Drug-free contact lens based on quaternized chitosan and tannic acid for bacterial keratitis therapy and corneal repair

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Abstract

Bacterial keratitis (BK) and related inflammatory diseases causes irreversible damage to the corneal tissue. In this study, a novel polyacrylamide semi-interpenetrating network hydrogel including quaternized chitosan and tannic acid (PAM-QCS-TA) were used to construct a novel antibacterial and antioxidant contact lens. The obtained hydrogels showed high water content (>85%), swelling resistance, light transmittance (>90%) and adjustable mechanical property. Both quantitative and qualitative antibacterial experiments against Staphylococcus aureus and Escherichia coli (E. coli) indicated excellent sterilization function especially against E. coli (almost 100%). Due to the presence of tannin acid, it showed obvious antioxidant properties, which relieved oxidative stress and protect cells from reactive oxygen species-induced cytotoxicity. Animal experiments also indicated the shortened treatment time of BK (only 3 days) as well as the protection of eye tissue structure. Therefore, such drug-free antibacterial and antioxidant contact lens avoiding the development of drug resistance is a potential candidate in ocular infectious and inflammatory diseases treatment.

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Magdalena L. Circu, Tak Aw (2010)

Reactive oxygen species (ROS) are products of normal metabolism and xenobiotic exposure, and depending on their concentration, ROS can be beneficial or harmful to cells and tissues. At physiological low levels, ROS function as "redox messengers" in intracellular signaling and regulation, whereas excess ROS induce oxidative modification of cellular macromolecules, inhibit protein function, and promote cell death. Additionally, various redox systems, such as the glutathione, thioredoxin, and pyridine nucleotide redox couples, participate in cell signaling and modulation of cell function, including apoptotic cell death. Cell apoptosis is initiated by extracellular and intracellular signals via two main pathways, the death receptor- and the mitochondria-mediated pathways. Various pathologies can result from oxidative stress-induced apoptotic signaling that is consequent to ROS increases and/or antioxidant decreases, disruption of intracellular redox homeostasis, and irreversible oxidative modifications of lipid, protein, or DNA. In this review, we focus on several key aspects of ROS and redox mechanisms in apoptotic signaling and highlight the gaps in knowledge and potential avenues for further investigation. A full understanding of the redox control of apoptotic initiation and execution could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders. Copyright 2010 Elsevier Inc. All rights reserved.

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Antibacterial and Anti-Inflammatory pH-Responsive Tannic Acid-Carboxylated Agarose Composite Hydrogels for Wound Healing

Neethu Ninan, Anton Blencowe, Aurélien Forget … (2016)

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Role of the Toll Like Receptor (TLR) Radical Cycle in Chronic Inflammation: Possible Treatments Targeting the TLR4 Pathway

Kurt Lucas, Michael Maes (2013)

Activation of the Toll-like receptor 4 (TLR4) complex, a receptor of the innate immune system, may underpin the pathophysiology of many human diseases, including asthma, cardiovascular disorder, diabetes, obesity, metabolic syndrome, autoimmune disorders, neuroinflammatory disorders, schizophrenia, bipolar disorder, autism, clinical depression, chronic fatigue syndrome, alcohol abuse, and toluene inhalation. TLRs are pattern recognition receptors that recognize damage-associated molecular patterns and pathogen-associated molecular patterns, including lipopolysaccharide (LPS) from gram-negative bacteria. Here we focus on the environmental factors, which are known to trigger TLR4, e.g., ozone, atmosphere particulate matter, long-lived reactive oxygen intermediate, pentachlorophenol, ionizing radiation, and toluene. Activation of the TLR4 pathways may cause chronic inflammation and increased production of reactive oxygen and nitrogen species (ROS/RNS) and oxidative and nitrosative stress and therefore TLR-related diseases. This implies that drugs or substances that modify these pathways may prevent or improve the abovementioned diseases. Here we review some of the most promising drugs and agents that have the potential to attenuate TLR-mediated inflammation, e.g., anti-LPS strategies that aim to neutralize LPS (synthetic anti-LPS peptides and recombinant factor C) and TLR4/MyD88 antagonists, including eritoran, CyP, EM-163, epigallocatechin-3-gallate, 6-shogaol, cinnamon extract, N-acetylcysteine, melatonin, and molecular hydrogen. The authors posit that activation of the TLR radical (ROS/RNS) cycle is a common pathway underpinning many “civilization” disorders and that targeting the TLR radical cycle may be an effective method to treat many inflammatory disorders.