Effects of Carbazole Derivatives on Neurite Outgrowth and Hydrogen Peroxide-Induced Cytotoxicity in Neuro2a Cells

Furukawa, Yoshiko; Sawamoto, Atsushi; Yamaoka, Mizuki; Nakaya, Makiko; Hieda, Yuhzo; Choshi, Tominari; Hatae, Noriyuki; Okuyama, Satoshi; Nakajima, Miki; Hibino, Satoshi

doi:10.3390/molecules24071366

Cited by 17 publications

(8 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neuro2a cells were maintained and cultured, as previously described [28,29]. Dulbecco's Modified Eagle Medium (DMEM), fetal bovine serum (FBS), and antibiotics were purchased from Thermo Fisher Scientific (Waltham, MA, USA).…”

Section: Cell Culturementioning

confidence: 99%

Citrus Auraptene Induces Expression of Brain-Derived Neurotrophic Factor in Neuro2a Cells

et al. 2020

Self Cite

View full text Add to dashboard Cite

(1) Background: Our published data have indicated that (1) auraptene (AUR), a citrus ingredient, has neuroprotective effects on the mouse brain, owing to its ability to suppress inflammation, such as causing a reduction in hyperactivation of microglia and astrocytes; (2) AUR has the ability to trigger phosphorylation (activation) of extracellular signal-related kinase (ERK) and cAMP response element-binding protein (CREB) in neuronal cells; (3) AUR has the ability to induce glial cell line-derived neurotrophic factor (GDNF) synthesis/secretion in rat C6 glioma cells. The well-established fact that the ERK-CREB pathway plays an important role in the production of neurotrophic factors, including GDNF and brain-derived neurotrophic factor (BDNF), prompted us to investigate whether AUR would also have the ability to induce BDNF expression in neuronal cells. (2) Methods: Mouse neuroblastoma neuro2a cells were cultured and the effects of AUR on BDNF mRNA expression and protein content were evaluated by RT-PCR and ELISA, respectively. (3) Results: The levels of BDNF mRNA and secreted BDNF were significantly increased by AUR in a dose- and time-dependent manner in neuro2a cells. (4) Conclusion: The induction of BDNF in neuronal cells might be, in part, one of the mechanisms accounting for the neuroprotective effects of AUR.

show abstract

Section: Cell Culturementioning

confidence: 99%

Citrus Auraptene Induces Expression of Brain-Derived Neurotrophic Factor in Neuro2a Cells

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…In addition, the same trend of increasing TUJ1+ cells as seen in neurospheres was observed, suggesting that infection may lead to interruption (or, at least, a delay) in TUJ1 to NF-200 progression. Neurite outgrowth has been evaluated in Neuro2a cells by other groups under different stimuli/treatments, and it has been reported that this process can be modulated by carbazole derivatives (Furukawa et al, 2019), miRNA (You et al, 2020), Mob proteins (Lin et al, 2011) and polyphenols, including Resveratrol and Apigenin (Namsi et al, 2018). Interestingly, Resveratrol has been shown to revert T. gondii -induced cytokine release and purinergic signaling imbalance in neural progenitor cells (Bottari et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Infection of mouse neural progenitor cells by Toxoplasma gondii affects in vitro proliferation, differentiation and migration

Pires

Barbosa

Santiago

et al. 2021

Preprint

View full text Add to dashboard Cite

Congenital toxoplasmosis constitutes a major cause of pre- and post-natal complications. Fetal infection with Toxoplasma gondii influences development and can lead to microcephaly, encephalitis, and neurological abnormalities. Few studies have attempted to explain the impact of T. gondii infection on the physiology of mature nerve cells, and no systematic study concerning the effect of infection of neural progenitor cells by T. gondii in the biology of these progenitors is available. We infected cortical intermediate progenitor cell cultivated as neurospheres obtained from E16.5 Swiss Webster mice with T. gondii (Me49 strain) tachyzoites to mimic the developing mouse cerebral cortex in vitro. Infection decreased cell proliferation as detected by Ki67 staining at 48 and 72 hours post infection (hpi) in floating neurospheres, resulting in reduced cellularity at 96 hpi. Neurogenic and gliogenic potential, assessed in plated neurospheres, was shown to be impaired in infected cultures, as indicated by neurofilament heavy chain (NF-200) and GFAP staining, respectively. To further investigate the impact of infection on neuronal differentiation, Neuro2a neuroblasts were infected and after 24 hpi, neurogenic differentiation was induced with serum withdrawal. We confirmed that infection induces a decrease in neuroblast-neuron differentiation rates in cells stained for NF-200, with reduced neuritogenesis. Migration rates were analyzed in plated neurospheres. At 120 h after plating, infected cultures exhibited decreased overall migration rates and altered the radial migration of nestin-, GFAP- and NF-200-positive cells. These findings indicate that T. gondii infection of neural progenitor cells may lead to reduced neuro/gliogenesis due to an imbalance in cell proliferation alongside an altered migratory profile. If translated to the in vivo situation, these data could explain, in part, the cortical malformations observed in congenitally infected individuals.

show abstract

“…We have been interested in the synthesis of heterocyclic compounds by constructing fused pyridine ring systems based on a thermal electrocyclization of an azahexatriene moiety [14,15]. It has been hoped that the development of compounds with enhanced biological activity would be possible using these natural products and their derivatives [16][17][18]. We have previously reported the total syntheses of indolo [3,2-c]quinoline (isocryptolepine) [19], azaanthracenones (kalasinamide, marcanine A, and geovanine) [20], imidazo [4',5':4,5]pyrido [2,3-b]indole (grossularine-1 and -2) [21,22], imidazo [4,5-b]pyridine (2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine and 2-amino-1,6-dimethylimidazo [4,5-b]pyridine) [23], and imidazo [4,5-c]quinoline (imiquimod) [24] based on the electrocyclization of 2-azahexatriene involving an isocyanate moiety as the key intermediate.…”

Section: Introductionmentioning

confidence: 99%

Total synthesis of pyrrolo[2,3-c]quinoline alkaloid: trigonoine B

Nishiyama¹,

Hamada²,

Ishii³

et al. 2021

Beilstein J. Org. Chem.

Self Cite

View full text Add to dashboard Cite

The first total synthesis of the pyrrolo[2,3-c]quinoline alkaloid trigonoine B (1) was accomplished via a six-step sequence involving the construction of an N-substituted 4-aminopyrrolo[2,3-c]quinoline framework via electrocyclization of 2-(pyrrol-3-yl)benzene containing a carbodiimide moiety as a 2-azahexatriene system. The employed six-step sequence afforded trigonoine B (1) in 9.2% overall yield. The described route could be employed for the preparation of various N-substituted 4-aminopyrroloquinolines with various biological activities.

show abstract

Effects of Carbazole Derivatives on Neurite Outgrowth and Hydrogen Peroxide-Induced Cytotoxicity in Neuro2a Cells

Cited by 17 publications

References 40 publications

Citrus Auraptene Induces Expression of Brain-Derived Neurotrophic Factor in Neuro2a Cells

Citrus Auraptene Induces Expression of Brain-Derived Neurotrophic Factor in Neuro2a Cells

Infection of mouse neural progenitor cells by Toxoplasma gondii affects in vitro proliferation, differentiation and migration

Total synthesis of pyrrolo[2,3-c]quinoline alkaloid: trigonoine B

Contact Info

Product

Resources

About