Here, an integrated cascade nanozyme with a formulation of Pt@PCN222-Mn is developed to eliminate excessive reactive oxygen species (ROS). This nanozyme mimics superoxide dismutase by incorporation of a Mn–[5,10,15,20-tetrakis(4-carboxyphenyl)porphyrinato]–based metal-organic framework compound capable of transforming oxygen radicals to hydrogen peroxide. The second mimicked functionality is that of catalase by incorporation of Pt nanoparticles, which catalyze hydrogen peroxide disproportionation to water and oxygen. Both in vitro and in vivo experimental measurements reveal the synergistic ROS-scavenging capacity of such an integrated cascade nanozyme. Two forms of inflammatory bowel disease (IBD; i.e., ulcerative colitis and Crohn’s disease) can be effectively relieved by treatment with the cascade nanozyme. This study not only provides a new method for constructing enzyme-like cascade systems but also illustrates their efficient therapeutic promise in the treatment of in vivo IBDs.
Zhongyin Zhang,Lichan Yuan,Yufeng Liu,Ruobing Wang,Yihong Zhang,Yan Yang,Hui Wei,Junqing Ma
Temporomandibular joint osteoarthritis (TMJ OA) is a degenerative joint disease with no complete cure at present. Notably, the inflammatory microenvironment in TMJ OA is modulated by oxidative stress, which impacts cartilage metabolism, chondrocyte apoptosis, inflammatory cytokine release, and extracellular matrix (ECM) synthesis. Thus, it is reasoned that reducing excess reactive oxygen species (ROS) in the chondrocyte microenvironment may be an effective therapeutic strategy for TMJ OA. Recently, cascade nanozymes, including Pt@PCN222-Mn, have been exploited to treat ROS-associated diseases. Nevertheless, cascade nanozymes are not employed for TMJ OA therapy. To fill this gap, it is explored whether the Pt@PCN222-Mn cascade nanozyme could be applied to the treatment of TMJ OA. The in vitro results demonstrate that the Pt@PCN222-Mn nanozyme can inhibit the production of inflammatory factors, the degradation of ECM, and the apoptosis of chondrocytes by inhibiting the ROS-nuclear factor kappa-B (NF- κ B_ and mitogen-activated protein kinase signaling pathways. The in vivo results further demonstrate that the Pt@PCN222-Mn nanozyme can delay the progression of TMJ OA in the rat unilateral anterior crossbite model. It is believed that insightful perspectives on the application of nanozymes in TMJ OA will be provided here.
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