Metformin/Donepezil combination modulates brain antioxidant status and hippocampal endoplasmic reticulum stress in type 2 diabetic rats

Combined effect of metformin and gallic acid on inflammation, antioxidant status, endoplasmic reticulum (ER) stress and glucose metabolism in fructose-fed streptozotocin-induced diabetic rats

“…Evaluation of amplicons was done by electrophoresis in agarose gel (0.2 %) using 0.5 × TBE buffer adjusted to pH 8.3 with the sodium hydroxide pellet) with 5 μl EZ-vision (VWR Life Science). ImageJ software was used to quantify relative amount of complimentary DNA [ 39 ].…”

Metformin a Potential Pharmacological Strategy in Late Onset Alzheimer’s Disease Treatment

“…In general, interventional models will be effective for detecting symptomatic or therapeutic interventions as a disease model. These models can include valuable observations such as the streptozotocin (STZ)-induced AD model, scopolamine-mediated amnesia model that led to learning and memory loss and cognition dysfunction [ 76 , 77 , 78 , 79 , 80 ]. For instance, in scopolamine-induced amnesia models, inflammation is activated by endotoxins and the brain metabolism interacts with other chemical action models [ 73 ].…”

“…Since LOAD represents more than 95% of AD cases, associated animal models are valuable research resources for studying pathogenesis and designing experimental treatments for sporadic AD [ 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 ]. STZ is a diabetogenic agent that is widely used to induce diabetes in animals because it damages and induces IR in pancreatic beta cells.…”

“…STZ is a diabetogenic agent that is widely used to induce diabetes in animals because it damages and induces IR in pancreatic beta cells. Decrease of glucose/energy metabolism in brain, corresponds to the severity of dementia symptoms in AD, and is a well-established brain abnormality of sporadic AD [ 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 ]. In ICV-STZ animal models, BIR reduced brain glucose metabolism, tau and Aβ accumulation, gliosis, cholinergic deficits, oxidative stress, and learning and memory deficits [ 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 ].…”

“…Decrease of glucose/energy metabolism in brain, corresponds to the severity of dementia symptoms in AD, and is a well-established brain abnormality of sporadic AD [ 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 ]. In ICV-STZ animal models, BIR reduced brain glucose metabolism, tau and Aβ accumulation, gliosis, cholinergic deficits, oxidative stress, and learning and memory deficits [ 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 ]. Brain insulin signaling controls the metabolism of cerebral glucose, and impaired transduction of brain insulin signaling was reported in AD [ 82 ].…”