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2-BFI Provides Neuroprotection Against Fluorosis by Stabilizing Endoplasmic Reticulum–Mitochondria Contact Sites and Inhibiting Activation of the NLRP3 Inflammasome
by
Xie, Peng
, Tang, Xiaohong
, Xu, Wan
, Zhi, Zhongwen
, Sun, Yifu
, Zhang, Caiyi
, Zhi, Rongrong
, Chen, Rui
in
Alzheimer's disease
/ Animal cognition
/ Animal diseases
/ Animal models
/ Animals
/ Apoptosis
/ Biochemistry
/ Biomedical and Life Sciences
/ Biomedicine
/ Blood-brain barrier
/ Brain research
/ Cell Biology
/ Cell viability
/ Cerebral infarction
/ Cognitive ability
/ Endoplasmic Reticulum
/ Fluoridation
/ Fluorides
/ Fluorides - toxicity
/ Fluorosis
/ Glucose
/ Hospitals
/ Humans
/ Imidazoline
/ Inflammasomes
/ Laboratory animals
/ Medical research
/ Mitochondria
/ Neuroblastoma
/ Neurochemistry
/ Neurodegenerative diseases
/ Neurological complications
/ Neurology
/ Neurons
/ Neuroprotection
/ Neurosciences
/ Neurotoxicity
/ NLR Family, Pyrin Domain-Containing 3 Protein
/ Original Paper
/ Oxidative stress
/ Pyrin protein
/ Stroke
/ Toxicity
2023
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2-BFI Provides Neuroprotection Against Fluorosis by Stabilizing Endoplasmic Reticulum–Mitochondria Contact Sites and Inhibiting Activation of the NLRP3 Inflammasome
by
Xie, Peng
, Tang, Xiaohong
, Xu, Wan
, Zhi, Zhongwen
, Sun, Yifu
, Zhang, Caiyi
, Zhi, Rongrong
, Chen, Rui
in
Alzheimer's disease
/ Animal cognition
/ Animal diseases
/ Animal models
/ Animals
/ Apoptosis
/ Biochemistry
/ Biomedical and Life Sciences
/ Biomedicine
/ Blood-brain barrier
/ Brain research
/ Cell Biology
/ Cell viability
/ Cerebral infarction
/ Cognitive ability
/ Endoplasmic Reticulum
/ Fluoridation
/ Fluorides
/ Fluorides - toxicity
/ Fluorosis
/ Glucose
/ Hospitals
/ Humans
/ Imidazoline
/ Inflammasomes
/ Laboratory animals
/ Medical research
/ Mitochondria
/ Neuroblastoma
/ Neurochemistry
/ Neurodegenerative diseases
/ Neurological complications
/ Neurology
/ Neurons
/ Neuroprotection
/ Neurosciences
/ Neurotoxicity
/ NLR Family, Pyrin Domain-Containing 3 Protein
/ Original Paper
/ Oxidative stress
/ Pyrin protein
/ Stroke
/ Toxicity
2023
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2-BFI Provides Neuroprotection Against Fluorosis by Stabilizing Endoplasmic Reticulum–Mitochondria Contact Sites and Inhibiting Activation of the NLRP3 Inflammasome
by
Xie, Peng
, Tang, Xiaohong
, Xu, Wan
, Zhi, Zhongwen
, Sun, Yifu
, Zhang, Caiyi
, Zhi, Rongrong
, Chen, Rui
in
Alzheimer's disease
/ Animal cognition
/ Animal diseases
/ Animal models
/ Animals
/ Apoptosis
/ Biochemistry
/ Biomedical and Life Sciences
/ Biomedicine
/ Blood-brain barrier
/ Brain research
/ Cell Biology
/ Cell viability
/ Cerebral infarction
/ Cognitive ability
/ Endoplasmic Reticulum
/ Fluoridation
/ Fluorides
/ Fluorides - toxicity
/ Fluorosis
/ Glucose
/ Hospitals
/ Humans
/ Imidazoline
/ Inflammasomes
/ Laboratory animals
/ Medical research
/ Mitochondria
/ Neuroblastoma
/ Neurochemistry
/ Neurodegenerative diseases
/ Neurological complications
/ Neurology
/ Neurons
/ Neuroprotection
/ Neurosciences
/ Neurotoxicity
/ NLR Family, Pyrin Domain-Containing 3 Protein
/ Original Paper
/ Oxidative stress
/ Pyrin protein
/ Stroke
/ Toxicity
2023
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2-BFI Provides Neuroprotection Against Fluorosis by Stabilizing Endoplasmic Reticulum–Mitochondria Contact Sites and Inhibiting Activation of the NLRP3 Inflammasome
Journal Article
2-BFI Provides Neuroprotection Against Fluorosis by Stabilizing Endoplasmic Reticulum–Mitochondria Contact Sites and Inhibiting Activation of the NLRP3 Inflammasome
2023
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Overview
2-(2-benzofu-ranyl)-2-imidazoline (2-BFI) is a drug that has attracted much attention in recent years. It has a therapeutic effect on brain diseases in animal models such as Alzheimer’s disease and cerebral infarction. However, whether 2-BFI affords neuroprotection against the toxicity of fluoride, which can cross the blood–brain barrier and cause neurological dysfunction is not known. We investigated the cell viability and apoptosis of SH-SY5Y cells and primary cultures of cortical neurons exposed to fluoride, and 2-BFI was used to protect both two kinds of cells against the effects of fluoride. We found that 2-BFI can provide neuroprotection on SH-SY5Y cells and primary cultures of cortical neurons upon fluorosis by maintaining the stability of endoplasmic reticulum–mitochondria contact sites and inhibiting activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome. This study may provide a new method for protecting against the neurotoxicity induced by fluoride exposure.
Publisher
Springer US,Springer Nature B.V
Subject
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