Interaction between hyperphosphorylated tau and pyroptosis in forskolin and streptozotocin induced AD models

Li, Yinjie; Xu, Pu; Shan, Jiajing; Sun, Wei; Ji, Xuefei; Chi, Tianyan; Liu, Peng; Zou, Libo

doi:10.1016/j.biopha.2019.109618

Cited by 29 publications

(22 citation statements)

References 82 publications

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“…However, emerging new studies suggest that a model based on tau protein pathology should also be considered in terms of the development and propagation of the disease. Tau burden correlates with clinical symptoms and is needed in some in vitro studies or animal models of AD for the appearance of neuronal damage [64,65,67,68]. Therefore, the inclusion of tau protein in future research, in addition to amyloid-β, could result in a new and better understanding of the mechanisms leading to AD pathology, especially as there are still few experiments considering tau hyperphosphorylation as more than just an Aβ-induced phenomenon [68][69][70][71].…”

Section: Discussionmentioning

confidence: 99%

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

Wiatrak

Balon

2020

Mol Neurobiol

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Amyloid-β (Aβ), the influence of which is considered the pathomechanism of Alzheimer’s disease, is also present in healthy people. The microbiome’s impact is also taken into account, where bacterial lipopolysaccharide (LPS) activates inflammatory processes and stimulates microglia via TLRs. Molecules of bacterial origin can co-create senile plaques with Aβ. This study evaluated the activity of physiological Aβ concentrations on neuronal and microglial cells after preincubation with LPS. Two cell lines were used in the study: PC12 cells differentiated with NGF and THP-1 cells differentiated with phorbol 12-myristate 13-acetate (PMA). Cells were incubated with LPS at concentrations of 1–100 μM for 24 h and then with Aβ25–35 at a concentration of 0.001 μM or 1.0 μM for another 24 h. The viability of the culture and free oxygen radicals and the number of DNA strand breaks in both cell lines were evaluated. Additionally, for PC12 cells, neural features were assessed. Stimulation of repair processes in the presence of Aβ was observed for both studied cell lines. There was a decrease in free radical level and DNA damage number compared to control cultures (cells treated with LPS and without Aβ). The neurotrophic activity of Aβ was observed—the effect on neurites’ growth even after the preincubation of PC12 cells with LPS. At the lowest concentration of LPS used, the increase in neurite length was about 50% greater than in the negative control. At low concentrations, Aβ has a protective effect on neuron-like PC12 cells pretreated with LPS.

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Section: Discussionmentioning

confidence: 99%

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

Wiatrak

Balon

2020

Mol Neurobiol

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“…Streptozotocin (STZ) is a nitrosourea compound used for modeling type 1 [17] and type 2 [18] diabetes mellitus in experimental animals when administered parenterally. When administered intracerebroventricularly in a low dose, streptozotocin causes brain oxidative stress [19], mitochondrial dysfunction [20], neuroinflammation [21, 22], cholinergic deficits [23], metabolic dysregulation [24], insulin system dysfunction [25], glucose hypometabolism[26], pathological accumulation of amyloid β [27] and hyperphosphorylated tau protein [25, 28]. Most importantly, neuropathological changes are accompanied by the progressive development of cognitive deficits following the administration of STZ [25, 29].…”

Section: Introductionmentioning

confidence: 99%

Failure of the brain glucagon-like peptide-1-mediated control of intestinal redox homeostasis in a rat model of sporadic Alzheimer’s disease

Homolak

Perhoč

Knezović

et al. 2021

Preprint

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Objective: The gastrointestinal system might be involved in the etiopathogenesis of the insulin-resistant brain state (IRBS) and Alzheimer′s disease. Gastrointestinal hormone glucagon-like peptide-1 (GLP-1) is being explored as a potential therapy as activation of brain GLP-1 receptors (GLP-1R) exerts neuroprotection and controls peripheral metabolism. Intracerebroventricular administration of streptozotocin (STZ-icv) is used to model IRBS and previous reports indicate GLP-1 dyshomeostasis as one of the possible pathophysiological mechanisms involved. The aim was to explore i) gastrointestinal homeostasis in the STZ-icv ii) assess whether the brain GLP-1 is involved in the regulation of gastrointestinal redox homeostasis and iii) analyze whether brain-gut GLP-1 is functional in the STZ-icv. Methods: Acute intracerebroventricular treatment with exendin-3(9-39)amide was used for pharmacological inhibition of brain GLP-1R in control and STZ-icv rats. Nitrocellulose redox permanganometry (NRP), thiobarbituric acid reactive substances (TBARS), and 1,2,3-trihydroxybenzene autooxidation (THB) were measured in plasma, and NRP, TBARS, THB, low molecular weight thiols, protein sulfhydryls, and catalase activity were measured in duodenum and ileum. Treatment effects and treatment-treatment interactions were modeled. Results: Pharmacological inhibition of brain GLP-1R reduced plasma superoxide dismutase (SOD) activity, reductive capacity, and TBARS. Acute inhibition of brain GLP-1R increased TBARS, and decreased LMWT, SH, and SOD in the duodenum, but not in the ileum of the controls. In the STZ-icv, TBARS and CAT were increased, LMWT and SH were decreased at baseline, and no further increment of oxidative stress was observed upon central GLP-1R inhibition. Conclusions: Brain GLP-1 signaling is involved in systemic redox regulation, and the brain-gut GLP-1 axis maintains duodenal redox homeostasis. Markers of oxidative stress are increased in the duodenum of the STZ-icv rats. Failure of the brain GLP-1R inhibition to further increase oxidative stress in the STZ-icv model indicates a dysfunctional brain-gut GLP-1 axis.

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“…3) leads to destruction of the blood-brain barrier, in ammation, and oxidative stress, and eventually results in brain damage [22,24,25] . Moreover, pyroptosis, a pro-in ammatory form of programmed cell death, also contributes to the pathogeneses of neurodegenerative diseases such as AD and Parkinson's disease (PD) [26,27] . Nod-like receptor protein 3 (NLRP3) in ammasome is known to contribute to upstream signaling of pyroptosis [28][29][30] .…”

Section: Introductionmentioning

confidence: 99%

Curcumin protects against cognitive impairments in a rat model of chronic cerebral hypoperfusion combined with diabetes mellitus by suppressing neuroinflammation, apoptosis, and pyroptosis

Zheng

Zhang

Zhao

et al. 2021

International Immunopharmacology

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Interaction between hyperphosphorylated tau and pyroptosis in forskolin and streptozotocin induced AD models

Cited by 29 publications

References 82 publications

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

Failure of the brain glucagon-like peptide-1-mediated control of intestinal redox homeostasis in a rat model of sporadic Alzheimer’s disease

Curcumin protects against cognitive impairments in a rat model of chronic cerebral hypoperfusion combined with diabetes mellitus by suppressing neuroinflammation, apoptosis, and pyroptosis

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