Effect of amyloid-β on the redox system activity in SH-SY5Y cells preincubated with lipopolysaccharide or co-cultured with microglia cells

Wiatrak, Benita; Jawień, Paulina; Matuszewska, Agnieszka; Szeląg, Adam; Kubis-Kubiak, Adriana

doi:10.1016/j.biopha.2022.112880

Cited by 9 publications

(8 citation statements)

References 43 publications

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“…The physiological role of amyloid peptides in LTP formation and synaptogenesis has been demonstrated in numerous studies [ 44 , 45 ]. Earlier studies also showed a strong antioxidant effect by influencing the parameters of oxidative stress of Aβ at the physiological concentrations of all fragments (1–40, 25–35, 1–42) [ 5 ]. Additionally, the regenerative effect of Aβ 25–35 and 1–40 was observed on DNA strand damage caused by the earlier preincubation of PC12 cell culture with lipopolysaccharide [ 6 ].…”

Section: Discussionmentioning

confidence: 99%

“…Our research used nanomolar concentrations of freshly prepared Aβ, i.e., mainly in monomeric forms. The literature also indicates the antioxidant effects of Aβ observed at pico- and nanomolar concentrations, and these effects disappear as the concentration of amyloid peptides increases [ 5 ]. The mechanism of β-amyloid antioxidant activity is probably related to the chelating properties of the peptide, which have an affinity, especially for copper ions, and iron ions, i.e., metal ions strongly catalyzing oxidative processes [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

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Impact of NMDA receptor activation on DNA damage in PC12 neuron-like cell cultures in the presence of β-amyloid peptides

2022

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Objective This study aimed to investigate the effect of low nanomolar concentrations of Aβ1–40 and Aβ25–35 on DNA double-strand breaks following NMDA activation of cells. Materials and methods After incubating the differentiated PC12 cells with Aβ25−35, Aβ1−40 or Aβ1−42 for 24 h, the culture was washed and stimulated for 15 min with NMDA. Then, tests were performed at four-time intervals from stimulation to assess the viability of the culture, the level of oxygen free radicals, and the γH2AX and pATM kinase. NMDAR1 expression was also evaluated by performing immunocytochemical staining. Results It was found that amyloid peptides in nanomolar concentrations reduce double-stranded DNA breaks after NMDA neuron activation. A slight antioxidant effect was also demonstrated when measured 120 min after NMDA cell activation. Conclusion The NMDA stimulation of PC12 cells led to a rapid increase in the number of double-stranded DNA breaks in the cells and is assumed to be the initial step in IEG activation and LTP induction. The effect of Aβ on the reduction of double-strand breaks after NMDA cell stimulation indicates that at concentrations similar to physiological amyloid peptides, it may reduce the mobilization of the neuronal response to stimuli, leading to inhibition of LTP induction and decreasing synaptic plasticity in the early stages of Alzheimer’s disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impact of NMDA receptor activation on DNA damage in PC12 neuron-like cell cultures in the presence of β-amyloid peptides

2022

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“…During the rst 7 days of rats' habituation to the new environment, the rats were observed to detect abnormalities. If no abnormality was detected, the rats were randomly divided into ve groups (n = 10) as follows: (i) control, (ii) LPS 5 mg/kg [7], (iii) LPS treated with minocycline 25 mg/kg (15), (iv) LPS treated with minocycline 50 mg/kg (15) and (v) LPS treated with memantine 10 mg/kg [7]. Minocycline (USP, 12601 Twinbrook Pkwy, Rockville, MD) and memantine (USP, 12601 Twinbrook Pkwy, Rockville, MD) treatments were administered intraperitoneally for 14 days and LPS, obtained from E. coli 0111: B4 (Sigma-Aldrich, St. Louis, MO), was injected intraperitoneally once on day 5 of the experiment.…”

Section: Experimental Designmentioning

confidence: 99%

Minocycline mitigates tau pathology via modulating the TLR-4/NF-кβ signalling pathway in the hippocampus of Alzheimer disease’s rat model

Qaid

Abdullah

Zakaria

et al. 2023

Preprint

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Introduction: The neuroinflammatory response was seen to impact the formation of phosphorylated tau protein in Alzheimer’s disease (AD). This study aims to investigate the molecular mechanism of minocycline in reducing phosphorylated tau protein formation in the hippocampus of lipopolysaccharide (LPS)-induced rats. Methods Fifty adult male Sprague Dawley (SD) rats were randomly allocated to 1 of 5 groups: control, LPS (5 mg/kg), LPS + minocycline (25 mg/kg), LPS + minocycline (50 mg/kg) and LPS + memantine (10 mg/kg). Minocycline and memantine were administered intraperitoneally (i.p) for two weeks, and LPS was injected i.p. once on day 5. ELISA was used to determine the level of phosphorylated tau protein in SD rats' hippocampal tissue. The density and expression of Toll-like receptor-4 (TLR-4), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-кβ), tumour necrosis factor-alpha (TNF-α), and cyclooxygenase (COX)-2 were determined using Western blot and immunohistochemistry. Results Minocycline, like memantine, prevented LPS-induced increase in phosphorylated tau protein level via reduced density and expression of TLR-4, NF-кβ, TNF-α and COX-2 proteins in rat hippocampal tissue. Interestingly, higher doses were shown to be more neuroprotective than lower doses. Conclusion This study suggests that minocycline suppresses the neuroinflammation signalling pathway and decreased phosphorylated tau protein formation induced by LPS in a dose-dependent manner. Minocycline has been recommended can be used as a preventative and therapeutic drug for neuroinflammatory diseases such as AD.

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“…So far, two causes of Alzheimer’s disease have been intensively studied: amyloid plaques and neurofibrillary tangles, which, after more than a hundred years of research, did not explain the etiology of the disease. This was ultimately confirmed by research into anti-amyloid drugs, which showed that amyloid also has several beneficial properties, such as antibacterial, antioxidant, and neurotrophic effects [ 20 , 21 , 22 ]. In addition, the complete removal of amyloid can cause swelling and bleeding in the brain [ 22 ].…”

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confidence: 93%

“…As an example, it is estimated that in Poland the total number of people living with cognitive deficits will more than double from 525,084 in 2018 to 1,075,099 in 2050. So people with dementia will make up 3.23% of the population in 2050 compared to 1.38% in 2018 [ 21 ]. Despite the vast amount of research investigating the causes and mechanisms leading to dementia, and projects to seek dementia-modifying or preventive therapies, there is still a lack of breakthroughs that will have a decisive impact on post-ischemic neurodegeneration and the development of Alzheimer’s disease.…”

mentioning

confidence: 99%

Ischemic Brain Neurodegeneration

Pluta¹

2022

IJMS

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Effect of amyloid-β on the redox system activity in SH-SY5Y cells preincubated with lipopolysaccharide or co-cultured with microglia cells

Cited by 9 publications

References 43 publications

Impact of NMDA receptor activation on DNA damage in PC12 neuron-like cell cultures in the presence of β-amyloid peptides

Impact of NMDA receptor activation on DNA damage in PC12 neuron-like cell cultures in the presence of β-amyloid peptides

Minocycline mitigates tau pathology via modulating the TLR-4/NF-кβ signalling pathway in the hippocampus of Alzheimer disease’s rat model

Ischemic Brain Neurodegeneration

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