|
| Number | Author | Nature of study | Mechanism of antibacterial action |
|
| [54] | Kon and Rai, 2013 | Review | Increases the surface area contacting the wound surface |
| [55] | Morones et al., 2005 | In vitro | Have a direct interaction on the cell surface and within the bacteria with a diameter of around 1–10 nm |
| [56] | Pal et al., 2007 | In vitro | The bactericidal action of nAg with a truncated triangular shape exceeds that of nAg with a spherical or rod shape |
| [57] | Matsumura et al., 2003 | In vitro | Interacts with the thiol group of respiratory enzymes |
| [58] | Gordon et al., 2010 | Animal study | Inactivates the key enzyme by blinding the thiol group, forming free radicals, and subsequently damaging DNA |
| [59] | Pandian et al., 2010 | In vitro | Interacts with and condenses phosphorus-containing DNA and cytoplasm (apoptosis) and inhibits cell replication |
| [60] | Dibrov et al., 2002 | In vitro | Binds to the modified phospholipid bilayer and induces a massive leakage of protons |
| [61] | Sondi and Salopek-Sondi, 2004 | In vitro | Attaches the negatively charged cell membrane by forming “pits,” making the membrane porous and resulting in leakage of intracellular content |
| [62] | Kim et al., 2007 | In vitro | Bacteria release cellular content after the permeability of the cell membrane increases, leading to cell death |
| [63] | Mirzajani et al., 2011 | In vitro | Destroyed the bonds of glycan strands composed of N-acetylglucosamine and N-acetylmuramic acid in the cell membrane of Gram +ve bacteria and causing “pits” to form |
| [64] | McQuillan et al., 2012 | In vitro | Interacts with the outer and inner membrane of Gram −ve bacteria, and then membrane dissolves; Ag+ releases into the cell and affects a transcriptional response |
| [65] | Mijakovic et al., 2006 | In vitro | Phosphorylation of the protein substrate in bacteria can influence bacterial sign transduction and cell cycle progression |
| [66] | Shrivastava et al., 2007 |
|
| Number | Author | Nature of study | Mechanism of anti-inflammatory action |
|
| [67] | Wright et al., 2002 | Animal study | Reduces the activity of MMPs and stimulates the apoptosis of PMNs, leading to a decrease in the release of cytotoxic compounds such as proteases and oxygen radicals |
| [68] | Bhol et al., 2004 | Animal study | Effectively decreases allergic contact dermatitis on a guinea pig model, similar to topical steroids |
| [69] | Bhol and Schechter, 2005 | Animal study | Suppresses the activities of TNF-α and IL-12 and induces the apoptosis of inflammatory cells |
| [70] | Wong et al., 2009 | Animal study | Downregulates the production of TNF-α without having a significant toxic effect on a peritoneal adhesion model |
| [71] | Nadworny et al., 2010 | Animal study | Decreases TNF-α and IL-8 and increases IL-4, EGF, KGF, and KGF-2 |
| [72] | Nadworny et al., 2010 | Animal study | Downregulates TNF-α and IL-8 and upregulates IL-4, IL-10, EGF, KGF, and KGF-2 |
| [73] | Bisson et al., 2013 | Animal study | Demonstrates a significant inflammatory effect, equivalent to that which results from using topical steroid cream |
| [74] | Shin et al., 2007 | In vivo | TNF-α and interferon-γ are significantly inhibited at low concentrations of nAg |
| [75] | Mani et al., 2015 | In vivo | TNF-α, IL-1β, and IL-6 are inhibited at concentrations ranging from 10 to 20 μg/mL |
|
