ArticleIranian journal of basic medical sciences2022
Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation.
Article in Iranian journal of basic medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Spinosin: A Critical Updated Review on Pharmacology, Pharmacokinetics, Toxicity and Translational Bottlenecks.Molecules (Basel, Switzerland) · 2026Review
- Insulin Resistance Triggers Atherosclerosis: Caveolin 1 Cooperates with PKCzeta to Block Insulin Signaling in Vascular Endothelial Cells.Cardiovascular drugs and therapy · 2024Article
- Establishment of fingerprint of phenolic compounds inFrontiers in chemistry · 2024Article
- Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases.Journal of inflammation research · 2023Review
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Authors and funding
5 authors.
Funding
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Abstract
Objectives: Spinosin is the predominant C-glycoside flavonoid derived from the seeds of Materials and Methods: The anti-IR effect of spinosin was evaluated in a high-fat diet (HFD) treated mice model. The effects of spinosin pretreatment on reactive oxygen species (ROS)-associated inflammation in Human umbilical vein endothelial cells (HUVEC) were evaluated by western blot analysis and reverse transcription-polymerase chain reaction. The effect of spinosin on insulin-mediated endothelium-dependent vasodilation of rat aortae was further evaluated. Results: Spinosin at 20 mg/kg alleviates increased mice's body weight, fasting serum glucose, oral glucose tolerance, serum insulin, insulin resistance index, and serum lipid of HFD-treated mice. Spinosin at 20 μM suppressed ROS overproduction, and inhibited ROS-related HUVEC inflammation by inhibiting mRNA expression of tumor necrosis factor-α and interleukin-6. In addition, spinosin at 0.1 μM showed a vasodilation effect of isoprenaline-pretreated rat aortae and increased insulin-mediated NO production in endothelial cells. These effects were shown to be related to the spinosin regulating serine/tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) facilitated/phosphoinositide 3-kinase (PI3K) signaling. Conclusion: Spinosin may ameliorate IR and ROS-associated inflammation, and increase endothelial NO production by mediating IRS-1/PI3K/endothelial nitric oxide synthase (eNOS) pathway.
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