Effect of atorvastatin on A β1–42‐induced alteration of SESN2, SIRT1, LC3II and TPP1 protein expressions in neuronal cell cultures

This study was undertaken whether A β‐induced changes of SESN2 and SIRT1 protein expression, autophagy marker LC3II and lysosomal enzyme TPP1 affected by atorvastatin (Western blot) and its possible role in Aβ neurotoxicity (ELISA).Key findings/resultsWe showed that SESN2 and LC3II expressions were elevated, whereas SIRT1 and TPP1 expressions were decreased in the A β1 –42‐exposed human neuroblastoma cells (SH‐SY5Y). Co‐administration of atorvastatin with Aβ1 –42 compensates SESN2 increase and recovers SIRT1 decline by reducing oxidative stress, decreasing SESN2 expression and increasing SIRT1 expression by its neuroprotective action. Atorvastatin induced LC3II but not TPP1 level in the A β1 –42‐exposed cells suggested that atorvastatin is effective in the formation of autophagosome but not on the expression of the specific lysosomal enzyme TPP1.Discussion and conclusionTogether, these results indicate that atorvastatin induced SESN2, SIRT1 and LC3II levels play a protective role against A β1 –42 neurotoxicity.
Source: Journal of Pharmacy and Pharmacology - Category: Drugs & Pharmacology Authors: Tags: Research Paper Source Type: research

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Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
CONCLUSIONS Silencing ACAT1 attenuates Aβ₂₅₋₃₅-induced cytotoxicity and cell apoptosis in SH-SY5Y cells, which may due to the synergistic effect of ACAT1 and COX2 through PKC/ERK pathways. PMID: 30541014 [PubMed - in process]
Source: Medical Science Monitor - Category: Research Tags: Med Sci Monit Source Type: research
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Source: Redox Biology - Category: Biology Source Type: research
The β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) initiates the production of amyloid-β peptide (Aβ), which is central to the pathogenesis of Alzheimer's disease (AD). Changes in brain cholesterol homeostasis have been suggested to affect Aβ metabolism. Cholesterol homeostasis is maintained in the brain by apolipoprotein E (apoE). The apoE4 isoform constitutes the major risk factor for AD. Here, we investigated the effect of apoE forms on Aβ generation and on BACE1 levels. We also examined the potential involvement in these processes of cholesterol transporters ABCG1 and ABCG4 or the l...
Source: Biochemical Journal - Category: Biochemistry Authors: Tags: Research Articles Source Type: research
Conclusions: In the cell cultures, we observed that seladin-1 protein levels increased after aromatase enzyme inhibition. The hippocampal aromatase protein levels decreased following chronic seladin-1 inhibition in icv inhibitor-administered rats; however, the aromatase levels in the dentate gyrus of seladin-1 knockout (SelKO) AD male mice increased. These findings indicate a partial relationship between these proteins and their roles in AD pathology.Pharmacology 2018;102:42 –52
Source: Pharmacology - Category: Drugs & Pharmacology Source Type: research
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Source: The Biochemical Journal - Category: Biochemistry Authors: Tags: Biochem J Source Type: research
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Source: Neuroscience Bulletin - Category: Neuroscience Source Type: research
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Source: CNS Neuroscience and Therapeutics - Category: Neuroscience Authors: Tags: CNS Neurosci Ther Source Type: research
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