Autism spectrum disorder (ASD) is an extreme neuropsychotic disturbance with both environmental and genetic origins. Sodium propionate (PPA) a metabolic bioproduct of gut microbiota is well-thought-out as a successful autism animal model. Nevertheless, Liposomal drug delivery system possess the advantagous of biocompatibility, targeting organs, ability to carry large drug payloads and skipping macrophages for this purpose the current study was carried out to investigate the hypothesis that Calcium Voltage-Gated channel subunit alpha 1 C (CACNA1C) and glial fibrillary acidic protein (GFAP) signaling pathways crosstalk with the efficacy of Co-enzyme Q10 (Co-Q10) and liposomal loaded Co-enzyme Q10 (L Co-Q10) in PPA mediated autistic rat model. Autism was conducted by buffered PPA (500 mg/Kg b.wt) daily for 5 consecutive days subsequently treatment via Co-Q10 in a dose of (10 mg/kg b.wt) and L Co-Q10 (2 mg/kg b.wt) for four weeks then the autistic model was followed for signs of autism at different time intervals of (one, two and four weeks). The control, PPA intoxicated, and treated groups were subjected to behavioral tests (Y-Maze and open field), antioxidant analysis, gene expression analysis, and histological examination at different time intervals of the study. The results revealed that Co-Q10 and L Co-Q10 significantly elevated antioxidative stress biomarkers, comprising superoxide dismutase (SOD), glutathione (GSH), and total antioxidant capacity (TAC). In addition, they significantly ameliorated the oxidative stress biomarker malondialdehyde (MDA). Meanwhile, they significantly downregulated GFAP and CACNA1C mRNA gene expressions, Co-Q10 and LCo-Q10 showed improvement in almost brain regions post PPA histopathological alterations, even better results were manifested via LCo-Q10 groups. These results showed the superiority of LCo-Q10 over Co-Q10 in competing autism. In conclusion The administration of anti-inflammatory and antioxidant agents such as Co-Q10 and L Co-Q10 may represent a promising strategy to counteract pathological behaviors in ASD model via targeting organs, increasing retention time, and reducing side effects
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http://dx.doi.org/10.1016/j.toxrep.2022.12.003 | DOI Listing |
Front Neurosci
December 2024
The Neuro's Early Drug Discovery Unit (EDDU), McGill University, Montreal, QC, Canada.
This study aimed to evaluate different combinations of three dietary supplements for potential additive or synergistic effects in an Parkinson's Disease model. The complex and diverse processes leading to neurodegeneration in each patient with a neurodegenerative disorder cannot be effectively addressed by a single medication. Instead, various combinations of potentially neuroprotective agents targeting different disease mechanisms simultaneously may show improved additive or synergistic efficacy in slowing the disease progression and allowing the agents to be utilized at lower doses to minimize side effects.
View Article and Find Full Text PDFInt J Syst Evol Microbiol
January 2025
Key Laboratory of Marine Genetic Resources, Third Institute of Oceanography, Ministry of Natural Resources of China; Key Laboratory of Marine Genetic Resources of Fujian Province, Xiamen 361005, PR China.
Int J Syst Evol Microbiol
January 2025
China General Microbiological Culture Collection Center (CGMCC), Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, PR China.
Int J Syst Evol Microbiol
January 2025
Environment and Plant Protection Institute, Chinese Academy of Tropical Agricultural Sciences, Haikou 571101, PR China.
A bacterial strain, designated as A6, was isolated from the rhizosphere soil of a healthy muskmelon in Wenchang, Hainan Province, China. The cells of strain A6 were Gram-negative, aerobic, short rod and motile with a single polar flagellum. Strain A6 could tolerate up to 55.
View Article and Find Full Text PDFAm J Med
January 2025
the University of Nevada, Reno School of Medicine, Reno, NV. Electronic address:
Background: A wide array of products in the category of complementary or alternative medicine products for cardiovascular disease and prevention are readily available on online retail platforms. However, a critical assessment of these products including their therapeutic claims has not been previously performed.
Methods: "Heart failure supplement" and similar terms were entered into the Amazon.
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