Study summary · research use only
Acetyl-L-carnitine and/or liposomal co-enzyme Q10 prevent propionic acid-induced neurotoxicity by modulating oxidative tissue injury, inflammation, and ALDH1A1-RA-RARα signaling in rats
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study, researchers examined whether acetyl-L-carnitine (ALCAR) and/or liposomal coenzyme Q10 (CoQ10) altered propionic acid (PPA)-induced neurotoxicity, an autism-like model, over a 5-day treatment period, assessing cerebral cortex and cerebellum tissue. The abstract reports PPA was associated with histopathological alterations and increased malondialdehyde (MDA), NF-κB p65, TNF-α, and IL-6, along with decreased reduced glutathione (GSH) and antioxidant enzymes. Concurrent ALCAR and/or CoQ10 treatment was associated with reduced tissue injury markers, decreased MDA, NF-κB p65, and pro-inflammatory cytokines, increased cellular antioxidants, upregulated Bcl-2, decreased Bax and caspase-3, and upregulated ALDH1A1 and RARα, with the combination showing more pronounced effects than either treatment alone in the reported data.
Abstract
Propionic acid (PPA) is a short-chain fatty acid produced endogenously by gut microbiota and found in foodstuffs and pharmaceutical products as an additive. Exposure to PPA has been associated with the development of autism spectrum disorder (ASD). The purpose of this study was to investigate the protective effect of acetyl-L-carnitine (ALCAR) and liposomal Co-enzyme Q10 (CoQ10) against cerebral and cerebellar oxidative injury, inflammation, and cell death, and alterations in ALDH1A1-RA-RARα signaling in an autism-like rat model induced by PPA. The rats were treated with PPA and concurrently received ALCAR and/or CoQ10 for 5 days. The animals were sacrificed, and the cerebral cortex and cerebellum were collected for analysis. PPA caused histopathological alterations along with increased malondialdehyde (MDA), NF-κB p65, TNF-α, and IL-6 in the cerebrum and cerebellum of rats. Reduced glutathione (GSH) and antioxidant enzymes were declined in the brain of rats that received PPA. Concurrent treatment with ALCAR and/or CoQ10 prevented tissue injury, decreased MDA, NF-κB p65, and pro-inflammatory cytokines, and enhanced cellular antioxidants in PPA-administered rats. ALCAR and/or CoQ10 upregulated Bcl-2 and decreased Bax and caspase-3 in the brain of rats. In addition, ALCAR and/or CoQ10 upregulated cerebral and cerebellar ALDH1A1 and RARα in PPA-treated rats. The combination of ALCAR and CoQ10 showed more potent effects when compared with the individual treatments. In conclusion, ALCAR and/or CoQ10 prevented tissue injury, ameliorated oxidative stress, inflammatory response, and apoptosis, and upregulated ALDH1A1-RA-RARα signaling in the brain of autistic rats.
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