Neuroprotective effects of Tanshinone IIA in an acrylamide-induced in-vivo zebrafish model: Behavioral, biochemical and molecular restoration.

Acrylamide is a neurotoxic chemical widely present in carbohydrate-rich foods due to thermal processing. Chronic exposure to acrylamide can lead to oxidative stress, neuroinflammation, and neurodegeneration, resulting in motor dysfunction and cognitive impairments. In this study, we evaluated the neuroprotective potential of Tanshinone IIA (TIIA), a bioactive compound derived from Salvia miltiorrhiza (Danshen), on an adult zebrafish model induced with acrylamide. Zebrafish were exposed to acrylamide to induce neurotoxic stress, followed by treatment with varying concentrations of TIIA. Our results highlight that TIIA significantly improved survival rates and restored behavioral deficits caused by acrylamide, including impaired exploratory behavior and increased anxiety-like responses. Biochemically, TIIA restored antioxidant enzyme activities such as superoxide dismutase (SOD) and catalase (CAT), which were reduced by acrylamide exposure, thereby mitigating oxidative stress. TIIA also decreased lactate dehydrogenase (LDH) activity, indicative of reduced cellular damage, and restored acetylcholinesterase (AChE) activity, crucial for cholinergic neurotransmission. At the molecular level, TIIA reduced the activity of pro-inflammatory genes by stopping transcription, which acrylamide had increased, and brought the levels of neuroprotective genes like bdnf and nrf back to normal. Additionally, histological investigation showed that TIIA treatment significantly restored the morphological damage caused by acrylamide in the brain tissue of zebrafish. We draw conclusions on TIIA's neuroprotective effectiveness against acrylamide-induced neurotoxicity, demonstrating its potential as a treatment to stop acrylamide processed foods from causing neurodegenerative diseases.