Messenger Nanozyme for Reprogramming the Microenvironment of Rheumatoid Arthritis,ACS Applied Materials & Interfaces

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Messenger Nanozyme for Reprogramming the Microenvironment of Rheumatoid Arthritis
ACS Applied Materials & Interfaces ( IF 8.3 ) Pub Date : 2022-12-29 , DOI: 10.1021/acsami.2c16458
Ming Jia ₁ , Wei Ren _{2,

3} , Yan Liu ₁ , Chenglong Wang ₁ , Xiu Zheng ₁ , Dan Zhang ₄ , Xiaoqiu Tan _{5,

6} , Chunhong Li _{1,

7}

Affiliation

Dysregulation of superoxide anion (O₂^–) and hydrogen peroxide (H₂O₂) metabolism in the microenvironment of rheumatoid arthritis (RA) drives the feedback loops of TNF-α and IL-1β thereby inducing an inflammatory storm between immune cells and joint tissue cells. Here, we combine nanoscale manganese dioxide (MnO₂) with microvesicles derived from macrophage (MMV). The former possesses superoxide dismutase (SOD) and catalase (CAT)-like activities that can modulate this imbalance, and we amplify the enzyme-like activities by using the amorphous hollow mesoporous structure and surface modification. The latter is a natural endogenous component with the parent cell-like inflammatory homing ability and a unique function of transmitting information to surrounding and distant cells (″messenger function″), which helps amorphous hollow MnO₂ (H–MnO₂) nanozymes to cloak in the blood and reach the site of inflammation, where they can not only accumulate in activated macrophages but also pretend to be ″messengers″ that are utilized by fibroblast-like synoviocytes (FLS) and chondrocytes. In addition, we also load dexamethasone sodium phosphate (DSP) for helping the nanozymes work. Messenger nanozyme (MMV-MnO₂@DSP) inherits the natural properties of MMV and mimics the enzymatic activity of SOD and CAT. It accumulates in activated macrophages to restore the metabolism of O₂^– and H₂O₂ while promoting repolarization and inhibits the feedback loops of TNF-α and IL-1β among macrophages, fibroblast-like synoviocytes, and chondrocytes, leading to anti-rheumatoid arthritis effects in vitro and in vivo.

中文翻译：

用于重编程类风湿性关节炎微环境的信使纳米酶

类风湿关节炎 (RA) 微环境中超氧阴离子 (O ₂^– ) 和过氧化氢 (H ₂ O ₂ ) 代谢失调驱动 TNF-α 和 IL-1β 的反馈回路，从而在免疫细胞和关节之间引发炎症风暴组织细胞。在这里，我们将纳米级二氧化锰 (MnO ₂) 与来自巨噬细胞 (MMV) 的微泡。前者具有超氧化物歧化酶 (SOD) 和过氧化氢酶 (CAT) 样活性，可以调节这种不平衡，我们通过使用无定形中空介孔结构和表面修饰来放大类酶活性。后者是一种天然的内源性成分，具有亲本细胞样炎症归巢能力和独特的向周围和远处细胞传递信息的功能（“信使功能”），有助于非晶空心MnO ₂ (H-MnO ₂) 纳米酶隐藏在血液中并到达炎症部位，在那里它们不仅可以在活化的巨噬细胞中积聚，还可以伪装成成纤维细胞样滑膜细胞 (FLS) 和软骨细胞利用的“信使”。此外，我们还加载了地塞米松磷酸钠（DSP）以帮助纳米酶发挥作用。信使纳米酶 (MMV-MnO ₂ @DSP) 继承了 MMV 的天然特性并模拟了 SOD 和 CAT 的酶活性。它在活化的巨噬细胞中积累以恢复 O ₂^–和 H ₂ O _2的代谢同时促进复极化并抑制 TNF-α 和 IL-1β 在巨噬细胞、成纤维细胞样滑膜细胞和软骨细胞之间的反馈回路，从而在体外和体内产生抗类风湿性关节炎作用。

更新日期：2022-12-29

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