ArticleJournal of thrombosis and thrombolysis2017
Novel sila-amide derivatives of N-acetylcysteine protects platelets from oxidative stress-induced apoptosis.
Article in Journal of thrombosis and thrombolysis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Novel Strategies in the Early Detection and Treatment of Endothelial Cell-Specific Mitochondrial Dysfunction in Coronary Artery Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Phosphorylation of GntR reduces Streptococcus suis oxidative stress resistance and virulence by inhibiting NADH oxidase transcription.PLoS pathogens · 2023Article
- Principles behind SLE treatment withImmunometabolism (Cobham, Surrey) · 2022Review
- Autophagy Ameliorates Reactive Oxygen Species-Induced Platelet Storage Lesions.Oxidative medicine and cellular longevity · 2022Article
- The pneumococcal two-component system SirRH is linked to enhanced intracellular survival of Streptococcus pneumoniae in influenza-infected pulmonary cells.PLoS pathogens · 2020Article
- Pharmacological Basis for Use ofOxidative medicine and cellular longevity · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress-induced platelet apoptosis is one among the many causes for the development and progression of many disorders like cardiovascular diseases, arthritis, Alzheimer's disease and many chronic inflammatory responses. Many studies have demonstrated the less optimal effect of N-acetyl cysteine (NAC) in oxidative stress-induced cellular damage. This could be due to its less lipophilicity which makes it difficult to enter the cellular membrane. Therefore in the present study, lipophilic sila-amide derivatives (6a and 6b) synthesized through the reaction of NAC with 3-Aminopropyltrimethylsilane and aminomethyltrimethylsilane were used to determine their protective property against oxidative stress-induced platelet apoptosis. At a concentration of 10 µM, compound 6a and 6b were able to significantly inhibit Rotenone/H
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