2. Academic Validation
  3. Multifaceted roles of a bioengineered nanoreactor in repressing radiation-induced lung injury

Multifaceted roles of a bioengineered nanoreactor in repressing radiation-induced lung injury

  • Biomaterials. 2021 Oct;277:121103. doi: 10.1016/j.biomaterials.2021.121103.
Tao Liu 1,  Qunfang Yang 1,  Haiping Zheng 2,  Honglin Jia 3,  Yufeng He 3,  Xuan Zhang 1,  Junfeng Zheng 1,  Yue Xi 1,  Haigang Zhang 1,  Renshan Sun 3,  Xiaohong Chen 4,  Wenjun Shan 5
Affiliations

Affiliations

  • 1 Department of Pharmacology, College of Pharmacy and Laboratory Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, PR China.
  • 2 School of Medicine, Xiamen University, Xiamen, 361102, PR China.
  • 3 Department of Dermatology, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, PR China.
  • 4 Department of Pharmacology, College of Pharmacy and Laboratory Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, PR China. Electronic address: [email protected].
  • 5 Department of Pharmacology, College of Pharmacy and Laboratory Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038, PR China. Electronic address: [email protected].
PMID: 34478930 DOI: 10.1016/j.biomaterials.2021.121103
Abstract

Radiation-induced lung injury (RILI) is a potentially fatal and dose-limiting complication of thoracic Cancer radiotherapy. However, effective therapeutic agents for this condition are limited. Here, we describe a novel strategy to exert additive effects of a non-erythropoietic EPO derivative (ARA290), along with a free radical scavenger, superoxide dismutase (SOD), using a bioengineered nanoreactor (SOD@ARA290-HBc). ARA290-chimeric nanoreactor makes SOD present in a confined reaction space by encapsulation into its interior to heighten stability against denaturing stimuli. In a RILI mouse model, intratracheal administration of SOD@ARA290-HBc was shown to significantly ameliorate acute radiation pneumonitis and pulmonary fibrosis. Our investigations revealed that SOD@ARA290-HBc performs its radioprotective effects by protecting against radiation induced alveolar epithelial cell Apoptosis and Ferroptosis, suppressing oxidative stress, inhibiting inflammation and by modulating the infiltrated macrophage phenotype, or through a combination of these mechanisms. In conclusion, SOD@ARA29-HBc is a potential therapeutic agent for RILI, and given its multifaceted roles, it may be further developed as a translational nanomedicine for other related disorders.

Keywords

Alveolar epithelial cell; Cytoprotection; Nanoreactor; Non-erythropoietic EPO derivative; Radiation-induced lung injury.

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