Neuroprotective effect of curcumin on hippocampal injury in 6-OHDA-induced Parkinson's disease rat

Yang, Jiaqing; Song, Shilei; Li, Jian; Liang, Tao

doi:10.1016/j.prp.2014.02.005

Cited by 83 publications

(41 citation statements)

References 23 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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“…Song et al demonstrated that curcumin protected against neural impairments induced by 6-OHDA in the substantia nigra region, as evidenced by enhanced memory abilities, elevated levels of SOD and GSH-Px, and reduced concentration of MDA [28]. Yang et al indicated that curcumin had a neuroprotective function against 6-OHDA-induced hippocampus neurons in rats, and the underlying mechanism promoted neural regeneration of hippocampal tissue by activating the brain derived neurotrophic factor/Tropomyosin receptor kinase B-dependent pathway [29], which was consistent with our results.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Curcumin Against Oxidative Stress-Induced Injury in Rats with Parkinson’s Disease Through the Wnt/ β-Catenin Signaling Pathway

Wang

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: The study aimed to investigate the protective effect of curcumin against oxidative stress-induced injury of Parkinson’s disease (PD) through the Wnt/β-catenin signaling pathway in rats. Methods: The successfully established PD rat models and normal healthy rats were randomly assigned into the 6-hydroxydopamine (6-OHDA), the curcumin (Cur) and the control groups. Immunohistochemistry was used to detect the positive expression of tyrosine hydroxylase (TH), dopamine transporter (DAT) and glial fibrillary acidic protein (GFAP). Deutocerebrum primary cells were extracted and classified into the control, 6-OHDA, Cur (5, 10, 15 µmol/L), Dickkopf-1 (DKK-1) and Cur + DKK-1 groups. MTT assays, adhesion tests and TUNEL staining were used to assess cell viability, adhesion and apoptosis, respectively. Western blotting and qRT-PCR were used to examine the protein and mRNA expressions of Wnt3a and β-catenin and the c-myc and cyclinD1 mRNA expressions. Results: TH and DAT expressions in the Cur group were elevated and GFAP was reduced compared with the 6-OHDA group. Curcumin enhanced viability, survival and adhesion and attenuated apoptosis of deutocerebrum primary cells by activating the Wnt/β-catenin signaling pathway. Higher Wnt3a and β-catenin mRNA and protein expressions and c-myc and cyclinD1 mRNA expressions, enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) contents, decreased malondialdehyde (MDA) content and elevated mitochondrial membrane potential (∆ψm) were found in the 10 and 15 µmol/L Cur groups compared with the 6-OHDA group. However, opposite tendencies were found in the Cur + DKK-1 group compared to the 10 µmol/L Cur group. Conclusion: This study suggests that curcumin could protect against oxidative stress-induced injury in PD rats via the Wnt/β-catenin signaling pathway.

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“…Cur, or diferuloylmethane, is a natural ingredient extracted from Curcuma longa rhizome [5,6]. It has attracted great interest for its numerous pharmacological properties such as anti-inflammation, antioxidant, anti-tumor and anti-nerve degeneration [2,7]. Previous studies suggested that Cur could be used in PD treatment in vivo [8].…”

Section: Introductionmentioning

confidence: 99%

“…Cui et al emphasized its mitigation on PD dopaminergic neural damage, of which increased tyrosine hydroxylase (TH) activity was included as a parameter [8]. However, the underlying mechanism of Cur being anti-PD has not been fully understood [7].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Protects an SH-SY5Y Cell Model of Parkinson’s Disease Against Toxic Injury by Regulating HSP90

Sang

Liu

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: We aimed to explore the protective role of curcumin (Cur) in a cell model of Parkinson’s disease (PD) and its underlying mechanism. Methods: In this study, genes concerned with PD-related keywords were screened within DiGSeE database. The association network between Cur and selected genes was downloaded from STITCH, with the interactions analyzed by STRING. We built a mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP⁺)-induced SH-SY5Y cell model of PD. Cell morphology was observed under an electron microscope. MTT assay was applied to detect cell proliferation rate. Western blot assay was conducted to determine the level of apoptotic markers, including cleaved caspase 3, Bcl-2-associated X protein (Bax) and B-cell lymphoma-extra-large (Bcl-xl). Tyrosine hydroxylase (TH), dopamine transporter (DAT) protein levels and dopamine (DA) concentration were identified as dopaminergic neuron markers and measured by western blotting or Enzyme-linked immunosorbent assay (ELISA). Results: Cur rescued the toxicity effects of MPP⁺ on SH-SY5Y cells, by controlling morphological change, promoting cell proliferation and inhibiting apoptosis. Of all PD-related genes, HSP90 played an important role in Cur-gene network. HSP90 protein level was elevated by MPP⁺, whereas Cur could reverse this effect. Silencing of HSP90 significantly attenuated the curative effect introduced by Cur, while HSP90 overexpression enhanced the impact of Cur on PD. Conclusion: Cur can effectively inhibit the toxic effect of MPP⁺ on SH-SY5Y cells and significantly reduce the adverse effects of MPP⁺ on dopaminergic neurons via up-regulation of HSP90.

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Neuroprotective effect of curcumin on hippocampal injury in 6-OHDA-induced Parkinson's disease rat

Cited by 83 publications

References 23 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

Protective Effect of Curcumin Against Oxidative Stress-Induced Injury in Rats with Parkinson’s Disease Through the Wnt/ β-Catenin Signaling Pathway

Curcumin Protects an SH-SY5Y Cell Model of Parkinson’s Disease Against Toxic Injury by Regulating HSP90

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