Curcumin micelles improve mitochondrial function in neuronal PC12 cells and brains of NMRI mice – Impact on bioavailability

Hagl, Stephanie; Kocher, Alexa; Schiborr, Christina; Kolesova, Natalie; Frank, Jan; Eckert, Gunter P.

doi:10.1016/j.neuint.2015.07.026

Cited by 81 publications

(42 citation statements)

References 51 publications

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“…GSSG, as an oxidized form of glutathione, can be easily converted to GSH by glutathione reductase, and hence, a lower concentration can easily lead to low GSH. In our study, VPA-exposed rats were under stressful conditions, so the unexpected increase of GSSG in valproate-treated animals that were also treated with curcumin, is supported by the previous study by Hagl et al [32], who reported that when under non-stressful conditions, curcumin induces the synthesis of GSH and many detoxifying enzymes (as shown in group IV). This might also be attributed to the low absorption and quick elimination of curcumin from the body.…”

Section: Discussionsupporting

confidence: 87%

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Postnatal treatment using curcumin supplements to amend the damage in VPA-induced rodent models of autism

Al-Askar

Bhat

Selim

et al. 2017

BMC Complement Altern Med

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BackgroundValproic acid (VPA) is used as a first-line antiepileptic agent and is undergoing clinical trials for use as a treatment for many disorders. Mothers undergoing VPA treatment during early pregnancy reportedly show increased rates of autism among their offspring. The benefits of curcumin supplementation were investigated using an animal model of VPA-induced autism.MethodsThe study was performed using a rodent model of autism by exposing rat fetuses to valproic acid (VPA) on the 12.5th day of gestation. At 7 days from their birth, the animals were supplemented with a specific dose of curcumin. Forty neonatal male Western Albino rats were divided into four groups. Rats in group I received only phosphate-buffered saline, rats in group II were the prenatal VPA exposure newborns, rats in group III underwent prenatal VPA exposure supplemented with postnatal curcumin, and rats in group IV were given only postnatal curcumin supplements.ResultsVPA rats exhibited delayed maturation and lower body and brain weights with numerous signs of brain toxicity, such as depletion of IFN-γ, serotonin, glutamine, reduced glutathione, glutathione S-transferase, lipid peroxidase with an increase in CYP450, IL-6, glutamate, and oxidized glutathione. A curcumin supplement moderately corrected these dysfunctions and was especially noticeable in improving delayed maturation and abnormal weight.ConclusionsCurcumin plays a significant therapeutic role in attenuating brain damage that has been induced by prenatal VPA exposure in rats; however, its therapeutic role as a dietary supplement still must be certified for use in humans.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-017-1763-7) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 87%

“…This might also be attributed to the low absorption and quick elimination of curcumin from the body. Hagl et al proved that low bioavailability of curcumin can be ameliorated through administration with secondary plant compounds, micronization and micellation, which might help to increase its therapeutic potency [32]. …”

Section: Discussionmentioning

confidence: 99%

Postnatal treatment using curcumin supplements to amend the damage in VPA-induced rodent models of autism

Al-Askar

Bhat

Selim

et al. 2017

BMC Complement Altern Med

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“…Hagl et al 126 prepared new CUR micelles and investigated the bioavailability in vivo in NMRI mice and the effects of native CUR and a newly developed CUR micelles formulation on mitochondrial function in vitro in PC12 cells and ex vivo in isolated mouse brain mitochondria. CUR micelles improved bioavailability of native CUR around 10–40 fold in plasma and brain of mice.…”

Section: Biological Activities Of Various Curcuminoid Formulationsmentioning

confidence: 99%

Biological activities of curcuminoids, other biomolecules from turmeric and their derivatives – A review

Amalraj¹,

Pius

Gopi

et al. 2017

Journal of Traditional and Complementary Medicine

731

413

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In recent years, several drugs have been developed deriving from traditional products and current drug research is actively investigating the possible therapeutic roles of many Ayruvedic and Traditional Indian medicinal therapies. Among those being investigated is Turmeric. Its most important active ingredient is curcuminoids. Curcuminoids are phenolic compounds commonly used as a spice, pigment and additive also utilized as a therapeutic agent used in several foods. Comprehensive research over the last century has revealed several important functions of curcuminoids. Various preclinical cell culture and animals studies suggest that curcuminoids have extensive biological activity as an antioxidant, neuroprotective, antitumor, anti-inflammatory, anti-acidogenic, radioprotective and arthritis. Different clinical trials also suggest a potential therapeutic role for curcuminoids in numerous chronic diseases such as colon cancer, lung cancer, breast cancer, inflammatory bowel diseases. The aim of this review is to summarize the chemistry, analog, metal complex, formulations of curcuminoids and their biological activities.

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“…Similarly, improvements in drug delivery and targeting will greatly assist in enhancing bioavailablity and aid in the development of more effective therapeutic agents. For example, Hagl and colleagues review improvements in the bioavailability of curcumin compounds as potential treatments for neurodegenerative disease (Hagl et al ., ). Curcumin micelles had improved effectiveness in protecting PC12 cells from nitrosative stress, compared with curcumin alone.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Redox‐based therapeutics in neurodegenerative disease

McBean

López

Wallner

2016

British J Pharmacology

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This review describes recent developments in the search for effective therapeutic agents that target redox homeostasis in neurodegenerative disease. The disruption to thiol redox homeostasis in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and multiple sclerosis is discussed, together with the experimental strategies that are aimed at preventing, or at least minimizing, oxidative damage in these diseases. Particular attention is given to the potential of increasing antioxidant capacity by targeting the Nrf2 pathway, the development of inhibitors of NADPH oxidases that are likely candidates for clinical use, together with strategies to reduce nitrosative stress and mitochondrial dysfunction. We describe the shortcomings of compounds that hinder their progression to the clinic and evaluate likely avenues for future research. LINKED ARTICLESThis article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc Abbreviations 6(OH)DA, 6-hydroxydopamine; AD, Alzheimer's disease; ADME(T), absorption, distribution, metabolism and excretion/toxicity; ALS, amyotrophic lateral sclerosis; APP, amyloid precursor protein; ARE, antioxidant response element; ASSNAC, S-allylmercapto-N-acetyl cysteine; Aβ, amyloid-β; CA, carnosic acid; DMF, dimethylfumarate; EAE, experimental autoimmune encephalomyelitis; EpRE, electrophile response element; GCL, glutamate cysteine ligase; GR, glutathione reductase; Grx, glutaredoxin; GSK-3β, glycogen synthase kinase-3β; Keap1, Kelch-like ECH-associated protein-1; MMF, monomethylfumarate; MPTP, 1-methyl, 4-phenyl-1,2,3,6-tetrahydropyridine; MS, multiple sclerosis; MPO, myeloperoxidase; NAC, N-acetylcysteine; NACA, N-acetylcysteine amide; NOX, NADPH oxidase; NQO1, NAD(P)H quinone oxidoreductase-1; Nrf2, nuclear factor (erythroid-derived 2)-like 2; PD, Parkinson's disease; PS1, pre-senelin-1; RNS, reactive nitrogen species; SN, substantia nigra; Trx, thioredoxin; TrxR, thioredoxin reductase; xCT, functional subunit of the x c À exchanger Disruption of cerebral redox homeostasis is a common occurrence in a range of human neurodegenerative disorders, and although much is understood of mechanistic dysfunction, the gap between knowledge and the availability of effective therapies remains wide. In this review, we focus on the potential for developing therapeutic agents that promote the availability of thiol redox antioxidants or boost the antioxidant capacity of cells via stimulation of the transcription factor, nuclear factor (erythroid-derived 2)-like 2 (Nrf2). In addition, we discuss options for reducing ROS production by inhibition of NADPH oxidases (NOXs), limiting nitrative stress or targeting mitochondrial dysfunction. Other potential strategies for limiting oxidative stress in neurodegenerative disease include nutrient and vitamin supplementation and metal chelators, which are excluded from the discussion. These approaches are t...

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Curcumin micelles improve mitochondrial function in neuronal PC12 cells and brains of NMRI mice – Impact on bioavailability

Cited by 81 publications

References 51 publications

Postnatal treatment using curcumin supplements to amend the damage in VPA-induced rodent models of autism

Postnatal treatment using curcumin supplements to amend the damage in VPA-induced rodent models of autism

Biological activities of curcuminoids, other biomolecules from turmeric and their derivatives – A review

Redox‐based therapeutics in neurodegenerative disease

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