ArticleJournal of diabetes investigation2018
Curcumin attenuates high glucose-induced inflammatory injury through the reactive oxygen species-phosphoinositide 3-kinase/protein kinase B-nuclear factor-κB signaling pathway in rat thoracic aorta endothelial cells.
Article in Journal of diabetes investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Review of the Protective Mechanism of Curcumin on Cardiovascular Disease.Drug design, development and therapy · 2024Review
- Role of oxidative stress in impaired type II diabetic bone repair: scope for antioxidant therapy intervention?Frontiers in dental medicine · 2024Review
- Jiawei Shengjiangsan's Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB Signaling Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Asprosin Exacerbates Endothelium Inflammation Induced by Hyperlipidemia Through Activating IKKβ-NF-κBp65 Pathway.Inflammation · 2023Article
- Curcumin activates autophagy and attenuates high glucose-induced apoptosis in HUVECs through the ROS/NF-κB signaling pathway.Experimental and therapeutic medicine · 2022Article
- RI75, a curcumin analogue, inhibits tumor necrosis factor-α and interleukin-6 production and exhibits antiallodynic and antiedematogenic activities in mice.Inflammopharmacology · 2022Article
- Evaluation of the anti-inflammatory and antioxidant pharmcodynamic compoents of naoxintong capsules as a basis of broad spectrum effects.Pharmaceutical biology · 2021Article
- Curcumin improves necrotising microscopic colitis and cell pyroptosis by activating SIRT1/NRF2 and inhibiting the TLR4 signalling pathway in newborn rats.Innate immunity · 2020Article
- Hypoxia destroys the microstructure of microtubules and causes dysfunction of endothelial cells via the PI3K/Stathmin1 pathway.Cell & bioscience · 2019Article
- Curcumin attenuates high glucose-induced inflammatory injury through the reactive oxygen species-phosphoinositide 3-kinase/protein kinase B-nuclear factor-κB signaling pathway in rat thoracic aorta endothelial cells.Journal of diabetes investigation · 2018Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AIMS/
introductionEndothelial cell inflammatory injury is likely required for barrier dysfunction under hyperglycemic conditions. Curcumin (CUR) is well known for its anti-inflammatory effect. However, there have been few reports about the anti-inflammatory effect of CUR induced by high glucose in endothelial cells. The aim of the present study was to investigate the inflammatory effect of high glucose and the anti-inflammatory effect of CUR induced by high glucose in rat thoracic aorta endothelial cells (TAECs). MATERIALS AND
methodsWell characterized TAECs were established and cell viability was assayed by the cell counting kit-8 method, messenger ribonucleic acid and protein expression were identified by real-time polymerase chain reaction, western blot or enzyme-linked immunosorbent assay, respectively. The production of reactive oxygen species was observed by a fluorescence microscope.
resultsHigh glucose (30 mmol/L) significantly decreased the cell viability of TAECs after being co-cultivated for 12 h and showed a time-dependent manner, and increased interleukin (IL)-1β, IL-6 and tumor necrosis factor-α secretion in TAECs. The injury effect of high glucose was involved in the reactive oxygen species-phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)-nuclear factor (NF)-κB signaling pathway. Anti-oxidant N-acetylcysteine, PI3K and NF-κB-specific pathway inhibitors can abolish the secretion of these inflammatory factors; pretreatment with anti-oxidant N-acetylcysteine significantly decreased PI3K expression, the level of phosphorylated AKT and nuclear NF-κB; pretreatment of LY294002 can significantly decrease the NF-κB level in nuclei. After treatment with CUR for 12 h, IL-1β, IL-6 and tumor necrosis factor-α secretion were markedly decreased, and PI3K expression, the phosphorylation of AKT and nuclear NF-κB level were also decreased.
conclusionCurcumin attenuates high glucose-induced inflammatory injury through the reactive oxygen species-PI3K/AKT-NF-κB signaling pathway in rat thoracic aorta endothelial cells.
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