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

El-Din, Shimaa Saad; Elwahab, Sahar Abd; Rashed, Laila Ahmed; Fayez, Salwa; Aboulhoda, Basma Emad; Heikal, Ola A.; Galal, Asmaa F.; Nour, Zeinab A.

doi:10.1007/s11011-021-00741-4

Cited by 11 publications

(10 citation statements)

References 33 publications

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“…It has been demonstrated that peripheral macrophages enhance infiltration of the hippocampus in DSS-induced mice, along with the increased frequency of M1-like microglia and increased release of proinflammatory cytokines [ 6 ]. Several studies have shown that in the disease process of AD, PPAR-γ plays an essential role in inhibiting the M1 polarization of microglia and promoting M2 polarization [ 46 , 47 , 48 ]. Like macrophages, iNOS is also a marker of M1 polarization in microglia and is widely recognized [ 49 , 50 , 51 ].…”

Section: Discussionmentioning

confidence: 99%

Shared Genes of PPARG and NOS2 in Alzheimer’s Disease and Ulcerative Colitis Drive Macrophages and Microglia Polarization: Evidence from Bioinformatics Analysis and Following Validation

Dong

Shen

et al. 2023

IJMS

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Emerging evidence shows that peripheral systemic inflammation, such as inflammatory bowel disease (IBD), has a close even interaction with central nervous disorders such as Alzheimer’s disease (AD). This study is designed to further clarify the relationship between AD and ulcerative colitis (UC, a subclass of IBD). The GEO database was used to download gene expression profiles for AD (GSE5281) and UC (GSE47908). Bioinformatics analysis included GSEA, KEGG pathway, Gene Ontology (GO), WikiPathways, PPI network, and hub gene identification. After screening the shared genes, qRT-PCR, Western blot, and immunofluorescence were used to verify the reliability of the dataset and further confirm the shared genes. GSEA, KEGG, GO, and WikiPathways suggested that PPARG and NOS2 were identified as shared genes and hub genes by cytoHubba in AD and UC and further validated via qRT-PCR and Western blot. Our work identified PPARG and NOS2 are shared genes of AD and UC. They drive macrophages and microglia heterogeneous polarization, which may be potential targets for treating neural dysfunction induced by systemic inflammation and vice versa.

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Section: Discussionmentioning

confidence: 99%

Shared Genes of PPARG and NOS2 in Alzheimer’s Disease and Ulcerative Colitis Drive Macrophages and Microglia Polarization: Evidence from Bioinformatics Analysis and Following Validation

Dong

Shen

et al. 2023

IJMS

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“…BBR has been found to partially improve neuroinflammation by reducing IL-6 and TNF-α levels in LPS-induced BV-2 cells, indicating a potential preventive or delayed onset of early AD ( 255 ). Rice bran extract (RBE), a novel PPARγ regulator that enhances cognitive function in rats ( 256 ), also exerts anti-inflammatory effects by regulating microglia phenotype in LPS-induced mice ( 257 ). RBE and PIO can both regulate microglia M1 to M2 phenotype, significantly reducing the expression of NF-κB and pro-inflammatory microglia markers (CD45), while increasing the expression of anti-inflammatory microglia markers and PPARγ ( 257 ).…”

Section: Pparmentioning

confidence: 99%

“…Rice bran extract (RBE), a novel PPARγ regulator that enhances cognitive function in rats ( 256 ), also exerts anti-inflammatory effects by regulating microglia phenotype in LPS-induced mice ( 257 ). RBE and PIO can both regulate microglia M1 to M2 phenotype, significantly reducing the expression of NF-κB and pro-inflammatory microglia markers (CD45), while increasing the expression of anti-inflammatory microglia markers and PPARγ ( 257 ). Additionally, RBE can reduce Aβ 42 deposition and p-tau protein levels, thereby effectively ameliorating AD pathology ( 257 ).…”

Section: Pparmentioning

confidence: 99%

Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review)

Zheng,

Zhang,

Zhang

et al. 2023

Int J Mol Med

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The intricate nature of Alzheimer's disease (AD) pathogenesis poses a persistent obstacle to drug development. In recent times, neuroinflammation has emerged as a crucial pathogenic mechanism of AD, and the targeting of inflammation has become a viable approach for the prevention and management of AD. The present study conducted a comprehensive review of the literature between October 2012 and October 2022, identifying a total of 96 references, encompassing 91 distinct pharmaceuticals that have been investigated for their potential impact on AD by inhibiting neuroinflammation. Research has shown that pharmaceuticals have the potential to ameliorate AD by reducing neuroinflammation mainly through regulating inflammatory signaling pathways such as NF-κB, MAPK, NLRP3, PPARs, STAT3, CREB, PI3K/Akt, Nrf2 and their respective signaling pathways. Among them, tanshinone IIA has been extensively studied for its anti-inflammatory effects, which have shown significant pharmacological properties and can be applied clinically. Thus, it may hold promise as an effective drug for the treatment of AD. The present review elucidated the inflammatory signaling pathways of pharmaceuticals that have been investigated for their therapeutic efficacy in AD and elucidates their underlying mechanisms. This underscores the auspicious potential of pharmaceuticals in ameliorating AD by impeding neuroinflammation.

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“…Such strategies have been explored in clinical trials for neurological diseases, such as Alzheimer’s disease. Compounds as pioglitazone or D (dendrimer)-tesaglitazar (a dendrimer-PPARα/γ dual agonist conjugate to pass BBB), as well as extracts of a variety of rice seem to significantly decrease 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) 137 , 182 (H) In recent years, many studies have addressed the possibility of blocking receptors that trigger the microglial pro-inflammatory response 146 , 147 using antibody therapies or specific drugs. 183 In this regard, substances like BLZ945 inhibit the colony-stimulating factor 1 receptor 183 and it may also be possible to use other novel antibodies that block pro-inflammatory substances.…”

Section: Potential Strategies To Combat Ad Based On Modifying the Act...mentioning

confidence: 99%

Section: Potential Strategies To Combat Ad Based On Modifying the Act...mentioning

confidence: 99%

The relationships between neuroglial and neuronal changes in Alzheimer’s disease, and the related controversies II: gliotherapies and multimodal therapy

Toledano-Dı́az¹,

Álvarez

Toledano

2022

J Cent Nerv Syst Dis

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Since the original description of Alzheimer´s disease (AD), research into this condition has mainly focused on assessing the alterations to neurons associated with dementia, and those to the circuits in which they are involved. In most of the studies on human brains and in many models of AD, the glial cells accompanying these neurons undergo concomitant alterations that aggravate the course of neurodegeneration. As a result, these changes to neuroglial cells are now included in all the “pathogenic cascades” described in AD. Accordingly, astrogliosis and microgliosis, the main components of neuroinflammation, have been integrated into all the pathogenic theories of this disease, as discussed in this part of the two-part monograph that follows an accompanying article on gliopathogenesis and glioprotection. This initial reflection verified the implication of alterations to the neuroglia in AD, suggesting that these cells may also represent therapeutic targets to prevent neurodegeneration. In this second part of the monograph, we will analyze the possibilities of acting on glial cells to prevent or treat the neurodegeneration that is the hallmark of AD and other pathologies. Evidence of the potential of different pharmacological, non-pharmacological, cell and gene therapies (widely treated) to prevent or treat this disease is now forthcoming, in most cases as adjuncts to other therapies. A comprehensive AD multimodal therapy is proposed in which neuronal and neuroglial pharmacological treatments are jointly considered, as well as the use of new cell and gene therapies and non-pharmacological therapies that tend to slow down the progress of dementia.

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

Cited by 11 publications

References 33 publications

Shared Genes of PPARG and NOS2 in Alzheimer’s Disease and Ulcerative Colitis Drive Macrophages and Microglia Polarization: Evidence from Bioinformatics Analysis and Following Validation

Shared Genes of PPARG and NOS2 in Alzheimer’s Disease and Ulcerative Colitis Drive Macrophages and Microglia Polarization: Evidence from Bioinformatics Analysis and Following Validation

Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review)

The relationships between neuroglial and neuronal changes in Alzheimer’s disease, and the related controversies II: gliotherapies and multimodal therapy

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