Rice Bran Extract Compensates Mitochondrial Dysfunction in a Cellular Model of Early Alzheimer's Disease

Hagl, Stephanie; Grewal, Rekha; Ciobanu, Ion; Helal, Amr M.; Khayyal, Mohamed T.; Müller, Walter E.; Eckert, Gunter P.

doi:10.3233/jad-132084

Cited by 44 publications

(47 citation statements)

References 46 publications

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“…Several researchers have used RBE to activate various types of cells [17–19]. Hagl et al found that RBE, which contains oryzanols and tocopherol components, compensated age-related mitochondrial dysfunction by increasing the mitochondrial respiration and membrane potential in a neurodegenerative mouse model.…”

Section: Discussionmentioning

confidence: 99%

Pigmentation Effect of Rice Bran Extracted Minerals Comprising Soluble Silicic Acids

Jang

Seo

2016

Evidence-Based Complementary and Alternative Medicine

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Our investigation focused on identifying melanogenesis effect of soluble minerals in rice bran ash extract (RBE) which include orthosilicic acid (OSA). Melanocytes were apparently normal in terms of morphology. It was, however, shown that they were stressed a little in the RBE and OSA added media in aspect of LDH activity. Melanin synthesis and intracellular tyrosinase activity were increased by treatment of RBE which is similar to that of OSA. The Western blotting results showed that TRP-1, tyrosinase, and MITF expression levels were 2-3 times higher in the OSA and RBE groups compared to the control group which promoted melanin synthesis through CREB phosphorylation. Moreover, histology and immunohistochemistry were shown to have similar result to that of protein expression. As a result, minerals which comprise orthosilicic acid has the potential to promote melanogenesis and both RBE and OSA have similar cell viability, protein expression, and immunostaining results, suggesting that RBE comprises specific minerals which promote melanin synthesis through increasing of MITF and CREB phosphorylation. Therefore, RBE could be used as a novel therapeutic approach to combat melanin deficiency related diseases by stimulating melanocytes via its soluble Si and mineral components.

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Section: Discussionmentioning

confidence: 99%

Pigmentation Effect of Rice Bran Extracted Minerals Comprising Soluble Silicic Acids

Jang

Seo

2016

Evidence-Based Complementary and Alternative Medicine

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“…Elevates ATP production and respiratory rates as well as PGC1α protein levels in PC12APPsw cells, thereby ameliorating the altered mitochondrial function AD [142] Astragaloside IV Augments the viability of neuronal cells, reduces apoptosis and the generation of intracellular ROS. Moreover, it also reduces mitochondrial superoxide in the presence of Aβ 1-42 AD [143] Asiatic acid (AA) Protects against glutamate toxicity, rotenone-induced mitochondrial dysfunction and oxidative stress-mediated apoptosis in differentiated SH-SYS5Y cells PD [144] Ghrelin Protects dopaminergic neurons against rotenone via reinstating mitochondrial dysfunction and inhibiting mitochondrial dependent apoptosis PD [145] Ursodeoxycholic acid (UDCA)…”

Section: Methazolamide (Mtz)mentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

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“…We recently reported that a stabilized rice bran extract containing vitamin E congeners and c-oryzanol had beneficial effects on mitochondrial function in PC12 cells (Hagl et al 2015a) and in the brains of young guinea pigs (Hagl et al 2013). Furthermore, the extract improved mitochondrial dysfunction in a cell culture model of AD (Hagl et al 2015b) as well as in the brains of aged NMRI mice (Hagl et al 2016). Until now, the effects of rice bran extract have only been examined in short-term in vivo studies (feeding period 3-4 weeks) using oral gavage.…”

Section: Introductionmentioning

confidence: 95%

Effects of Long-Term Rice Bran Extract Supplementation on Survival, Cognition and Brain Mitochondrial Function in Aged NMRI Mice

et al. 2016

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Aging represents a major risk factor for the development of neurodegenerative diseases like Alzheimer's disease (AD). As mitochondrial dysfunction plays an important role in brain aging and occurs early in the development of AD, the prevention of mitochondrial dysfunction might help to slow brain aging and the development of neurodegenerative diseases. Rice bran extract (RBE) contains high concentrations of vitamin E congeners and γ-oryzanol. We have previously shown that RBE increased mitochondrial function and protected from mitochondrial dysfunction in vitro and in short-term in vivo feeding studies. To mimic the use of RBE as food additive, we have now investigated the effects of a long-term (6 months) feeding of RBE on survival, behavior and brain mitochondrial function in aged NMRI mice. RBE administration significantly increased survival and performance of aged NMRI mice in the passive avoidance and Y-maze test. Brain mitochondrial dysfunction found in aged mice was ameliorated after RBE administration. Furthermore, data from mRNA and protein expression studies revealed an up-regulation of mitochondrial proteins in RBE-fed mice, suggesting an increase in mitochondrial content which is mediated by a peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α)-dependent mechanism. Our findings suggest that a long-term treatment with a nutraceutical containing RBE could be useful for slowing down brain aging and thereby delaying or even preventing AD.

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Rice Bran Extract Compensates Mitochondrial Dysfunction in a Cellular Model of Early Alzheimer's Disease

Cited by 44 publications

References 46 publications

Pigmentation Effect of Rice Bran Extracted Minerals Comprising Soluble Silicic Acids

Pigmentation Effect of Rice Bran Extracted Minerals Comprising Soluble Silicic Acids

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Effects of Long-Term Rice Bran Extract Supplementation on Survival, Cognition and Brain Mitochondrial Function in Aged NMRI Mice

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