ArticleNutrients2016
Effect of Cudrania tricuspidata and Kaempferol in Endoplasmic Reticulum Stress-Induced Inflammation and Hepatic Insulin Resistance in HepG2 Cells.
Article in Nutrients, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 29 citations in OpenAlex.
- Chemical Profiling and Anti-Inflammatory Mechanisms ofMetabolites · 2026Article
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- Kaempferol attenuates particle-induced osteogenic impairment by regulating ER stress via the IRE1α-XBP1s pathway.The Journal of biological chemistry · 2024Article
- Review
- In Vitro Antithrombotic, Hematological Toxicity, and Inhibitor Studies of Protocatechuic, Isovanillic, andMolecules (Basel, Switzerland) · 2022Article
- A Comparative Study on Physicochemical, Photocatalytic, and Biological Properties of Silver Nanoparticles Formed Using Extracts of Different Parts ofNanomaterials (Basel, Switzerland) · 2020Article
- Anti-Metastatic Effect of Gold Nanoparticle-ConjugatedInternational journal of nanomedicine · 2020Article
- In Vivo Rodent Models of Type 2 Diabetes and Their Usefulness for Evaluating Flavonoid Bioactivity.Nutrients · 2019Review
- Simultaneous UPLC-TQ-MS/MS determination of six active components in rat plasma: application in the pharmacokinetic study ofChinese medicine · 2019Article
- Article
- Long-chain bases from sea cucumber mitigate endoplasmic reticulum stress and inflammation in obesity mice.Journal of food and drug analysis · 2017Article
- Flavonoids, Inflammation and Immune System.Nutrients · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we quantitated kaempferol in water extract from Cudrania tricuspidata leaves (CTL) and investigated its effects on endoplasmic reticulum (ER) stress-induced inflammation and insulin resistance in HepG2 cells. The concentration of kaempferol in the CTL was 5.07 ± 0.08 mg/g. The HepG2 cells were treated with 300 µg/mL of CTL, 500 µg/mL of CTL, 1.5 µg/mL of kaempferol or 2.5 µg/mL of kaempferol, followed immediately by stimulation with 100 nM of thapsigargin for ER stress induction for 24 h. There was a marked increase in the activation of the ER stress and inflammation response in the thapsigargin-stimulated control group. The CTL treatment interrupted the ER stress response and ER stress-induced inflammation. Kaempferol partially inhibited the ER stress response and inflammation. There was a significant increase in serine phosphorylation of insulin receptor substrate (IRS)-1 and the expression of C/EBPα and gluconeogenic genes in the thapsigargin-stimulated control group compared to the normal control. Both CTL and kaempferol suppressed serine phosphorylation of IRS-1, and the treatments did not interrupt the C/EBPα/gluconeogenic gene pathway. These results suggest that kaempferol might be the active compound of CTL and that it might protect against ER stress-induced inflammation and hyperglycemia.
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