ArticleJournal of diabetes and metabolic disorders2022
Morin hydrate protects type-2-diabetic wistar rats exposed to diesel exhaust particles from inflammation and oxidative stress.
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 4 papers.
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4 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular Docking, Dynamics, and Preclinical Studies Reveal Morin Hydrate as a Potent PPARγ and Nrf2 Agonist That Mitigates Colon Inflammation.Pharmacology research & perspectives · 2025Article
- In silico analysis of Rutin and Morin against diabetes-associated molecular targets.In silico pharmacology · 2025Article
- Hepatoprotective Effect of Morin Hydrate in Type 2 Diabetic Wistar Rats Exposed to Diesel Exhaust Particles.Applied biochemistry and biotechnology · 2023Article
- Effect of the Combination of Probiotics and Korean Red Ginseng on Diabetic Wound Healing Exposed to Diesel Exhaust Particles(DEPs).Medicina (Kaunas, Lithuania) · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Background: Studies have demonstrated that exposure to diesel exhaust particle (DEP) aggravates diabetes condition by inducing oxidative and pro-inflammatory effects. Morin hydrate (MH), a flavonol found in common guava, among others has been demonstrated to possess a variety of biological activities. The present study was designed to investigate the effects of morin hydrate (MH) on the pancreas of type-2 diabetic (T2D) wistar rats exposed to DEP. Methods: Rats were induced with type 2 diabetes by oral fructose therapy for 14 days followed by injection of streptozotocin (45 mg/kg). These rats were pre-treated with DEP (0.4 mg/kg and 0.5 mg/kg) through nasal instillation prior to receiving oral MH (30 mg/kg).This study determined oxidative stress parameters using biochemical assay, and some pancreatic genes involved in oxidative stress, inflammation and glucose uptake were quantified using RT-polymerase chain reaction (PCR). Results: The results indicate that MH reverses oxidative stress in T2D rats exposed to DEP via substantial increase in superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity and reduced glutathione (GSH) levels, but a decrease in malondialdehyde (MDA) and conjugated diene (CD) levels. Moreover, PCR assay showed that MH mitigate inflammation and oxidative stress but promote glucose uptake by increasing the mRNA expression of IL-10, HO-1, and GLUT 4; decreasing mRNA expression of IL-1 and modulating AKT/PI3K/GLUT4 and AMPK/GLUT4 signaling. Histopathological examination revealed that MH reverses DEP induced pancreatic fibrosis and necrosis. Conclusion: The results suggest that MH alleviate inflammation and oxidative stress and promote glucose uptake in the pancreas of type-2 diabetic rats, either in the presence or absence of DEP.
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