator expression in mice brains. It also decreased PPAR-γ sumoylation without significant effect on IκB expression or NFκB binding to its response element. The majority of the effects were attenuated in presence of PPAR-γ antagonist (GW9662). Level of significance was set to P < 0.05. Such findings highlight the agonistic effect of RBE component(s) on PPAR-γ and support the hypothesis of involvement of PPAR-γ activation in its neuroprotective effect.

show abstract

Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model

et al. 2021

View full text Add to dashboard Cite

Enhancement of cognitive functions by rice bran extract in a neuroinflammatory mouse model via regulation of PPARγ

Cited by 16 publications

References 48 publications

Pyrroloquinoline Quinone Enhances Cognition of Neuroinflammatory Alzheimer’s Disease Mouse Model via Mitochondrial Biogenesis Regulation

Pyrroloquinoline Quinone Enhances Cognition of Neuroinflammatory Alzheimer’s Disease Mouse Model via Mitochondrial Biogenesis Regulation

Rice Bran Extract Protected against LPS-Induced Neuroinflammation in Mice through Targeting PPAR-γ Nuclear Receptor

Possible role of rice bran extract in microglial modulation through PPAR-gamma receptors in alzheimer’s disease mice model

Contact Info

Product

Resources

About