RESUMO
Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by tau pathology and accumulations of neurofibrillary tangles (NFTs) along with amyloid-beta (Aß). It has been associated with neuronal damage, synaptic dysfunction, and cognitive deficits. The current review explained the molecular mechanisms behind the implications of Aß aggregation in AD via multiple events. Beta (ß) and gamma (γ) secretases hydrolyzed amyloid precursor protein (APP) to produce Aß, which then clumps together to form Aß fibrils. The fibrils increase oxidative stress, inflammatory cascade, and caspase activation to cause hyperphosphorylation of tau protein into neurofibrillary tangles (NFTs), which ultimately lead to neuronal damage. Acetylcholine (Ach) degradation is accelerated by upstream regulation of the acetylcholinesterase (AChE) enzyme, which leads to a deficiency in neurotransmitters and cognitive impairment. There are presently no efficient or disease-modifying medications for AD. It is necessary to advance AD research to suggest novel compounds for treatment and prevention. Prospectively, it might be reasonable to conduct clinical trials with unclean medicines that have a range of effects, including anti-amyloid and anti-tau, neurotransmitter modulation, anti-neuroinflammatory, neuroprotective, and cognitive enhancement.
RESUMO
PURPOSE: The present study was aimed at evaluating the role of Momordica charantia L. fruit and Genistein on beta cell, insulin resistance/sensitivity and lipid profile in type 2 diabetic rats. METHODS: Thirty-five (35) albino rats were divided into seven (7) groups of 5 rats each comprising of five (5) non-diabetic and thirty (30) diabetic rats. Groups 1 and 2 served as the normal control and diabetic control groups respectively and received distill water, groups 3 and 4 received Mormodica charantia L. at 250 mg/kg and 500 mg/kg respectively. Groups 5 and 6 received Genistein at 10 mg/kg and 20 mg/kg respectively while group 7 received Metformin at 500 mg/kg the experiment lasted for four weeks. All the rats were euthanized at the end of the fourth week. RESULTS: Lipid profile, glucose and insulin levels were determined from the analysis of serum parameters and the histology of the pancreas. A significant reduction (p < 0.05) in blood glucose levels was noticed in rats that received Momordica charantia L. (MC) and genistein when compared with diabetic control rats. A significant decrease (p < 0.05) in cholesterol, triglyceride, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) levels were also noted in rats that received MC and Genistein when compared with the diabetic control rats. MC and Genistein significantly increased (P < 0.05) serum insulin level compared to the diabetic control rats. MC and Genistein significantly decreased (p < 0.05) homeostatic model assessment-insulin resistance (HOMA-IR) level compared with the diabetic control group. Pancreas of rats that received MC and Genistein showed regenerating beta-cells. CONCLUSION: Momordica charantia L. fruit and Genistein were able to enhance beta cell function and prevent lipid accumulation and insulin resistance in type 2 diabetic rats.