ArticleJournal of cellular and molecular medicine2014
Inhibition of JNK by compound C66 prevents pathological changes of the aorta in STZ-induced diabetes.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Combination of Tramiprosate, Curcumin, and SP600125 Reduces the Neuropathological Phenotype in Familial Alzheimer Disease PSEN1 I416T Cholinergic-like Neurons.International journal of molecular sciences · 2024Article
- TXNIP in liver sinusoidal endothelial cells ameliorates alcohol-associated liver disease via nitric oxide production.International journal of biological sciences · 2024Article
- Efficacy of the monocarbonyl curcumin analog C66 in the reduction of diabetes-associated cardiovascular and kidney complications.Molecular medicine (Cambridge, Mass.) · 2022Review
- The Role of PKC-MAPK Signalling Pathways in the Development of Hyperglycemia-Induced Cardiovascular Complications.International journal of molecular sciences · 2022Review
- Epigenetics in the pathogenesis of diabetic nephropathy.Acta biochimica et biophysica Sinica · 2022Review
- The Potential Role of Curcumin in Modulating the Master Antioxidant Pathway in Diabetic Hypoxia-Induced Complications.Molecules (Basel, Switzerland) · 2021Review
- Unfolding Nrf2 in diabetes mellitus.Molecular biology reports · 2021Review
- Protective role of NRF2 in macrovascular complications of diabetes.Journal of cellular and molecular medicine · 2020Review
- Hypoglycemic Mechanism of the Berberine Organic Acid Salt under the Synergistic Effect of Intestinal Flora and Oxidative Stress.Oxidative medicine and cellular longevity · 2018Article
- Novel Curcumin C66 That Protects Diabetes-Induced Aortic Damage Was Associated with Suppressing JNK2 and Upregulating Nrf2 Expression and Function.Oxidative medicine and cellular longevity · 2018Article
- High glucose enhances the metastatic potential of tongue squamous cell carcinoma via the PKM2 pathway.Oncotarget · 2017Article
- Exacerbation of diabetic cardiac hypertrophy in OVE26 mice by angiotensin II is associated with JNK/c-Jun/miR-221-mediated autophagy inhibition.Oncotarget · 2017Article
- Antioxidative Effects of Natural Products on Diabetic Cardiomyopathy.Journal of diabetes research · 2017Review
- The Role of Nrf2 in Cardiovascular Function and Disease.Oxidative medicine and cellular longevity · 2017Review
- C66 ameliorates diabetic nephropathy in mice by both upregulating NRF2 function via increase in miR-200a and inhibiting miR-21.Diabetologia · 2016Article
- Bacterial Flora Changes in Conjunctiva of Rats with Streptozotocin-Induced Type I Diabetes.PloS one · 2015Article
- Diabetic cardiomyopathy and its prevention by nrf2: current status.Diabetes & metabolism journal · 2014Review
- Ventral prostate fibrosis in the Akita mouse is associated with macrophage and fibrocyte infiltration.Journal of diabetes research · 2014Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases as leading causes of the mortality world-wide are related to diabetes. The present study was to explore the protective effect of curcumin analogue C66 on diabetes-induced pathogenic changes of aortas. Diabetes was induced in male C57BL/6 mice with a single intraperitoneal injection of streptozotocin. Diabetic mice and age-matched non-diabetic mice were randomly treated with either vehicle (Control and Diabetes), C66 (C66 and Diabetes/C66) or c-Jun N-terminal kinase (JNK) inhibitor (sp600125, JNKi and Diabetes/JNKi). All three treatments were given by gavage at 5 mg/kg every other day for 3 months. Aortic inflammation, oxidative stress, fibrosis, cell apoptosis and proliferation, Nrf2 expression and transcription were assessed by immunohistochemical staining for the protein level and real-time PCR method for mRNA level. Diabetes increased aortic wall thickness and structural derangement as well as JNK phosphorylation, all of which were attenuated by C66 treatment as JNKi did. Inhibition of JNK phosphorylation by C66 and JNKi also significantly prevented diabetes-induced increases in inflammation, oxidative and nitrative stress, apoptosis, cell proliferation and fibrosis. Furthermore, inhibition of JNK phosphorylation by C66 and JNKi significantly increased aortic Nrf2 expression and transcription function (e.g. increased expression of Nrf2-downstream genes) in normal and diabetic conditions. These results suggest that diabetes-induced pathological changes in the aorta can be protected by C66 via inhibition of JNK function, accompanied by the up-regulation of Nrf2 expression and function.
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