Scholarlink

<p>Acrylamide (ACR) has gained worldwide attention as a thermal process contaminant because of its neurotoxic actions and widespread presence. Prolonged exposure to ACR results in the degeneration of neuronal cells, loss of motor function, and potential impairment of antioxidant defence systems, especially during brain development. The widespread exposure and neurotoxic effects of acrylamide, there is an urgent need​ to identify natural compounds capable of mitigating its detrimental impact on the nervous system. Therefore, this study aimed to determine the neuroprotective effect of swertiamarin (SWE) on ACR-induced neurotoxicity in zebrafish larvae. Zebrafish larvae at 3 days post-fertilisation (dpf) were exposed to 0.75 mM ACR for 3 days to induce neurotoxicity and co-treated with SWE (100 µM) to evaluate its potential neuroprotective effects. All behavioural and biochemical assays, including locomotor activity, glutathione levels, antioxidant enzyme activity, and acetylcholinesterase function in the head region, were conducted at 6 days post-fertilization (dpf). ACR exposure disrupted glutathione redox balance in zebrafish larvae, and subsequent SWE treatment significantly restored this balance, which is essential for acrylamide detoxification and clearance. Furthermore, it reduced the expression of pro-inflammatory cytokines, including <i>tnf-α</i>,<i> il-1β</i>, and <i>il-6</i>, in the zebrafish larvae head, alleviated oxidative stress, and improved synaptic vesicle cycling. Motor responses were partially restored, suggesting an improvement in neuronal function. In conclusion, this study demonstrates that SWE exhibits neuroprotective effects against acrylamide-induced damage by modulating neuroinflammation, synaptic function, and oxidative stress. These results support the potential of SWE as a treatment option for neurodegenerative illnesses linked to oxidative stress.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Swertiamarin Attenuates Acrylamide-Induced Neurotoxicity in Zebrafish: Imaging and Mechanistic Insights Via Nrf-2/HO-1 Signalling Pathway

  • 期刊论文

  • 发表日期：

    2025年12月3日

查看全文
  • Monita Wahengbam,
  • Siva Satya Sreedhar P,
  • C. Priya,
  • Sundhar Singh Pitta,
  • S. Navaneethan,
  • S. Nithyanandh,
  • S. Divyapriya

摘要

Acrylamide (ACR) has gained worldwide attention as a thermal process contaminant because of its neurotoxic actions and widespread presence. Prolonged exposure to ACR results in the degeneration of neuronal cells, loss of motor function, and potential impairment of antioxidant defence systems, especially during brain development. The widespread exposure and neurotoxic effects of acrylamide, there is an urgent need​ to identify natural compounds capable of mitigating its detrimental impact on the nervous system. Therefore, this study aimed to determine the neuroprotective effect of swertiamarin (SWE) on ACR-induced neurotoxicity in zebrafish larvae. Zebrafish larvae at 3 days post-fertilisation (dpf) were exposed to 0.75 mM ACR for 3 days to induce neurotoxicity and co-treated with SWE (100 µM) to evaluate its potential neuroprotective effects. All behavioural and biochemical assays, including locomotor activity, glutathione levels, antioxidant enzyme activity, and acetylcholinesterase function in the head region, were conducted at 6 days post-fertilization (dpf). ACR exposure disrupted glutathione redox balance in zebrafish larvae, and subsequent SWE treatment significantly restored this balance, which is essential for acrylamide detoxification and clearance. Furthermore, it reduced the expression of pro-inflammatory cytokines, including tnf-α, il-1β, and il-6, in the zebrafish larvae head, alleviated oxidative stress, and improved synaptic vesicle cycling. Motor responses were partially restored, suggesting an improvement in neuronal function. In conclusion, this study demonstrates that SWE exhibits neuroprotective effects against acrylamide-induced damage by modulating neuroinflammation, synaptic function, and oxidative stress. These results support the potential of SWE as a treatment option for neurodegenerative illnesses linked to oxidative stress.