Abstract

The efficacy of an extract from Asparagus racemosus seeds in protecting zebrafish neurons from acrylamide-induced neurotoxicity was the focus of this investigation. ACR treatment induced neurotoxicity in zebrafish by reducing glutathione reductase levels by a factor of 3, increasing lipid peroxidation activity by a factor of 3.4, elevating nitrite levels by a factor of 1.7, raising acetylcholinesterase levels by a factor of 3.9, and decreasing total protein levels by a factor of 1.4, when compared to wild-type zebrafish. Vinpocetine demonstrated neuroprotective properties in ACR-induced zebrafish. These results indicate a 2.7-fold increase in glutathione reductase, a 3.4-fold reduction in lipid peroxidation activity, a 1.5-fold decrease in nitrite levels, a 3.2-fold decrease in acetylcholinesterase levels, and a 1.4-fold increase in total protein levels. Zebrafish with inherent genetic traits had similar outcomes. Treatment with solvent seed extracts from A. racemosus effectively reduced the damage caused by ACR. Following this intervention, levels of glutathione reductase, lipid peroxides, nitrite, protein, and acetylcholinesterase activity reverted back to levels seen in control group. The ethanolic extract exhibited superior neuroprotective effects compared to the solvent extract in zebrafish treated with ACR. After administering an ethanolic seed extract therapy at a concentration of 440 mg/l, the levels of glutathione reductase rose by a factor of 2.7. Simultaneously, there was a decrease in lipid peroxidation activity by 3.1, nitrite by 1.4, and acetylcholinesterase by 2.7. The protein content of zebrafish exposed to ACR rose by a factor of 1.3. Wild zebrafish had comparable results

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