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Background <p>Neuroinflammation driven by TNF-α is increasingly recognized as a central mechanism in Parkinson’s disease (PD) progression. This study aimed to evaluate a polydopamine-coated zinc oxide (PDZ) nanocomposite for its TNF-α interaction potential and biosafety profile through integrated computational and experimental approaches. </p> Methods <p>The PDZ composite was synthesized via oxidative self-polymerization and characterized using UV-Vis, FTIR, XRD, TGA, and HR-TEM. Density Functional Theory (DFT) calculations examined electronic structure and surface reactivity, while molecular docking simulated binding interactions with TNF-α (PDB: 2AZ5). Hemocompatibility and cytotoxicity assays were performed, and ADMET properties were predicted using pkCSM. </p> Results <p>Spectroscopic and microscopic analyses confirmed successful polydopamine layer was formed on the surface of the zinc oxide nanocrystals with a thickness of ~ 14&#xa0;nm, but without compromising the crystalline structure of the ZnO core. The DFT results indicated that the surface of the PDZ was electronically adaptable (bandgap: 0.20&#xa0;eV) with abundant electron-rich oxygen sites available for hydrogen bonding. Docking results showed that PDZ had a significant binding affinity to TNF-α, Vina score: -10.0&#xa0;kcal/mol, at the C5 binding pocket of TNF-α, and that this binding affinity was mediated by multiple hydrogen bonds and hydrophobic interactions. PDZ demonstrated low hemolysis (1.13%, below the 2% safety limit) and high biocompatibility (&gt; 90% cell viability). ADMET predictions indicated that PDZ had good absorption, did not interact with CPY enzymes, and did not cause toxicity or mutagenesis. </p> Coclusion <p>PDZ demonstrates promising TNF-α interaction potential combined with excellent biosafety, supporting its further investigation as a neuroinflammation-targeting agent for Parkinson’s disease.</p>

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Hemocompatible ZnO-Polydopamine Nanocomposite (PDZ): Computational Insights into TNF-α Interaction Potential and Experimental Validation of Biosafety

  • 期刊论文

  • 发表日期：

    2026年6月17日

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  • Yasin Albarqouni,
  • Ghada Said I. Abdulwahed,
  • Roney Miah,
  • Amit Dubey,
  • Aisha Tufail,
  • Md Towhidul Islam Tarun,
  • Arman Bin Abdullah

摘要

Background

Neuroinflammation driven by TNF-α is increasingly recognized as a central mechanism in Parkinson’s disease (PD) progression. This study aimed to evaluate a polydopamine-coated zinc oxide (PDZ) nanocomposite for its TNF-α interaction potential and biosafety profile through integrated computational and experimental approaches.

Methods

The PDZ composite was synthesized via oxidative self-polymerization and characterized using UV-Vis, FTIR, XRD, TGA, and HR-TEM. Density Functional Theory (DFT) calculations examined electronic structure and surface reactivity, while molecular docking simulated binding interactions with TNF-α (PDB: 2AZ5). Hemocompatibility and cytotoxicity assays were performed, and ADMET properties were predicted using pkCSM.

Results

Spectroscopic and microscopic analyses confirmed successful polydopamine layer was formed on the surface of the zinc oxide nanocrystals with a thickness of ~ 14 nm, but without compromising the crystalline structure of the ZnO core. The DFT results indicated that the surface of the PDZ was electronically adaptable (bandgap: 0.20 eV) with abundant electron-rich oxygen sites available for hydrogen bonding. Docking results showed that PDZ had a significant binding affinity to TNF-α, Vina score: -10.0 kcal/mol, at the C5 binding pocket of TNF-α, and that this binding affinity was mediated by multiple hydrogen bonds and hydrophobic interactions. PDZ demonstrated low hemolysis (1.13%, below the 2% safety limit) and high biocompatibility (> 90% cell viability). ADMET predictions indicated that PDZ had good absorption, did not interact with CPY enzymes, and did not cause toxicity or mutagenesis.

Coclusion

PDZ demonstrates promising TNF-α interaction potential combined with excellent biosafety, supporting its further investigation as a neuroinflammation-targeting agent for Parkinson’s disease.