ArticleChinese medicine2025
Cinnamic acid alleviates endothelial dysfunction and oxidative stress by targeting PPARδ in obesity and diabetes.
Article in Chinese medicine, 2025. 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.
- Hepatoprotective effects of cinnamic acid against carbon tetrachloride-induced liver injury in a mouse model.Molecular biology reports · 2026Article
- Article
- Liensinine Ameliorating Oxidative Damage to Vascular Endothelium In Vitro via Upregulating eNOS and Nrf2/HO-1 Signaling.Food science & nutrition · 2026Article
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Targeting hypertension through natural phenolics: The multifaceted role of cinnamic acid and its derivatives.Pflugers Archiv : European journal of physiology · 2026Review
- Celafolin A-1 Ameliorates Subretinal Fibrosis via Inhibition of Crystallin Alpha B in a Laser-Induced Choroidal Neovascularization Mouse Model.Biomolecules & therapeutics · 2026Article
- Semi-Synthetic HACS medicinal chemistry letters · 2026Article
- Anti-diabetic retinopathy molecular mechanism of Dihuang Yinzi: insights from network pharmacology, metabolomics, and microbiome analysis.Frontiers in medicine · 2026Article
- Optimization of the Extraction of Bioactive Compounds and Metabolomic Profile ofPlants (Basel, Switzerland) · 2025Article
- Anti-obesity effects of Wumeishanzhayin: an integrated lipidomics and transcriptomics study.Frontiers in pharmacology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
objectiveCinnamic acid (CA) is a bioactive compound isolated from cinnamon. It has been demonstrated to ameliorate inflammation and metabolic diseases, which are associated with endothelial dysfunction. This study was aimed to study the potential protective effects of CA against diabetes-associated endothelial dysfunction and its underlying mechanisms.
methodsHigh-fat diet (HFD) with 60 kcal% fat was used to induce obesity/diabetes in C57BL/6 mice for 12 weeks. These diet-induced obese (DIO) mice were orally administered with CA at 20 or 40 mg/kg/day, pioglitazone (PIO) at 20 mg/kg/day or same volume of vehicle during the last 4 weeks. Isolated mouse aortic segments and primary culture rat aortic endothelial cells (RAECs) were induced with high glucose (HG) to mimic hyperglycemia and co-treated with different concentrations of CA.
resultsIn DIO mice, four-week administration of CA, particularly at 40 mg/kg/day, diminished the body weights, blood pressure, fasting blood glucose and plasma lipid levels, and ameliorated endothelium-dependent relaxations (EDRs) and oxidative stress in aortas. The beneficial effects of CA were comparable to the positive control group, PIO. Western blotting results indicated that CA treatment upregulated the expression of peroxisome proliferator-activated receptor delta (PPARδ), and activated nuclear factor erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) and AMP-activated protein kinase (AMPK)/ protein kinase B (Akt)/ endothelial nitric oxide synthase (eNOS) signaling pathways in mouse aortas in vivo and ex vivo. HG stimulation impaired EDRs in mouse aortas and inhibited nitric oxide (NO) production but elevated reactive oxygen species (ROS) levels in RAECs. CA reversed these impairments. Importantly, PPARδ antagonist GSK0660 abolished the vasoprotective effects of CA. Molecular docking analysis suggested a high likelihood of mutual binding between CA and PPARδ.
conclusionCA protects against endothelial dysfunction and oxidative stress in diabetes and obesity by targeting PPARδ through Nrf2/HO-1 and Akt/eNOS signaling pathways.
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