ArticleMolecules (Basel, Switzerland)2016
Zerumbone, a Bioactive Sesquiterpene, Ameliorates Diabetes-Induced Retinal Microvascular Damage through Inhibition of Phospho-p38 Mitogen-Activated Protein Kinase and Nuclear Factor-κB Pathways.
Article in Molecules (Basel, Switzerland), 2016. 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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10 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Review
- Zerumbone Protects Rats from Collagen-Induced Arthritis by Inhibiting Oxidative Outbursts and Inflammatory Cytokine Levels.ACS omega · 2023Article
- Beneficial effects of protocatechuic acid on diabetic retinopathy in streptozocin-induced diabetic rats.International journal of ophthalmology · 2023Article
- Healthy Zerumbone: From Natural Sources to Strategies to Improve Its Bioavailability and Oral Administration.Plants (Basel, Switzerland) · 2022Review
- Zerumbone Protects against Carbon Tetrachloride (CClMolecules (Basel, Switzerland) · 2019Article
- Zerumbone Exhibits Antiphotoaging and Dermatoprotective Properties in Ultraviolet A-Irradiated Human Skin Fibroblast Cells via the Activation of Nrf2/ARE Defensive Pathway.Oxidative medicine and cellular longevity · 2019Article
- Atrial Transcriptional Profiles of Molecular Targets Mediating Electrophysiological Function in Aging andFrontiers in physiology · 2019Article
- Gene and Protein Expression Profile of Selected Molecular Targets Mediating Electrophysiological Function inInternational journal of molecular sciences · 2018Article
- Phytochemicals: Target-Based Therapeutic Strategies for Diabetic Retinopathy.Molecules (Basel, Switzerland) · 2018Review
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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
Zerumbone ameliorates retinal damage by blocking advanced glycation end products and their receptor system in streptozotocin-diabetic rats. Because of the multiple factors involved in diabetic retinopathy (DR) etiology, the mechanisms of zerumbone that are mainly responsible for its ameliorative effect on DR need to be further clarified. In the present study, zerumbone (20 mg or 40 mg/kg) or fenofibric acid (100 mg/kg) was orally administered to diabetic rats by intragastric gavage once daily for three consecutive months. Zerumbone displayed similar characteristics to fenofibric acid in reducing retinal vascular permeability and leukostasis in diabetic rats. Fundus photographs showed that large retinal vessel diameters were decreased in zerumbone-treated diabetic rats. Zerumbone not only down-regulated the gene expression of retinal angiogenic parameters, but also reduced the expression of inflammatory cytokines and chemokines in the retina of diabetic rats. Moreover, zerumbone reduced the p38 MAPK phosphorylation and abrogated the nuclear translocation of NF-κB p65 in the retina of diabetic rats. In conclusion, treatment of diabetic rats with zerumbone attenuates the severity of retinal inflammation and angiogenesis, via inhibition of p38 MAPK and NF-κB signaling pathways. These benefits of zerumbone for DR appear to be linked to its antihyperglycemic and antihyperlipidemic effects.
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