Thymoquinone Can Improve Neuronal Survival and Promote Neurogenesis in Rat Hippocampal Neurons

Beker, Merve; Dalli, Tugce; Elibol, Birsen

doi:10.1002/mnfr.201700768

Cited by 16 publications

(10 citation statements)

References 70 publications

(129 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Firstly, we evaluated the acute effect of TQ administration for 4 weeks on young neurogenesis and secondly, chronic effect of TQ administration for 12 weeks on adult neurogenesis. In consistent with previous study [79], we did not observe any difference on memory improvement, hippocampal neurogenesis, and BDNF/CREB signaling in hippocampus (Supplementary Fig. 2) after 4 weeks of TQ treatment in our acute time-point study.…”

Section: Discussionsupporting

confidence: 93%

“…Recently, the role of TQ in neuroprotection via BDNF pathways, which control NPCs/NSCs proliferation and differentiation, has attracted much attention. Acute administration of TQ for 15 days (20 mg kg-1 day-1) in young rats has been shown to enhance neuronal survival and to promote neurogenesis in rat hippocampal neurons via ERK/JNK and CREB signaling pathways, though no upregulation of BDNF was observed [79]. In the present study design, we have conducted two study to evaluate neurogenesis after 4 weeks of TQ administration in young and after 12 weeks of TQ administration in adult rats.…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway

et al. 2021

View full text Add to dashboard Cite

Thymoquinone is a pharmacologically active component of Nigella sativa Linn. seeds. Despite the diverse neuropharmacological attributes of TQ, limited reports related to adult neurogenesis and memory research are available. In this study, we investigated the effects of TQ on the proliferation and neural differentiation of cultured neural stem/progenitor cells (NSCs/ NPCs). We also investigated the effect of TQ chronic administration on neurogenesis and memory in adult rats. Under proliferation conditions, TQ (0.05-0.3 μM) significantly increased NSCs/NPCs viability, neurosphere diameter, and cell count. TQ treatment under differentiation conditions increased the proportion of cells positive for Tuj1 (a neuronal marker). Furthermore, chronic oral administration of TQ (25 mg/kg/day for 12 weeks) to adult rats increased the number of bromodeoxyuridine (BrdU)-immunopositive cells double-stained with a mature neuronal marker, neuronal nuclei (NeuN), and a proliferation marker, doublecortin (Dcx), in the dentate gyrus of the hippocampus. TQ-administered rats showed a profound beneficial effect on avoidance-related learning ability, associated with an increase in the hippocampal mRNA and protein levels of brain-derived neurotrophic factor (BDNF), as measured by both real-time PCR and ELISA. Western blot analysis revealed that TQ stimulates the phosphorylation of cAMP-response element-binding protein (CREB), the upstream signaling molecule in the BDNF pathway. Furthermore, chronic administration of TQ decreased lipid peroxide and reactive oxygen species levels in the hippocampus. Taken together, our results suggest that TQ plays a role in memory improvement in adult rats and that the CREB/BDNF signaling pathways are involved in mediating the actions of TQ in hippocampal neurogenesis.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 98%

Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In the current study, we found that TQ treatment significantly increased the expression of DCX protein. This result confirmed our previous findings that TQ administration had a positive effect on the neurogenesis [47]. As seen, it can be interpreted elevated neurogenesis in the hippocampus could be as a result of TQ-triggered protective effect against the pathophysiology of AD.…”

Section: Discussionsupporting

confidence: 91%

Thymoquinone (TQ) demonstrates its neuroprotective effect via an anti-inflammatory action on the Aβ_(1–42)-infused rat model of Alzheimer's disease

Elibol

Terzioglu-Usak

Beker

et al. 2019

Psychiatry and Clinical Psychopharmacology

Self Cite

View full text Add to dashboard Cite

OBJECTIVES: Alzheimer's disease (AD) is a severe neurodegenerative disease with presentation of the neuronal death, memory loss and cognitive decline. The relationship between neuroinflammation and AD has been well documented. However, the options of antiinflammatory treatment are very limited in patients with AD. Previous studies showed that flavonoids might be an effective treatment and thymoquinone (TQ), an aromatic hydrocarbon found in Nigella sativa suggested as a candidate molecule due to having strong anti-inflammatory effects. Our study aimed to investigate the effects of TQ on neuroinflammation and neuroprotection in Aβ (1-42) infused rat model of AD. METHODS: A rat model of AD was established in 6 month-old rats (n = 23) by intra-hippocampal infusion during 14 days via a micro-osmotic pump containing aggregated Aβ (1-42) . After model establishment, TQ at a dosage of 20 mg/kg/day was intubated intragastrically for 15 days. The functional recovery was determined using the Morris Water Maze task by measuring memory consolidation. The content of cytokine levels of Tumour Necrosis Factor-alpha (TNF-α), Interleukin-1 beta (IL-1β), Interleukin-1 alpha (IL-1α) and Interferon-gamma (IFN-γ) in the hippocampus was assessed by Magnetic Luminex assay. In order to reveal the functional molecular changes in hippocampal tissue upon TQ administration, the protein expression profile of neuronal migration protein Doublecortin (DCX), synaptic plasticity marker Mitogen Activated Protein Kinase2 (MAP2) and apoptosis related protein Poly (ADP-ribose) Polymerase (PARP) was analyzed by Western blotting. RESULTS: Aβ (1-42) infused group had worse memory performance than sham control group on Day 4 with an amelioration in this behaviour by TQ. In our study, the levels of TNF-α, IL-1α and IL-1β did not significantly alter among groups. On the other hand, Aβ (1-42) infusion slightly decreased the level of IFN-γ compared to sham control group. TQ treatment ameliorated both impaired memory performance and IFN-γ levels. It was found that TQ treatment increased the protein levels of DCX compared to the sham control group. Also, the levels of MAP2 and the activation of PARP protein markedly decreased in both Aβ (1-42) and Aβ (1-42) +TQ groups compared to the sham control groups Pearson's correlation test showed a positive relation between IL-1β and DCX in the Aβ (1-42) group. DISCUSSION: Our data suggested that TQ-related functional improvement might result from the increasing level of neurogenesis and ameliorating the level of IFN-γ in the Aβ (1-42) infused rat model of AD.

show abstract

“…This volatile oil is reported to include 30–48% thymoquinone (TQ), the main active ingredient 8,9 . TQ is important in relieving oxidative stress, improve the neuronal survival and therapeutic effects for the treatment of central nervous system tumors 7,10,11 . Oxidative stress was blamed for the harmful effects of higher concentrations of sodium nitrite 12 .…”

Section: Introductionmentioning

confidence: 99%

Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives

Hamdan

Al‐Gayyar

Shams

et al. 2019

Sci Rep

View full text Add to dashboard Cite

Continuous exposure to preservatives such as nitrite salts has deleterious effects on different organs. Meanwhile, Nigella sativa oil can remediate such organ dysfunction. Here, we studied the effect of consumption of thymoquinone (TQ); the main component of Nigella sativa oil on the brain damage induced by sodium nitrite. Forty adult male rats were daily given oral gavage of sodium nitrite (80 mg/kg) with or without thymoquinone (50 mg/kg). Oxidative stress, cytokines of inflammation, fibrotic elements and apoptotic markers in brain tissue were measured. Exposure to sodium nitrite (SN) resulted in increased levels of malondialdehyde, TGF-β, c-reactive protein, NF-κB, TNF-α, IL-1β and caspase-3 associated with reduced levels of glutathione, cytochrome c oxidase, Nrf2 and IL-10. However, exposure of rats’ brain tissues to thymoquinone resulted ameliorated all these effects. In conclusion, thymoquinone remediates sodium nitrite-induced brain impairment through several mechanisms including attenuation of oxidative stress, retrieving the reduced concentration of glutathione, blocks elevated levels of pro-inflammatory cytokines, restores cytochrome c oxidase activity, and reducing the apoptosis markers in the brain tissues of rats.

show abstract

Thymoquinone Can Improve Neuronal Survival and Promote Neurogenesis in Rat Hippocampal Neurons

Abstract: These findings suggest that TQ has an enhancing effect on cell survival and neurogenesis in healthy hippocampus, rather inducing apoptosis in damaged neurons. This may proceed via ERK/JNK and CREB signaling pathways as a candidate acting mechanism for TQ.

Cited by 16 publications

References 70 publications

Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway

Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway

Thymoquinone (TQ) demonstrates its neuroprotective effect via an anti-inflammatory action on the Aβ_(1–42)-infused rat model of Alzheimer's disease

Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives

Contact Info

Product

Resources

About

Thymoquinone Can Improve Neuronal Survival and Promote Neurogenesis in Rat Hippocampal Neurons

Abstract: These findings suggest that TQ has an enhancing effect on cell survival and neurogenesis in healthy hippocampus, rather inducing apoptosis in damaged neurons. This may proceed via ERK/JNK and CREB signaling pathways as a candidate acting mechanism for TQ.

Cited by 16 publications

References 70 publications

Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway

Chronic Administration of Thymoquinone Enhances Adult Hippocampal Neurogenesis and Improves Memory in Rats Via Regulating the BDNF Signaling Pathway

Thymoquinone (TQ) demonstrates its neuroprotective effect via an anti-inflammatory action on the Aβ(1–42)-infused rat model of Alzheimer's disease

Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives

Contact Info

Product

Resources

About

Thymoquinone (TQ) demonstrates its neuroprotective effect via an anti-inflammatory action on the Aβ_(1–42)-infused rat model of Alzheimer's disease