ArticleJournal of diabetes and metabolic disorders2022
1,8 cineole protects type 2 diabetic rats against diabetic nephropathy via inducing the activity of glyoxalase-I and lowering the level of transforming growth factor-1β.
Article in Journal of diabetes and metabolic disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- The Effects of 1,8-Cineole Treatment on Benign Prostatic Hyperplasia in Rats.Current pharmaceutical biotechnology · 2026Article
- The comprehensive review of eucalyptol: synthesis, metabolism, and therapeutic applications in disease treatment.Molecular biology reports · 2025Review
- Protective effect of 1, 8-cineole (eucalyptol) against lead-induced liver injury by ameliorating oxidative stress and inflammation and modulating TLR4/MyD88/NF-κB signaling.Iranian journal of basic medical sciences · 2024Article
- Role of cineole in alleviation of acute kidney injury and renal function recovery following gentamicin administration in rats.Iranian journal of basic medical sciences · 2023Article
- The Nicotinamide/Streptozotocin Rodent Model of Type 2 Diabetes: Renal Pathophysiology and Redox Imbalance Features.Biomolecules · 2022Review
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2 authors at 2 institutions in 1 country.
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Abstract
Purpose: Diabetes leading to the production and circulation of glycation products along with the reduction of the activity of glyoxalase-I (GLO-I) contribute to diabetic nephropathy. Therefore, we studied the effect of 1,8 cineole (Cin) on the formation of diverse glycation products and the activity of GLO-I as well as renal histopathological alterations in the type-2 diabetic rat. Methods: Type 2 diabetes was induced in rats with a combination of streptozotocin and nicotinamide (55 + 200 mg/kg). Two groups of rats, normal and diabetic, were treated intragastrically with Cin (200 mg/kg) once daily for 2 months. Fasting blood sugar, insulin resistance index, lipid profile, the activity of GLO-I, glycation products (Glycated albumin, Glycated LDL, Methylglyoxal, and advanced glycation end products), and oxidative stress (Advanced oxidation protein products, malondialdehyde, oxidized LDL, and reduced glutathione), inflammatory markers (Tumor necrosis factor-α and Transforming growth factor-1β), creatinine in the serum (Cre), and proteinuria (PU) in the urine of all rats was determined as well as renal histopathological alterations were investigated. Results: Cin reduced biochemical (Cre and PU) and histopathological (glomerulosclerosis) indicators of renal dysfunction in the diabetic rat compared to untreated diabetic rats. Moreover, the treatment decreased different glycation, oxidative stress, and pro-inflammatory markers Conclusions: Cin ameliorated diabetic nephropathy via reduction of TGF-1β following to decrease the formation of different glycation products, oxidative stress, and inflammatory process with the induction of the activity of glyoxalase-I in type 2 diabetic rats.
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