👤 Tarek Khamis

Microplastic (MPs) pollution is widespread in the environment and poses growing risks to food safety and human health. In a 60-day oral exposure study, male Swiss mice received MPs (10 mg/kg b.wt), and the neuroprotective potential of taurine (Tau, 200 mg/kg b.wt) was evaluated. MPs exposure induced pronounced anxiety-like behavior, evidenced by increased peripheral zone activity in the open field test (+ 81.1%) and elevated anxiety index in the elevated plus maze (+ 75.9%), along with significant memory and spatial learning impairments in the Y-maze (increased trials + 31.6% and latency + 75.2%). Neurochemically, MPs increased acetylcholinesterase (AChE) activity (+ 89.4%) while reducing dopamine (-29.4%) and γ-aminobutyric acid (GABA) (-17.9%) levels. MPs also triggered marked oxidative stress, as shown by elevated reactive oxygen species (+ 107.6%) and malondialdehyde (+ 249.0%), accompanied by reduced total antioxidant capacity (-26.2%). At the molecular level, MPs downregulated CREB1 (-82.2%) and BDNF (-80.2%) while markedly upregulating AKT1 (~ fivefold) and pro-inflammatory cytokines (TNF-α, IL-6, CXCL-10, and IL-1β; 5.2-7.2-fold). Histopathological analysis revealed severe neurodegenerative alterations across the cerebrum, hippocampus, and cerebellum. Tau co-treatment significantly ameliorated MPs' induced neurotoxicity by reducing anxiety and memory deficits, lowering AChE activity (- 17.3%), restoring dopamine (+ 28.8%) and GABA (+ 14.2%) levels, attenuating oxidative stress (ROS -45.4% and MDA -44.7%), suppressing inflammatory gene expression (-51.0 to -68.1%), and partially normalizing CREB1 and BDNF expression (+239% and +240%, respectively). Collectively, these findings identify Tau as a promising natural neuroprotective agent against MPs' induced neurotoxicity. Show less

Dyslipidemia is a major risk factor for the development of NAFLD, atherosclerosis and cardiovascular diseases. Rosuvastatin (ROS) is a lipid-lowering drug that protects against the development of NAFLD and atherosclerosis. However, the mechanism of this protection remains obscure. Therefore, the current study aims to explore the mechanism by which ROS-loaded glycerosomes (ROS-GLY) protect against NAFLD and atherosclerosis. Hence, for this purpose, hepatic lncRNA-H19/miR-130a/PPAR-γ and aortic PPAR-γ/LXRα/ABCA1 signaling pathways were assessed. In addition, these target pathways were predicted using molecular docking analysis. Thirty-five male Sprague Dawley rats were separated into control, dyslipidemic (poloxamer 407 (P 407)), P 407+ROS-GLY, P 407+NC, and P 407+ROS-GLY+NC groups. ROS-GLY improved lipid profile, hepatic MDA, SOD, catalase and total antioxidant capacity (TAC) in compared to P 407 group. In the dyslipidemic group, ROS-GLY downregulated hepatic lncRNA-H19 expression which leads to an upregulate of the miR-130a level and subsequent reduction of the PPAR-γ level. Consequently, the hepatic expression level of lipogenic genes such as, ACC-1, FASN and SCD-1 was significantly downregulated in the ROS-GLY group than the dyslipidemic one. Aortic PPAR-γ/LXRα/ABCA1 signaling pathway was significantly upregulated in the ROS-GLY group compared to the dyslipidemic group. Furthermore, ROS-GLY modulated IL-6 and IL-10 immunoprotein expression in hepatic and aortic tissues. Interestingly, ROS showed a substantial binding affinity with PPAR-γ, LXR-α, and FASN, according to a molecular docking study. The current study indicated that ROS-GLY protected against the progression of NAFLD and atherosclerosis in dyslipidemic rats via modulation of lipid profile, oxidative stress, pro-/anti-inflammatory cytokines, hepatic lncRNA-H19/miR-130a/PPAR-γ, and aortic PPAR-γ/LXRα/ABCA1 signaling pathways. Show less