Hydrogels and Hydrogel Nanocomposites: Enhancing Healthcare through Human and Environmental Treatment

Abstract

Humans are constantly exposed to exogenous chemicals throughout their life, which can lead to a multitude of negative health impacts. Advanced materials can play a key role in preventing or mitigating these impacts through a wide variety of applications. The tunable properties of hydrogels and hydrogel nanocomposites (e.g., swelling behavior, biocompatibility, stimuli responsiveness, functionality, etc.) have deemed them ideal platforms for removal of environmental contaminants, detoxification, and reduction of body burden from exogenous chemical exposures for prevention of disease initiation, and advanced treatment of chronic diseases, including cancer, diabetes, and cardiovascular disease. In this review, three main junctures where the use of hydrogel and hydrogel nanocomposite materials can intervene to positively impact human health are highlighted: 1) preventing exposures to environmental contaminants, 2) prophylactic treatments to prevent chronic disease initiation, and 3) treating chronic diseases after they have developed.

Keywords: chronic diseases; hydrogel nanocomposites; hydrogels; remediations; therapeutics.

Figure 1.

Hydrogels and hydrogel nanocomposites interventions to 1) prevent exposures to environmental contaminants, 2) prevent chronic disease initiation via prophylactic treatments, and 3) treat diseases after they have developed.

Figure 2.

A) Preparation of poly DMAPAA-Q hydrogel schematic. B) PFAS removal efficiencies for DMAPAA-Q hydrogels in varying pH solutions for GenX, ADONA, F-53B, PFBS, PFOS, PFBA, and PFOA at initial concentrations of 1000 ng L⁻¹ of each PFAS, an adsorbent dose of 70 mg L⁻¹, and contact time of 24 h with n = 3. Reproduced with permission.^[58] Copyright 2019, Elsevier.

Figure 3.

A) Redox-responsive behavior of carboxymethylcellulose hydrogels synthesized by Hou et al. i) reactant mixture, ii) formed hydrogel, iii) hydrogel after addition of 50 × 10⁻³ m DTT, and iv) regenerated gel after addition of 30% H₂O₂. B) Sol–gel transition schematic for redox-responsive hydrogel systems. C) Simultaneous increase in hydrogel redox potential (Eh) (solid lines) and reduction in concentration of Hg²⁺ (dashed lines). Agrochemical release (bars) of both GNA (red) and GBA (blue). Reproduced with permission.^[68] Copyright 2018, Royal Society of Chemistry.

Figure 4.

A) Schematic representation of binding studies conducted with PCB 126 in a 99:1 DI water:ethanol solvent. Room temperature adsorption isotherms for PCB 126 of the B) MNM systems and C) MP systems. PCB 126 initial concentrations from 0.003 to 0.1 ppm fitted using the Langmuir model. Reproduced with permission.^[71] Copyright 2020, Wiley.

Figure 5.

A) Experimental images and polymer-network schematics to show self-healing properties. B) Schematic to show the mechanism of light-assisted adsorption of copper ions (Cu²⁺) on the TiO₂ surface, and the image sequence of Cu²⁺ solution at different times of UV light exposure. C) Schematic to show the mechanism of light-assisted dye degradation, and the image sequence of the dye solution at different times of UV light exposure. Reproduced with permission.^[85] Copyright 2020, MDPI.

Figure 6.

Adsorption kinetics for A) TcdB and B) TcdA, showing remaining concentration over time for Enterosgel, charcodote, and positive control (no adsorbent) (mean ± sem). Equilibrium adsorption isotherm (Qe) of C) TcdB and D) TcdA against remaining concentration in solution (Ce) for Enterosgel and Charcodote. Reproduced with permission.^[93] Copyright 2019, Nature Publications.

Figure 7.

A) Scheme of the pH-controlled hydrogel loaded with erlotinib-encapsulated microspheres for peritumoral injection. B) In vivo degradation kinetics of scanned NIRF images of the control, Cy5.5, HP/HD/Cy5.5, HP9/HD/Cy5.5, and HP9/HD/ERTMS/Cy5.5 groups in mice from 0 to 672 h postperitumoral injection. Reproduced with permission.^[180] Copyright 2021, American Chemical Society.

Figure 8.

A) Schematic illustration of the formation of the biodegradable polymer-insulin complexes and mechanisms of glucose binding and insulin release. B) Representative IVIS images of diabetic mice treated with insulin and four different biodegradable polymer–insulin complexes from injection time (0 h) to 48 h post-treatment. Reproduced with permission. ^[212] Copyright 2021, American Chemical Society.

Figure 9.

A) Schematic showing the proposed mechanism of NO-RIG in inhibiting MI in mice. NO-RIG is composed of two biofuntional polymers: PArg-PEG-PArg, which generates NO by the activated macrophages in inflamed tissues, and PMNT-PEG-PMNT, which scavenges ROS to enhance NO activity. NO-RIG can sustainably control the NO delivery and redox equilibrium balance in the infarcted tissues. As the results, NO-RIG treatment significantly prevents the progression of MI and improve cardiac functions. SMC: smooth muscle cell; EC: endothelial cell. Reproduced with permission.^[244] Copyright 2018, Elsevier. B) Schematic representations of MMP-responsive hydrogel preparation and the process of drug release in the wound bed of MI model rats. (A) Preparation of GST-TIMP-bFGF via a recombinant protein expression method. (B) GSH was loaded into the hydrogel by a chemical crosslinking process to obtain Gel-GSH. C) GST-TIMP-bFGF was mixed with Gel-GSH, and the two components were linked with a bond between GST and GSH. D) Intramyocardial injection of the mixed hydrogel to the wound of a rat after MI. E) In the wound microenvironment, substrate peptides were degraded by MMP-2/9, and specific targeting peptides were released, achieving the dual functions of angiogenesis and MMP inhibition. Reproduced with permission.^[252] Copyright 2019, Wiley-VCH GmbH.

Figure 10.

Optimal range for delivery of siRNA using nanohydrogels. Reproduced with permission.^[168] Copyright 2021, Elsevier.