Famotidine has a neuroprotective effect on MK-801 induced toxicity via the Akt/GSK-3β/β-catenin signaling pathway in the SH-SY5Y cell line

Ünal, Gökhan; Dokumacı, Alim Hüseyin; Özkartal, Ceren Şahin; Yerer, Mükerrem Betül; Arıcıoğlu, Feyza

doi:10.1016/j.cbi.2019.108823

Cited by 11 publications

(7 citation statements)

References 37 publications

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“…Recently, the study has showed that famotidine treatment resulted in significant downregulation of LDH, TGF-β, bFGF and IL-9, respectively, and significant upregulation of Caspase-3 expression in diffuse large B-cell lymphoma[ 43 ]. Further analysis showed that famotidine prevented increment in oxidative stress markers and reduction of antioxidants during ischemia-reperfusion injury[ 44 ], in addition, the protective effect of famotidine was observed in neuroprotective[ 30 ]. However, no available direct reports about the famotidine in cell pyroptosis.…”

Section: Discussionmentioning

confidence: 99%

“…Pervious study have demonstrated that omeprazole suppressed de novo lipogenesis in gastric epithelial cells[ 28 ], and rabeprazole inhibited cell proliferation in gastric epithelial cells by targeting STAT3-mediated glycolysis[ 29 ]. While famotidine, a histamine H[ 2 ] receptor antagonist, has been reported to protect against cell death induced by MK-801 through glycogen synthase kinase 3 β (GSK-3β)/β-catenin signaling pathway in SK-SY5Y cells[ 30 ]. Further study showed that the novelty and importance of the famotidine in the management of cardiovascular diseases through NF-κB[ 31 ].…”

Section: Introductionmentioning

confidence: 99%

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Famotidine promotes inflammation by triggering cell pyroptosis in gastric cancer cells

Huang

Fan

Liu

et al. 2021

BMC Pharmacol Toxicol

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Background Cell pyroptosis has been characterized by cell swelling and pro-inflammatory factors release to aggravate inflammatory reaction., such as interlukin-1 beta (IL-1β) and interlukin18 (IL-18). However, the function of famotidine, an antagonist of histamine H2-receptor antagonists, in cell pyroptosis remained unknown. Methods Real-time quantitative PCR (qPCR), western blotting (WB), LDH release assay and enzyme linked immunosorbent assay (Elisa) combined with inhibitor were performed to analyze the effect of famotidine on cell pyroptosis-related gene expression. Results In this study, we found that famotidine (300 μm) treatment led to a phenomenon of cell pyroptosis as confirmed by LDH assay. Further results showed that famotidine triggered cell pyroptosis in gastric cancer cells by activation of NLPR3 inflammasomes including ASC, Caspase-1 and NLRP, leading to enhanced IL-18, not IL-1β, mature and secretion. What’s more, the results also showed GSDME, not GSDMD, was increased in response to famotidine stimulation in BGC823 and AGS cells. Mechanically, phosphorylation of ERK1/2 was drastically enhanced in present with famotidine treatment, while inhibition of ERK1/2 activity by U0126 could reverse the promotion of famotidine in IL-18 secretion. Conclusion These findings revealed a novel role of famotidine in cell pyroptosis in patients with gastric cancer, a comprehensive consideration is needed in treatment of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Famotidine promotes inflammation by triggering cell pyroptosis in gastric cancer cells

Huang

Fan

Liu

et al. 2021

BMC Pharmacol Toxicol

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“…These data support the constructive validity of the SH-SY5Y cell line. This cell line and its CRISPR-engineered derivatives may serve as valuable primary screening platforms for antipsychotic drugs [27][28][29]. A neurite outgrowth assay was applied to SH-SY5Y cells to investigate the effect of antipsychotics such as amisulpride and haloperidol on the regulation of neuronal morphology [30].…”

Section: Neuroblastoma Modelmentioning

confidence: 99%

Cellular Models in Schizophrenia Research

Abashkin

Kurishev

Карпов

et al. 2021

IJMS

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Schizophrenia (SZ) is a prevalent functional psychosis characterized by clinical behavioural symptoms and underlying abnormalities in brain function. Genome-wide association studies (GWAS) of schizophrenia have revealed many loci that do not directly identify processes disturbed in the disease. For this reason, the development of cellular models containing SZ-associated variations has become a focus in the post-GWAS research era. The application of revolutionary clustered regularly interspaced palindromic repeats CRISPR/Cas9 gene-editing tools, along with recently developed technologies for cultivating brain organoids in vitro, have opened new perspectives for the construction of these models. In general, cellular models are intended to unravel particular biological phenomena. They can provide the missing link between schizophrenia-related phenotypic features (such as transcriptional dysregulation, oxidative stress and synaptic dysregulation) and data from pathomorphological, electrophysiological and behavioural studies. The objectives of this review are the systematization and classification of cellular models of schizophrenia, based on their complexity and validity for understanding schizophrenia-related phenotypes.

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“…Several studies speculated that the H2R antagonist famotidine might be effective for certain ASD symptoms because it has been shown to improve certain symptoms in SCH, including improvements in eye contact avoidance, repetitive behaviors, social communication, and social interaction in children with ASD who had no history of gastrointestinal problems (Linday, 1997;Linday et al, 2001). Moreover, a very recent study showed that pretreatments of animals with famotidine prevented cell death induced by the NMDA antagonist MK-801, and therefore provided neuroprotective effects via modulation of the Akt/GSK-3b/b-catenin signaling pathway, an important mechanism in SCH neurobiology (Unal et al, 2019).…”

Section: H2r Antagonistsmentioning

confidence: 99%

Role of Neuroinflammation in Autism Spectrum Disorder and the Emergence of Brain Histaminergic System. Lessons Also for BPSD?

et al. 2020

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Many behavioral and psychological symptoms of dementia (BPSD) share similarities in executive functioning and communication deficits with those described in several neuropsychiatric disorders, including Alzheimer's disease (AD), epilepsy, schizophrenia (SCH), and autism spectrum disorder (ASD). Numerous studies over the last four decades have documented altered neuroinflammation among individuals diagnosed with ASD. The purpose of this review is to examine the hypothesis that central histamine (HA) plays a significant role in the regulation of neuroinflammatory processes of microglia functions in numerous neuropsychiatric diseases, i.e., ASD, AD, SCH, and BPSD. In addition, this review summarizes the latest preclinical and clinical results that support the relevance of histamine H1-, H2-, and H3-receptor antagonists for the potential clinical use in ASD, SCH, AD, epilepsy, and BPSD, based on the substantial symptomatic overlap between these disorders with regards to cognitive dysfunction. The review focuses on the histaminergic neurotransmission as relevant in these brain disorders, as well as the effects of a variety of H3R antagonists in animal models and in clinical studies.

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Famotidine has a neuroprotective effect on MK-801 induced toxicity via the Akt/GSK-3β/β-catenin signaling pathway in the SH-SY5Y cell line

Cited by 11 publications

References 37 publications

Famotidine promotes inflammation by triggering cell pyroptosis in gastric cancer cells

Famotidine promotes inflammation by triggering cell pyroptosis in gastric cancer cells

Cellular Models in Schizophrenia Research

Role of Neuroinflammation in Autism Spectrum Disorder and the Emergence of Brain Histaminergic System. Lessons Also for BPSD?

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