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Morin hydrate protects type-2-diabetic wistar rats exposed to diesel exhaust particles from inflammation and
Akeem O Lawal1, Ibukun M Folorunso1, Opeyemi Iwaloye1
1Bioinformatics and Molecular Biology Unit, Department of Biochemistry, School of Sciences, Federal University of Technology, P.M.B. 704, Akure, Ondo-State Nigeria.
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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