The curry spice curcumin attenuates beta-amyloid-induced toxicity through beta-catenin and PI3K signaling in rat organotypic hippocampal slice culture

Hoppe, Juliana Bender; Frozza, Rudimar Luiz; Pires, Elisa Nicoloso Simões; Meneghetti, André; Salbego, Christianne Gazzana

doi:10.1179/1743132813y.0000000225

Cited by 21 publications

(14 citation statements)

References 43 publications

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“…Curcumin has been recognized as an effective agent for neurodegenerative diseases, because of its neuroprotective effects in PD, AD, and ALS [45]. Curcumin also ameliorates neurotoxicity induced by various toxicants such as metals (fluoride, lead, and arsenic), solvents, 6-OHDA, and Aβ [36,37,[40][41][42][43][44]. Recently, we found that curcumin enhanced the adult hippocampal neurogenesis as well as improved learning and memory deficits in AD model via recruitment of the Wnt/β-catenin pathway [41].…”

Section: Discussionmentioning

confidence: 99%

“…Curcumin attenuates neurotoxicity induced by various toxicants such as fluoride, acrolein, okadaic acid, lead, ethanol, arsenic, sodium metabisulfite, 6-hydroxydopamine (6-OHDA), and amyloid-β (Aβ) [34][35][36][37][38][39][40][41][42][43][44]. Curcumin also provides neuroprotection in cellular and animal models of neurological and neurodegenerative disorders including Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), depression, multiple sclerosis, and schizophrenia [45][46][47][48].…”

Section: Introductionmentioning

confidence: 99%

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Bisphenol-A Mediated Inhibition of Hippocampal Neurogenesis Attenuated by Curcumin via Canonical Wnt Pathway

et al. 2015

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Bisphenol A (BPA) is an environmental xenoestrogenic endocrine disruptor, utilized for production of consumer products, and exerts adverse effects on the developing nervous system. Recently, we found that BPA impairs the finely tuned dynamic processes of neurogenesis (generation of new neurons) in the hippocampus of the developing rat brain. Curcumin is a natural polyphenolic compound, which provides neuroprotection against various environmental neurotoxicants and in the cellular and animal models of neurodegenerative disorders. Here, we have assessed the neuroprotective efficacy of curcumin against BPA-mediated reduced neurogenesis and the underlying cellular and molecular mechanism(s). Both in vitro and in vivo studies showed that curcumin protects against BPA-induced hippocampal neurotoxicity. Curcumin protects against BPA-mediated reduced neural stem cells (NSC) proliferation and neuronal differentiation and enhanced neurodegeneration. Curcumin also enhances the expression/levels of neurogenic and the Wnt pathway genes/proteins, which were reduced due to BPA exposure in the hippocampus. Curcumin-mediated neuroprotection against BPA-induced neurotoxicity involved activation of the Wnt/β-catenin signaling pathway, which was confirmed by the use of Wnt specific activators (LiCl and GSK-3β siRNA) and inhibitor (Dkk-1). BPA-mediated increased β-catenin phosphorylation, decreased GSK-3β levels, and β-catenin nuclear translocation were significantly reversed by curcumin, leading to enhanced neurogenesis. Curcumin-induced protective effects on neurogenesis were blocked by Dkk-1 in NSC culture treated with BPA. Curcumin-mediated enhanced neurogenesis was correlated well with improved learning and memory in BPA-treated rats. Overall, our results conclude that curcumin provides neuroprotection against BPA-mediated impaired neurogenesis via activation of the Wnt/β-catenin signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Bisphenol-A Mediated Inhibition of Hippocampal Neurogenesis Attenuated by Curcumin via Canonical Wnt Pathway

et al. 2015

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“…However, the role of Akt-GSK3β in regulating OS-induced osteoblast apoptosis is unknown. Furthermore, studies have indicated that curcumin exerts a protective effect against apoptosis via the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway [32,33]. However, whether curcumin treatment promotes osteoblast survival through prevention of OS-induced mitochondrial dysfunction and activation of Akt-GSK3β signaling remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of Oxidative Stress-Induced Osteoblast Apoptosis by Curcumin is Associated with Preservation of Mitochondrial Functions and Increased Akt-GSK3β Signaling

Dai

Mao

Sun

et al. 2017

Cell Physiol Biochem

102

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Background: Osteoblast apoptosis induced by oxidative stress plays a crucial role in the development and progression of osteoporosis. Curcumin, a natural antioxidant isolated from Curcuma longa, has highly protective effects against osteoporosis. However, the effects of curcumin on oxidative stressinduced osteoblast apoptosis remain unclear. This study aimed to explore the effect of curcumin on hydrogen peroxide (H 2 O 2 ) induced osteoblast apoptosis and the underlying mechanisms. Methods: An osteoblastic cell line (Saos-2) was exposed to various concentrations of H 2 O 2 with or without curcumin treatment. Cell viability was evaluated by MTT assays. The apoptosis rate was analyzed by flow cytometry and TUNEL assays. Mitochondrial ROS and membrane potential were determined using a fluorescence microscope. Mitochondrial respiratory enzyme activity was measured using a spectrophotometer. Protein levels were detected by western blotting. Results: Curcumin was cytoprotective because it greatly improved the viability of Saos-2 cells exposed to H 2 O 2 and attenuated H 2 O 2 -induced apoptosis. Curcumin treatment also preserved the mitochondrial redox potential, decreased the mitochondrial oxidative status, and improved the mitochondrial membrane potential and functions. Furthermore, curcumin treatment markedly increased levels of phosphorylated protein kinase B (Akt) and phosphorylated glycogen synthase kinase-3β (GSK3β). Conclusion: Curcumin administration ameliorates oxidative stress-induced apoptosis in osteoblasts by preserving mitochondrial functions and activation of Akt-GSK3β signaling. These data provide experimental evidence supporting the clinical use of curcumin for prevention or treatment of osteoporosis.P. Dai and Y. Mao contributed equally to this work.

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“…[7][8][9] Curcumin, which is extracted from Curcuma longa L, has been shown to exert a range of pharmacological effects, including antioxidative and anti-inflammatory activity, which may be useful for preventing cancer. [10][11][12] Curcumin can also reduce infarct volume and improve neurological function after middle cerebral artery occlusion (MCAO), [13][14][15][16] leading us to wonder whether curcumin may promote proliferation and differentiation of NSCs after stroke. Indeed, studies have shown that curcumin can influence proliferation and differentiation of nerve cells, 17,18 though whether this is also true in ischemic animals is unknown.…”

Section: Introductionmentioning

confidence: 99%

Curcumin protects against stroke and increases levels of Notch intracellular domain

Liu

Cao

et al. 2016

Neurological Research

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The curry spice curcumin attenuates beta-amyloid-induced toxicity through beta-catenin and PI3K signaling in rat organotypic hippocampal slice culture

Abstract: These results reinforce the neuroprotective effects of curcumin on Abeta toxicity and add some evidence that its mechanism may involve beta-catenin and PI3K signaling pathway in organotypic hippocampal slice culture.

Cited by 21 publications

References 43 publications

Bisphenol-A Mediated Inhibition of Hippocampal Neurogenesis Attenuated by Curcumin via Canonical Wnt Pathway

Bisphenol-A Mediated Inhibition of Hippocampal Neurogenesis Attenuated by Curcumin via Canonical Wnt Pathway

Attenuation of Oxidative Stress-Induced Osteoblast Apoptosis by Curcumin is Associated with Preservation of Mitochondrial Functions and Increased Akt-GSK3β Signaling

Curcumin protects against stroke and increases levels of Notch intracellular domain

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