Reactive oxygen species (ROS)-responsive biomaterials mediate tissue microenvironments and tissue regeneration

Yao, Yingming; Zhang, Haolan; Wang, Zhaoyi; Ding, Jie; Wang, Shuqin; Huang, Baiqiang; Ke, Shifeng; Gao, Changyou

doi:10.1039/c9tb00847k

Cited by 215 publications

(140 citation statements)

References 155 publications

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“…Among them, DNA damage is the most common type, mainly including purine and pyrimidine bases, changes in DNA protein cross-linking, and breakage of oligonucleotide chains and base sites. Protein damage is the cleavage of peptide chains induced by ROS, which leads to direct oxidative modification of amino acid side chains [ 26 ]. Lipid peroxidation reduces the fluidity of biofilm and increases the permeability of the cell membrane, which led to apoptosis [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

PPARγ Attenuates Interleukin‐1β‐Induced Cell Apoptosis by Inhibiting NOX2/ROS/p38MAPK Activation in Osteoarthritis Chondrocytes

Liu

Wei

et al. 2021

Oxidative Medicine and Cellular Longevity

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Introduction. Reactive oxygen species (ROS) induced by extracellular cytokines trigger the expression of inflammatory mediators in osteoarthritis (OA) chondrocyte. Peroxisome proliferator-activated receptor gamma (PPARγ) exerts an anti-inflammatory effect. The aim of this study was to elucidate the role of PPARγ in interleukin-1β- (IL-1β-) induced cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) expression through ROS generation in OA chondrocytes. Methods. IL-1β-induced ROS generation and chondrocyte apoptosis were determined by flow cytometry. Contents of NADPH oxidase (NOX), caspase-3, and caspase-9 were evaluated by biochemical detection. The involvement of NOX2 and mitogen-activated protein kinases (MAPKs) in IL-1β-induced COX-2 and PGE2 expression was investigated using pharmacologic inhibitors and further analyzed by western blotting. Activation of PPARγ was performed by using a pharmacologic agonist and was analyzed by western blotting. Results. IL-1β-induced COX-2 and PGE2 expression was mediated through NOX2 activation/ROS production, which could be attenuated by N-acetylcysteine (NAC; a scavenger of ROS), GW1929 (PPARγ agonist), DPI (diphenyleneiodonium chloride, NOX2 inhibitor), SB203580 (p38MAPK inhibitor), PD98059 (extracellular signal-regulated kinase, ERK inhibitor), and SP600125 (c-Jun N-terminal kinase, JNK inhibitor). ROS activated p38MAPK to enter the nucleus, which was attenuated by PPARγ. Conclusion. In OA chondrocytes, IL-1β induced COX-2 and PGE2 expression via activation of NOX2, which led to ROS production and MAPK activation. The activation of PPARγ exerted protective roles in the pathogenesis of OA.

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Section: Discussionmentioning

confidence: 99%

PPARγ Attenuates Interleukin‐1β‐Induced Cell Apoptosis by Inhibiting NOX2/ROS/p38MAPK Activation in Osteoarthritis Chondrocytes

Liu

Wei

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…[ 7 ] In addition, under laser irradiation, photosensitizers can generate ROS and effectively decompose ROS‐responsive covalent bonds, such as thioketal, arylboron ester, thioether, diselenide ether, and peroxyacetate. [ 8 ] We achieved this by introducing an ROS‐responsive prodrug (CPT‐TK‐2‐(1‐hexyloxyethyl)‐2‐devinyl pyropheophorbide‐a (HPPH)) that consisted of thioketal bond linked CPT and photosensitizer HPPH. The HPPH was a potential photosensitizer with good photodynamic activity, a high penetration rate for tumor tissue, and low phototoxicity.…”

Section: Introductionmentioning

confidence: 99%

Polymeric Nanoparticles with ROS‐Responsive Prodrug and Platinum Nanozyme for Enhanced Chemophotodynamic Therapy of Colon Cancer

et al. 2020

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The combination of chemotherapy and photodynamic therapy (PDT) has promising potential in the synergistic treatment of cancer. However, chemotherapy and photodynamic synergistic therapy are impeded by uncontrolled chemotherapeutics release behavior, targeting deficiencies, and hypoxia-associated poor PDT efficacy in solid tumors. Here, a platinum nanozyme (PtNP) loaded reactive oxygen species (ROS)-responsive prodrug nanoparticle (CPT-TK-HPPH/Pt NP) is created to overcome these limitations. The ROS-responsive prodrug consists of a thioketal bond linked with camptothecin (CPT) and photosensitizer-2-(1-hexyloxyethyl)-2-devinyl pyropheophorbide-a (HPPH). The PtNP in CPT-TK-HPPH/Pt NP can efficiently catalyze the decomposition of hydrogen peroxide (H 2 O 2) into oxygen to relieve hypoxia. The production of oxygen can satisfy the consumption of HPPH under 660 nm laser irradiation to attain the on-demand release of CPT and ensure enhanced photodynamic therapy. As a tumor diagnosis agent, the results of photoacoustic imaging and fluorescence imaging for CPT-TK-HPPH/Pt NP exhibit desirable long circulation and enhanced in vivo targeting. CPT-TK-HPPH/Pt NPs effectively inhibit tumor proliferation and growth in vitro and in vivo. CPT-TK-HPPH/Pt NP, with its excellent ROS-responsive drug release behavior and enhanced PDT efficiency can serve as a new cancer theranostic agent, and will further promote the research of chemophotodynamic synergistic cancer therapy.

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“…Indeed, sensing before being responsive is a need during relevant increase in oxidative stress. Such a kind of activation is ideal for clinical application of antioxidant biomaterials [ 72 ]. With the goal of reducing oxidative stress, new biomaterials can be exploitable in order to control the release of redox sensitive molecules, that is, disulphide containing biomaterials [ 73 ].…”

Section: New Opportunities For Natural Antioxidant Combination Witmentioning

confidence: 99%

Repositioning Natural Antioxidants for Therapeutic Applications in Tissue Engineering

Marrazzo

O’Leary

2020

Bioengineering

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Although a large panel of natural antioxidants demonstrate a protective effect in preventing cellular oxidative stress, their low bioavailability limits therapeutic activity at the targeted injury site. The importance to deliver drug or cells into oxidative microenvironments can be realized with the development of biocompatible redox-modulating materials. The incorporation of antioxidant compounds within implanted biomaterials should be able to retain the antioxidant activity, while also allowing graft survival and tissue recovery. This review summarizes the recent literature reporting the combined role of natural antioxidants with biomaterials. Our review highlights how such functionalization is a promising strategy in tissue engineering to improve the engraftment and promote tissue healing or regeneration.

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Reactive oxygen species (ROS)-responsive biomaterials mediate tissue microenvironments and tissue regeneration

Abstract: ROS-responsive biomaterials alleviate the oxidative stress in tissue microenvironments, promoting tissue regeneration and disease therapy.

Cited by 215 publications

References 155 publications

PPARγ Attenuates Interleukin‐1β‐Induced Cell Apoptosis by Inhibiting NOX2/ROS/p38MAPK Activation in Osteoarthritis Chondrocytes

PPARγ Attenuates Interleukin‐1β‐Induced Cell Apoptosis by Inhibiting NOX2/ROS/p38MAPK Activation in Osteoarthritis Chondrocytes

Polymeric Nanoparticles with ROS‐Responsive Prodrug and Platinum Nanozyme for Enhanced Chemophotodynamic Therapy of Colon Cancer

Repositioning Natural Antioxidants for Therapeutic Applications in Tissue Engineering

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