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<p>Oxidative stress is known to be associated with epilepsy, and antiseizure medication treatment, albeit with limited consensus on the specific oxidative stress pathways/proteins involved. Identifying these can reveal novel therapeutic targets for epilepsy management. This study utilized network pharmacology to identify potential protein targets of carbamazepine and valproic-acid that are implicated in oxidative stress and epilepsy, thereby highlighting their therapeutic potential. Drug targets for carbamazepine and valproic-acid were predicted using SuperPred/SwissTargetPrediction, while genes associated with epilepsy and oxidative stress were obtained from DisGeNET and GeneCards. Common proteins were identified, and a protein–protein interaction network was constructed using STRING, followed by analysis via Cytoscape. Hub proteins identified were EGFR, GSK3B, and STAT3 for carbamazepine, and PTGS2, mTOR, and TLR4 for valproic-acid. Molecular docking revealed a strong binding affinity of carbamazepine to its targets (ΔG<sub>bind</sub> &gt; − 5&#xa0;kcal/mol) and binding of valproic-acid to its targets (ΔG<sub>bind</sub> &gt; − 3&#xa0;kcal/mol), with PTGS2 showing the strongest interaction with valproic-acid (− 5.06&#xa0;kcal/mol). These findings underscore EGFR, GSK3B, and STAT3, for carbamazepine and PTGS2, mTOR, and TLR4 for valproic-acid as pivotal therapeutic targets in oxidative stress-associated epilepsy. These identified proteins can be targeted by add on antioxidants to alleviate oxidative stress generated by chronic antiseizure medication.</p>

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Decoding the relationship between oxidative stress and antiseizure medications using network pharmacology and molecular docking

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月26日

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  • Malhar Desai,
  • Sarangthem Dinamani Singh,
  • Selvaraman Nagamani,
  • Sunik Malik,
  • Anju Singh,
  • Ritushree Kukreti,
  • Shrikant Kukreti,
  • Gurpreet K. Grewal

摘要

Oxidative stress is known to be associated with epilepsy, and antiseizure medication treatment, albeit with limited consensus on the specific oxidative stress pathways/proteins involved. Identifying these can reveal novel therapeutic targets for epilepsy management. This study utilized network pharmacology to identify potential protein targets of carbamazepine and valproic-acid that are implicated in oxidative stress and epilepsy, thereby highlighting their therapeutic potential. Drug targets for carbamazepine and valproic-acid were predicted using SuperPred/SwissTargetPrediction, while genes associated with epilepsy and oxidative stress were obtained from DisGeNET and GeneCards. Common proteins were identified, and a protein–protein interaction network was constructed using STRING, followed by analysis via Cytoscape. Hub proteins identified were EGFR, GSK3B, and STAT3 for carbamazepine, and PTGS2, mTOR, and TLR4 for valproic-acid. Molecular docking revealed a strong binding affinity of carbamazepine to its targets (ΔGbind > − 5 kcal/mol) and binding of valproic-acid to its targets (ΔGbind > − 3 kcal/mol), with PTGS2 showing the strongest interaction with valproic-acid (− 5.06 kcal/mol). These findings underscore EGFR, GSK3B, and STAT3, for carbamazepine and PTGS2, mTOR, and TLR4 for valproic-acid as pivotal therapeutic targets in oxidative stress-associated epilepsy. These identified proteins can be targeted by add on antioxidants to alleviate oxidative stress generated by chronic antiseizure medication.