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. 2021 Oct;36(7):1903-1915.
doi: 10.1007/s11011-021-00741-4. Epub 2021 May 27.

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

Shimaa Saad El-Din  1 , Sahar Abd Elwahab  2 , Laila Rashed  2 , Salwa Fayez  2 , Basma Emad Aboulhoda  3 , Ola Ahmed Heikal  4 , Asmaa Fathi Galal  4 , Zeinab A Nour  2
Affiliations

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

Shimaa Saad El-Din et al. Metab Brain Dis. 2021 Oct.

Abstract

Alzheimer's Disease (AD), the most prevalent neurodegenerative disorder among elderly people, is ordinarily associated with progressive cognitive decline. Peroxisome proliferator-activated receptors-gamma (PPAR-γ) agonists can be targeted as a beneficial therapeutic strategy against AD. In the present study, we aimed to investigate the preventive and therapeutic effects of rice bran extract (RBE) as a possible PPAR-γ agonist on the microglial phenotype modulation in AD in mice compared to the effects of pioglitazone. This study included 64 adult male Swiss Albino mice divided into 8 groups, each group comprised 8 mice; control group, RBE group, lipopolysaccharide-induced neurodegeneration (a) (LPSa) group, (LPSb) group, RBE-preventive group (RBE + LPSa), pioglitazone-preventive group (PG + LPSa), RBE-treated group (RBE + LPSb), and pioglitazone-treated group (PG + LPSb). Cognitive functions were assessed by Y-maze and Morris water maze tests. The expression of PPAR-γ, CD45, arginase1, CD36, and CD163 genes was assessed by real time qPCR and the estimation of NF-kβ protein level was done by Western blot technique. Moreover, the assessment of Aβ42 and P-tau levels was performed by ELISA. Histopathological examination of brain tissues was performed for all the studied groups. Our results showed that RBE and pioglitazone could modulate microglial phenotype from M1 to M2 where they significantly decreased the expression of NF-κβ and the pro-inflammatory microglial marker (CD45) in parallel with increasing the expression of the anti-inflammatory microglial and phagocytic markers (arginase1, CD163, and CD36). In addition, RBE and pioglitazone significantly increased PPAR-γ expression and reduced Aβ42 deposition as well as p-tau protein levels. In conclusion, our study identified the possible role of PPAR-γ agonistic activity of RBE as a preventive and therapeutic agent in the treatment of the neuro-inflammation associated with AD.

Keywords: Alzheimer’s disease; Microglia; Neuro-inflammation; PPAR-γ; Pioglitazone; Rice bran extract.

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References

    1. Aboulhoda BE, Rashed LA, Ahmed H, Obaya EM, Ibrahim W, Alkafass M A, Abd El‐Aal SA, ShamsEldeen AM (2021): Hydrogen sulfide and mesenchymal stem cells‐extracted microvesicles attenuate LPS‐induced Alzheimer's disease. J Cellular Physiol https://doi.org/10.1002/jcp.30283
    1. Aghamohammadzadeh R, Unwin RD, Greenstein AS et al (2015) Effects of obesity on perivascular adipose tissue vasorelaxant function: nitric oxide, inflammation and elevated systemic blood pressure. J Vasc Res 52:299–305 - DOI
    1. Arai K, Matsuki N, Ikegaya Y et al (2001) Deterioration of spatial learning performances in lipopolysaccharide-treated mice. Jpn J Pharmacol 87:195–201 - DOI
    1. Bhatia HS, Baron J, Hagl S et al (2016) Rice bran derivatives alleviate microglia activation: Possible involvement of MAPK pathway. J Neuroinflammation 13:148 - DOI
    1. Bromley-Brits K, Deng Y, Song W (2011) Morris Water Maze Test for Learning and Memory Deficits in Alzheimer’s Disease Model Mice. J Vis Exp 53:2920

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