ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2020
Network Pharmacology Combined with Transcriptional Analysis to Unveil the Biological Basis of Astaxanthin in Reducing the Oxidative Stress Induced by Diabetes Mellitus.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2020. 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, 14 citations in OpenAlex.
- Synthesis and biological evaluation of 6-hydroxychromone based thiosemicarbazones as potential antidiabetic and antioxidant agents.Scientific reports · 2026Article
- Elucidating the Molecular Network Underpinning Hypoxia Adaptation in the Liver of Silver Carp (Animals : an open access journal from MDPI · 2025Article
- Exploring the role of glycolysis in the pathogenesis of erectile dysfunction in diabetes.Translational andrology and urology · 2025Article
- Uncovering the gene regulatory network of type 2 diabetes through multi-omic data integration.Journal of translational medicine · 2022Article
- Roles of NAD(P)H:quinone Oxidoreductase 1 in Diverse Diseases.Life (Basel, Switzerland) · 2021Review
- The diverse functionality of NQO1 and its roles in redox control.Redox biology · 2021Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAstaxanthin (Ast) has been reported to reduce oxidative stress induced by diabetes mellitus (DM). The aim of this research was to give a systematic overview of the biological basis for this process.
methodsAst-targeted proteins were collected from the BATMAN database, Comparative Toxicogenomics Database, and STITCH database. Putative DM-related protein targets were collected from the GeneCards database. A DM-rat model was then built with streptozotocin (STZ) combined with a high-sugar, high-fat diet for 30 days. Total cholesterol (TC), triglycerides (TGs), and insulin levels were examined using whole tail-vein blood from overnight-fasted rats. SOD, GSH, and MDA activy was detected in liver tissue (
resultsA total of 120 Ast-targeted proteins and 13,784 DM-related targets were collected. Ast functioned in reducing TC, TG, and MDA levels, promoting SOD activity and GSH expression, and alleviating islet-cell injury in Ast-fed DM rats compared with DM control rats. Furthermore, genes involved in MAPK, TNF, AMPK, and FOXO signaling pathways were differently expressed in Ast-treated DM rats compared with DM rats. The differentially expressed genes were enriched in euchromatin, thyroid cancer, and metaphase-plate congression. Three Ast-intersecting targets - Col5A1, Nqo1, and Notch2 - were then identified. We found possible binding patterns of Ast with Nqo1 and Notch2, respectively. Ast targets-pathway networks were finally built to show a systematic overview of how Ast works in multiple pathways to reduce oxidative stress. Taken together, Ast is predicted to target Col5A1, Nqo1, and Notch2 to form a network of systemic pharmacological effects to: 1) promote insulin-releasing balance and relieve insulin resistance, 2) reduce testicular cell apoptosis, and 3) maintain normal size in marginal-zone B cells and inhibit autoimmune DM, all of which contribute to the balance of lipid metabolism and reduction of oxidative stress in DM patients.
conclusionAst functions in reducing oxidative stress in DM rats by regulating a variety of targets to form a comprehensive antioxidative network.
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