Protective effects of lycopene against amyloid β-induced neurotoxicity in cultured rat cortical neurons

Qu, Mingyue; Li, Li; Chen, Chunhai; Li, Min; Pei, Liping; Chu, Fang; Yang, Ju Hye; Yu, Zhengping; Deng-gao, Wang; Zhou, Zhou

doi:10.1016/j.neulet.2011.10.048

Cited by 83 publications

(39 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our study, Ab treatment on PC12 cells induced neurotoxicity as indicated by increased cell death, elevated intracellular levels of ROS and calcium, loss of mitochondrial membrane potential, and decrease of the activity of caspase-3 and ratio of Bcl-2/Bax. These observations are consistent with the findings previously reported by others (Sul et al 2009;Qu et al 2011;Xian et al 2012). Treatment with pinostrobin significantly reversed these changes in PC12 cells, suggesting the protective effect of pinostrobin against Abinduced neurotoxicity.…”

Section: Discussionsupporting

confidence: 93%

“…It has also been extensively used to investigate factor-induced cellular toxicity, such as Ab, glutamate, and others (Hwang and Yen 2008;Qu et al 2011;Wang et al 2011). Treatment of PC12 cells with Ab induces oxidative stress, overload of intracellular calcium influx, mitochondrial membrane potential depolarization, tau phosphorylation expression, and apoptotic cell death (Sul et al 2009;Qu et al 2011). Based on these findings, the model of Abinduced PC12 cell injury was adopted for studying the neuroprotective effect of pinostrobin.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Protective Effects of Pinostrobin on β-Amyloid-Induced Neurotoxicity in PC12 Cells

Xian

Lin

et al. 2012

Cell Mol Neurobiol

View full text Add to dashboard Cite

Beta-Amyloid peptide (Aβ), a major protein component of brain senile plaques in Alzheimer's disease (AD), has been considered as a critical cause in the pathogenesis of AD. Pinostrobin, a potent flavonoid inducer, is the major and most active ingredient of Folium cajani. The present study aimed to investigate whether pinostrobin could provide protective effect against Aβ(25-35)-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The PC12 cells were pretreated with different concentrations of pinostrobin for 2 h, followed by the challenge with 20 μM Aβ(25-35) for 24 h. The results showed that pretreatment with pinostrobin significantly elevated cell viability, decreased the lactate dehydrogenase activity, the levels of intracellular reactive oxygen species and calcium, and mitochondrial membrane potential in Aβ(25-35)-treated PC12 cells. In addition, pinostrobin significantly suppressed the formation of DNA fragmentation and increased the ratio of Bcl-2/Bax. These results indicate that pinostrobin was able to exert a neuroprotective effect against Aβ(25-35)-induced neurotoxicity in PC12 cells, at least in part, via inhibiting oxidative damage and calcium overload, as well as suppressing the mitochondrial pathway of cellular apoptosis.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Protective Effects of Pinostrobin on β-Amyloid-Induced Neurotoxicity in PC12 Cells

Xian

Lin

et al. 2012

Cell Mol Neurobiol

View full text Add to dashboard Cite

show abstract

“…Lycopene protects the cell from lipid peroxidation and oxidative DNA damage as a highly efficient antioxidant (8,9). In addition, lycopene exhibits other properties, including antiapoptosis (10), anti-inflammation (11,12), antiamyloid (13), anti-ischemia (14), and antitumor properties (15). Since lycopene has a high liposolubility, it can cross the blood-brain barrier (16).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effects of lycopene pretreatment on transient global cerebral ischemia-reperfusion in rats: The role of the Nrf2/HO-1 signaling pathway

Lei

Zhang

et al. 2015

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. The present study aimed to investigate the neuroprotective effect of lycopene in a mouse model of bilateral common carotid artery occlusion (BCCAO) and the role of the Nrf2/HO-1 signaling pathway. A total of 60 male C57BL/6 mice, aged 12 weeks and weighing 20-24 g, were used in the present study. The mice were randomly assigned to three groups: Control, BCCAO and BCCAO + lycopene. The neurological score was assessed 24, 48 or 72 h following BCCAO. Hematoxylin and eosin staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) were performed to detect neuronal death and survival. The production of glutathione (GSH) and reactive oxygen species were detected to investigate the oxidative stress. The expression levels of nuclear factor erythroid 2-related factor (Nrf2) and Heme oxygenase-1 (HO-1) were determined by western blotting. Lycopene significantly improved the neurological score in the BCCAO mice. It attenuated neuronal apoptosis, as indicated by TUNEL staining, and attenuated the oxidative stress induced by global ischemia. Lycopene increased the expression levels of Nrf2 and HO-1, indicating that the Nrf2/HO-1 signaling pathway may be involved in the neuroprotective effect of lycopene. The present study revealed that lycopene protects the brain from global ischemic injury, which is associated with its antiapoptotic effect and the activation of the Nrf2/HO-1 signaling pathway.

show abstract

“…In a cell culture model of AD, lycopene was shown to efficiently attenuate Aβ-induced ROS formation, improve neuron viability and decrease the rate of apoptosis [38]. Low serum levels of lycopene, β-carotene, lutein and zeaxanthin have also been linked to impaired cognitive function and AD [39-42].…”

Section: Introductionmentioning

confidence: 99%

Cerebrospinal fluid levels of inflammation, oxidative stress and NAD+are linked to differences in plasma carotenoid concentrations

Guest

Grant

Garg

et al. 2014

J Neuroinflammation

View full text Add to dashboard Cite

BackgroundThe consumption of foods rich in carotenoids that possess significant antioxidant and inflammatory modulating properties has been linked to reduced risk of neuropathology. The objective of this study was to evaluate the relationship between plasma carotenoid concentrations and plasma and cerebrospinal fluid (CSF) markers of inflammation, oxidative stress and nicotinamide adenine dinucleotide (NAD+) in an essentially healthy human cohort.MethodsThirty-eight matched CSF and plasma samples were collected from consenting participants who required a spinal tap for the administration of anaesthetic. Plasma concentrations of carotenoids and both plasma and cerebrospinal fluid (CSF) levels of NAD(H) and markers of inflammation (IL-6, TNF-α) and oxidative stress (F2-isoprostanes, 8-OHdG and total antioxidant capacity) were quantified.ResultsThe average age of participants was 53 years (SD = 20, interquartile range = 38). Both α-carotene (P = 0.01) and β-carotene (P < 0.001) correlated positively with plasma total antioxidant capacity. A positive correlation was observed between α-carotene and CSF TNF-α levels (P = 0.02). β-cryptoxanthin (P = 0.04) and lycopene (P = 0.02) inversely correlated with CSF and plasma IL-6 respectively. A positive correlation was also observed between lycopene and both plasma (P < 0.001) and CSF (P < 0.01) [NAD(H)]. Surprisingly no statistically significant associations were found between the most abundant carotenoids, lutein and zeaxanthin and either plasma or CSF markers of oxidative stress.ConclusionTogether these findings suggest that consumption of carotenoids may modulate inflammation and enhance antioxidant defences within both the central nervous system (CNS) and systemic circulation. Increased levels of lycopene also appear to moderate decline in the essential pyridine nucleotide [NAD(H)] in both the plasma and the CSF.

show abstract

Protective effects of lycopene against amyloid β-induced neurotoxicity in cultured rat cortical neurons

Cited by 83 publications

References 23 publications

Protective Effects of Pinostrobin on β-Amyloid-Induced Neurotoxicity in PC12 Cells

Protective Effects of Pinostrobin on β-Amyloid-Induced Neurotoxicity in PC12 Cells

Neuroprotective effects of lycopene pretreatment on transient global cerebral ischemia-reperfusion in rats: The role of the Nrf2/HO-1 signaling pathway

Cerebrospinal fluid levels of inflammation, oxidative stress and NAD+are linked to differences in plasma carotenoid concentrations

Contact Info

Product

Resources

About