Evidence map›Paper›PMID 40636588›Full record

ArticleAnnals of neurosciences2025

N-acetyl L-cysteine and Growth Factors Impede Endoplasmic Reticulum Stress and Inflammatory Responses in Astrocytes to Amyloid-β in Serum-free Culture.

Diptesh Roy, Sukanya Sarkar, Subhas C Biswas

Abstract read
In one paragraph

Article in Annals of neurosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Diptesh RoyCell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, West Bengal, India.ORCID https://orcid.org/0009-0003-8663-3457
Sukanya SarkarCell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, West Bengal, India.ORCID https://orcid.org/0009-0003-8056-1341
Subhas C BiswasCell Biology and Physiology Division, CSIR-Indian Institute of Chemical Biology, Kolkata, West Bengal, India.ORCID https://orcid.org/0000-0002-1746-101X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Astrocytes play an integral role in Alzheimer's disease (AD) pathology, where they may act as a double-edged sword. The existing serum-supplemented in vitro astrocyte culture models are not suitable to study certain stress response mechanisms that occur in AD. Purpose: Here, we tried to develop a serum-free murine primary cortical astrocyte culture model to study endoplasmic reticulum (ER) stress and inflammation to investigate the effect of amyloid-beta (Aβ Methods: Astrocytes were cultured in a controlled serum-free environment to minimise interference from serum components. Serum-free astrocytes were exposed to oligomeric Aβ and subjected to imaging, immunocytochemistry, real-time PCR and western blot analysis. Results: Using an established protocol, no significant activation of eIF2α, a key marker of ER stress, was observed under serum-free conditions, but with the removal of N-acetyl cysteine (NAC), ER stress response was enhanced after 24 hours of Aβ exposure. Subsequently, the Aβ-induced inflammatory response, assessed through TNF-α expression, which was minimal in the presence of growth factors, became pronounced when these factors were withdrawn. Concomitantly, a significant increase in astrocytes reactivity, assessed by GFAP expression upon 24 hours of Aβ exposure, was observed. Transcript analysis revealed a time-dependent shift in the expression of inflammatory molecules, with early time points showing an increase in anti-inflammatory markers, while late exposure promoting pro-inflammatory responses. Conclusion: This study identifies that NAC and growth factors impede ER stress and inflammatory responses in astrocytes upon Aβ exposure in serum-free culture. These findings also highlight the potential of a serum-free culture system for studying ER stress and inflammation in astrocytes to understand the complex role of these cells in AD pathophysiology.

Indexed as

amyloid-betaAstrocytesendoplasmic reticulum stressinflammation

Identifiers

PMID40636588
PMCPMC12234514

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