Mulberry Fruit Prevents Diabetes and Diabetic Dementia by Regulation of Blood Glucose through Upregulation of Antioxidative Activities and CREB/BDNF Pathway in Alloxan-Induced Diabetic Mice
| Autor: | A Young Min, Mee Ree Kim, Jae-Myung Yoo, Dai-Eun Sok |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Blood Glucose
Male Aging medicine.medical_specialty Article Subject tau Proteins CREB Biochemistry Neuroprotection Antioxidants Diabetes Mellitus Experimental chemistry.chemical_compound Downregulation and upregulation Internal medicine Alloxan Diabetes mellitus Hyperlipidemia Animals Medicine Phosphorylation Cyclic AMP Response Element-Binding Protein Hypolipidemic Agents Mice Inbred ICR Kidney Amyloid beta-Peptides biology QH573-671 business.industry Brain-Derived Neurotrophic Factor Cell Biology General Medicine medicine.disease Malondialdehyde Up-Regulation Oxidative Stress medicine.anatomical_structure Endocrinology chemistry Organ Specificity Fruit biology.protein Dementia Lipid Peroxidation Morus business Cytology Research Article Signal Transduction |
| Zdroj: | Oxidative Medicine and Cellular Longevity, Vol 2020 (2020) Oxidative Medicine and Cellular Longevity |
| ISSN: | 1942-0994 1942-0900 |
| Popis: | Although mulberry fruit has various beneficial effects, its effect on diabetes-related dementia remains unknown. We investigated whether the ethyl acetate fraction of ethanolic extract of mulberry fruit (MFE) could alleviate biochemical and behavioral deficits in alloxan-induced diabetic mice. In the diabetic mice, MFE considerably abolished multiple deficits, e.g., body weight reduction; water and food intake increase; and hyperglycemia, hyperlipidemia, hypoinsulinism, and hypertrophy of the liver, kidneys, spleen, and brain. A 200 mg/kg MFE dose reduced malondialdehyde levels and improved antioxidant enzyme activity in the liver, kidney, and brain tissues. MFE attenuated hyperglycemia-induced memory impairments and acetylcholine deprivation, protected neuronal cells in CA1 and CA3 regions via p-CREB/BDNF pathway activation, and reduced amyloid-β precursor protein and p-Tau expressions in the brain tissue. In conclusion, MFE exerts antidiabetic and neuroprotective effects by upregulating antioxidative activities and p-CREB/BDNF pathway in chronic diabetes. Therefore, MFE may be used as a therapeutic agent for diabetes and diabetic neurodegenerative diseases. |
| Databáze: | OpenAIRE |
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