👤 Hassan M Fayed

This study aimed to investigate how nano curcumin (Nano-Cur) or nano-chromium chloride (Nano-CrCl) in comparison with metformin (Met), can reduce diabetic neuropathy caused by streptozotocin (STZ) in rats. Seventy Wistar albino male rats were randomly divided into seven groups (ten rats/group): control; STZ-induced diabetes; diabetic rats receiving daily oral doses of Nano-Cur, Cur, Nano-CrCl, CrCl, and Met. The present results show that all treated groups significantly alleviated diabetic neuropathy by restoring serum insulin and glucose levels, enhancing cerebral antioxidant activities and activating IR/PI3K/AKT, normalizing neurotransmitters, decreasing oxidative stress markers (MDA), and reducing inflammatory biomarkers and pyroptotic biomarkers. At the molecular level, the levels of GSK3B, JAK-2, STAT-3, AMPK, and BACE1 were significantly downregulated in all treated diabetic groups compared to the diabetic group, especially Nano-Cur and Met. However, Cur, Nano-CrCl, and CrCl did not cause any significant (p > 0.05) alteration in ACh levels compared to the diabetic group. Additionally, the Nano-Cur, Cur, and Met groups exhibited a marked increase in miRNA-223-3p and miRNA-124 levels, whereas Nano-CrCl and CrCl showed no significant changes in these miRNAs when compared to the diabetic group. Show less

Alzheimer's disease (AD) is the most common cause of dementia, a neurodegenerative disorder that progress overtime, which is best known for mood swings and loss of cognitive, behavioral and functional abilities. Quercetin is one of the most consumed flavonoids in the diet and has neuroprotective, anti-inflammatory and antioxidant effects. The purpose of this study was to assess the potential neurotherapeutic effect of quercetin and compare it with donepezil. 40 Wister male rats were used and separated into two main groups: Group I: control group; Group II: AD group, which was divided into four subgroups: Group IIA: untreated AD-rats; Group IIB: quercetin treated AD-rats; Group IIC: donepezil treated AD-rats and Group IID: combined group of quercetin and donepezil. Hydrated aluminum chloride (AlCl Show less

This study investigated the neuroprotective effect of ferulic acid (FA) against bisphenol A (BPA) induced Alzheimer's disease-like pathology in male rats. Rats were allocated into four groups, control, BPA, BPA + FA, and FA, respectively, for 40 days. Spatial working memory and recognition memory were evaluated. Moreover, the brain levels of oxidative stress biomarkers, proinflammatory cytokines, extracellular signal-regulated kinase (ERK), and phosphorylated serine/threonine protein kinase (p-Akt) were measured. We also determined the brain neuropathological protein levels, including Beta-Amyloid 1-42, total Tau (tTau), and phosphorylated Tau (pTau) proteins. Furthermore, brain levels of Acetylcholinesterase (AChE) and Beta-secretase (BACE) were assessed. Brain histological investigation and immunohistochemistry determination of glial fibrillar acidic protein (GFAP) were also performed. Moreover, docking simulation was adapted to understand the inhibitory role of FA on AChE, BACE-1, and ERK1/2. Interestingly, the BPA + FA treated group showed a reversal in the cognitive impairments induced by BPA, which was associated with improved brain redox status. They also exhibited a significant decrease in brain inflammatory cytokines, ERK, and p-Akt levels. Moreover, they revealed a decline in beta-amyloid 1-42 and a significant improvement in tTau expression and pTau protein levels in the brain tissue. Further, the brain levels of AChE and BACE were substantially reduced in BPA + FA rats. The neuroprotective effect of FA was confirmed by restoring the normal architecture of brain tissue, which was associated with decreasing GFAP. FA could be a potent neuroprotectant agent against AD with a possible prospect for its therapeutic capabilities and nutritional supplement value due to its antioxidant and antiapoptotic properties. Show less