ArticleMolecular biology reports2019
Protective effects of anthocyanin against apoptosis and oxidative stress induced by arsanilic acid in DF-1 cells.
Article in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 13 citations in OpenAlex.
- Black Elder and Its Constituents: Molecular Mechanisms of Action Associated with Female Reproduction.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Anthocyanin fromClinical, cosmetic and investigational dermatology · 2022Article
- Protective Effect of Phloretin against Hydrogen Peroxide-Induced Oxidative Damage by Enhancing Autophagic Flux in DF-1 Cells.Oxidative medicine and cellular longevity · 2022Article
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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
Anthocyanin is a natural plant pigment that acts as an antioxidant and scavenges free radicals. This study aimed to investigate the potential protective role of nightshade anthocyanin (NA), a natural flavonoid compound, against the arsanilic acid (ASA)-induced cell death of DF-1 cells. DF-1 cells were initially exposed to ASA, and then NA was applied to the treated cells. Cell viability, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and apoptosis were examined. Results showed that NA inhibited the ASA-induced decrease in cell viability, increase in ROS, and loss of MMP in DF-1 cells. Moreover, caspase-3 activation was inhibited by ASA supplementation and NA attenuated the ASA-induced increase in the percentage of apoptotic cells. In summary, our study suggested that NA can enhance ASA-induced cytotoxicity and apoptosis, thereby providing a basis for the molecular mechanisms of NA-mediated protection.
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