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<p>Chronic wound healing is associated with prolonged elevated inflammation and high levels of oxidative stress leading to cell death. The majority of wounds are colonized with antibiotic-resistant bacterial biofilms such as <i>Pseudomonas aeruginosa</i> and <i>Staphylococcus aureus</i>. An ideal wound treatment should include agents with antioxidant, anti-inflammatory, and antibiofilm behavior. Therefore, in this study, a combination of curcumin nanoparticle (Cur-NP) and silver nanoparticle (AgNP) (Cur-NP/AgNP) loaded PVA hydrogel was used to inhibit the bacterial attachment and subsequent biofilm formation of <i>P. aeruginosa</i> and <i>S. aureus</i>. Cur was known for its antioxidant and anti-inflammatory effect while being non-toxic to cells. Meanwhile, AgNP demonstrated superior anti-bacterial and antibiofilm activities against both <i>P. aeruginosa</i> and <i>S. aureus</i>. Cur-NP/AgNP loaded PVA hydrogels completely inhibited the bacterial attachment and biofilm formation, possibly due to synergistic effect of Cur-NPs and AgNPs in killing the bacterial cells. It should be highlighted that no surviving bacterial cells were noted for Cur-NP/AgNP loaded hydrogels. On the other hand, AgNPs or Cur-NPs alone loaded hydrogels were unable to achieve complete inhibition of biofilm formation, even though significant reduction in the biofilm mass was noted compared with control samples. Cur-NP and AgNP exerted oxidative-stress induced cell death in HaCaT cells via mitochondrial dysfunction, mitochondrial membrane potential (MMP) reduction, adenosine triphosphate inhibition, and increased cytochrome C release. The toxicity of formulation followed the decreasing trend: Cur-NP/AgNP &lt; AgNPs alone &lt; Cur-NPs alone. Taken together, the combination of Cur-NP/AgNP completely inhibited bacterial biofilm formation through bactericidal effect on the planktonic cells while exerted the least toxic effects towards skin cells.</p>

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Evaluation of hydrogel loading with curcumin and silver nanoparticles: biocompatibilities and anti-biofilm activities

  • 期刊论文

  • 发表日期：

    2025年2月20日

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  • Wei Qing Hong,
  • Wing-Hin Lee,
  • Siti Hajar Musa,
  • Nur Azzalia Kamaruzaman,
  • Ching-Yee Loo

摘要

Chronic wound healing is associated with prolonged elevated inflammation and high levels of oxidative stress leading to cell death. The majority of wounds are colonized with antibiotic-resistant bacterial biofilms such as Pseudomonas aeruginosa and Staphylococcus aureus. An ideal wound treatment should include agents with antioxidant, anti-inflammatory, and antibiofilm behavior. Therefore, in this study, a combination of curcumin nanoparticle (Cur-NP) and silver nanoparticle (AgNP) (Cur-NP/AgNP) loaded PVA hydrogel was used to inhibit the bacterial attachment and subsequent biofilm formation of P. aeruginosa and S. aureus. Cur was known for its antioxidant and anti-inflammatory effect while being non-toxic to cells. Meanwhile, AgNP demonstrated superior anti-bacterial and antibiofilm activities against both P. aeruginosa and S. aureus. Cur-NP/AgNP loaded PVA hydrogels completely inhibited the bacterial attachment and biofilm formation, possibly due to synergistic effect of Cur-NPs and AgNPs in killing the bacterial cells. It should be highlighted that no surviving bacterial cells were noted for Cur-NP/AgNP loaded hydrogels. On the other hand, AgNPs or Cur-NPs alone loaded hydrogels were unable to achieve complete inhibition of biofilm formation, even though significant reduction in the biofilm mass was noted compared with control samples. Cur-NP and AgNP exerted oxidative-stress induced cell death in HaCaT cells via mitochondrial dysfunction, mitochondrial membrane potential (MMP) reduction, adenosine triphosphate inhibition, and increased cytochrome C release. The toxicity of formulation followed the decreasing trend: Cur-NP/AgNP < AgNPs alone < Cur-NPs alone. Taken together, the combination of Cur-NP/AgNP completely inhibited bacterial biofilm formation through bactericidal effect on the planktonic cells while exerted the least toxic effects towards skin cells.