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. 2018 Feb 16;9(11):2927-2933.
doi: 10.1039/c7sc05476a. eCollection 2018 Mar 21.

ROS scavenging Mn3O4 nanozymes for in vivo anti-inflammation

Jia Yao  1 , Yuan Cheng  1 , Min Zhou  1 , Sheng Zhao  1 , Shichao Lin  1 , Xiaoyu Wang  1 , Jiangjiexing Wu  1 , Sirong Li  1 , Hui Wei  1   2
Affiliations

ROS scavenging Mn3O4 nanozymes for in vivo anti-inflammation

Jia Yao et al. Chem Sci. .

Abstract

Reactive oxygen species (ROS)-induced oxidative stress is linked to various diseases, including cardiovascular disease and cancer. Though highly efficient natural ROS scavenging enzymes have been evolved, they are sensitive to environmental conditions and hard to mass-produce. Therefore, enormous efforts have been devoted to developing artificial enzymes with ROS scavenging activities. Among them, ROS scavenging nanozymes have recently attracted great interest owing to their enhanced stability, multi-functionality, and tunable activity. It has been implicated that Mn-contained nanozymes would possess efficient ROS scavenging activities, however only a few such nanozymes have been reported. To fill this gap, herein we demonstrated that Mn3O4 nanoparticles (NPs) possessed multiple enzyme mimicking activities (i.e., superoxide dismutase and catalase mimicking activities as well as hydroxyl radical scavenging activity). The Mn3O4 nanozymes therefore significantly scavenged superoxide radical as well as hydrogen peroxide and hydroxyl radical. Moreover, they were not only more stable than the corresponding natural enzymes but also superior to CeO2 nanozymes in terms of ROS elimination. We showed that the Mn3O4 NPs not only exhibited excellent ROS removal efficacy in vitro but also effectively protected live mice from ROS-induced ear-inflammation in vivo. These results indicated that Mn3O4 nanozymes are promising therapeutic nanomedicine for treating ROS-related diseases.

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Figures

Fig. 1
Fig. 1. (A) TEM image of Mn3O4 NPs. (B) Powder X-ray diffraction pattern of Mn3O4 NPs (the red lines at the bottom mark the reference pattern of hausmannite Mn3O4 from the JCPDS database, card no. 24-0734).
Fig. 2
Fig. 2. (A) Fluorescent spectra of HE after reaction with X and XO, in the absence and presence of Mn3O4 NPs. X for xanthine and XO for xanthine oxidase, respectively. (B) Dependence between the elimination of ˙O2– and concentrations of Mn3O4 NPs, CeO2 NPs, and natural SOD.
Fig. 3
Fig. 3. (A) Fluorescent spectra of TA after reaction with H2O2, in the absence and presence of Mn3O4 NPs. (B) Dependence between the elimination of H2O2 and concentrations of Mn3O4 NPs, CeO2 NPs, and natural catalase.
Fig. 4
Fig. 4. (A) Absorption spectra of SA after reaction with Fe2+/H2O2, in the absence and presence of Mn3O4 NPs. SA alone, and SA reacted with Fe2+ or H2O2 were used as control. (B) Dependence between the elimination of ˙OH and concentration of Mn3O4 NPs and CeO2 NPs (mean ±S.D., **p < 0.05; n.s., not significant).
Fig. 5
Fig. 5. (A) Hela cell viability under different concentrations of Mn3O4 NPs. (B) Laser confocal fluorescence images of Hela cells with different treatments: (a–d) 0.01 mM DCFH-DA, (e–h) Rosup and DCFH-DA, (i–l) Rosup and DCFH-DA with 5 μg mL–1 Mn3O4 NPs, (m–p) Rosup and DCFH-DA with 10 μg mL–1 Mn3O4 NPs. (C) Corresponding fluorescent intensity of DCFH-DA in panel (B).
Fig. 6
Fig. 6. In vivo fluorescence imaging of mice with PMA-induced ear inflammation after treatment with (A) PMA, (B) DCFH-DA, (C) PMA and DCFH-DA, (D) PMA and DCFH-DA with 0.5 μg kg–1 Mn3O4 NPs, and (E) PMA and DCFH-DA with 1.25 μg kg–1 Mn3O4 NPs.
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