时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
LR-IL-22 preserves Lgr5⁺ intestinal stem cells and promotes barrier restoration, whereas LR-IFN-β preserves intestinal stem cells and barrier integrity and suppresses local inflammation120,121 (Figure 4D).Translational Constraints and Clinical EvaluationDose-Limiting Organs and Fractionated IrradiationThe intended clinical use should identify the dose-limiting organ, a clinically meaningful toxicity endpoint, and the tumor-control objective.
方法
EVs and cell-membrane-coated carriers provide additional delivery platforms,9 with sources including mesenchymal stem cells, adipose-derived cells, and microorganisms.10,11 Evidence from shielding materials or topical wound care should not be treated as evidence of systemic normal-tissue protection during cancer radiotherapy.Existing reviews provide complementary perspectives.；Extracellular vesicles should be described by measured size and biological identity rather than a universal exosome size cutoff.；Functional outcomes, acute symptoms, and late injury should be measured alongside dosimetry.Scavengers intended to prevent initial radiation damage must reach the relevant tissue during irradiation, whereas post-exposure mitigators target evolving inflammatory and regenerative processes.
核心结论
This preserves mitochondrial function and suppresses NF-κB signaling, thereby restoring intestinal epithelial tight junctions and reprogramming the immune microenvironment.74 Collectively, catalytic nanozymes extend radioprotection beyond passive ROS scavenging by coupling enzyme-mimetic catalysis with regulation of mitochondrial quality control, cell-death pathways, and tissue-specific repair (Table 1).；Physical enhancement also depends on beam energy, material concentration, intracellular distribution, and demonstrated tumor uptake.；SGs scavenge IR-induced ROS, restore CAT, SOD, and GPx activity, suppress MPO and pro-inflammatory cytokines, and recover ZO-1, occludin, and E-cadherin expression, thereby reinforcing intestinal redox homeostasis and barrier integrity.116Collectively, microbe-derived nanomaterials and micro/nano hybrid systems differ from conventional inorganic nanozymes by coupling intrinsic redox buffering with microbiota-, immune-, and barrier-regulatory functions (Figure 4A).
局限
However, radiation can also injure adjacent normal tissues, largely through the accumulation of unrepaired or misrepaired DNA damage, with DSBs representing a major determinant of irreversible cellular injury.1 Although cells possess robust DNA repair machinery, DSBs are among the most lethal forms of genomic damage.；NHEJ directly ligates broken DNA ends without requiring a homologous template and operates throughout the cell cycle, with predominant activity in G1; however, end processing can introduce small insertions or deletions.33 By contrast, HR uses the sister chromatid as a repair template, is therefore largely restricted to S and G2 phases, and depends on BRCA1, BRCA2, and RAD51 to support high-fidelity repair.
对本项目的价值
中高价值：属「线粒体质量控制与氧化应激」方向；线粒体功能与氧化应激栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.1/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 53,461 字符，题名指纹 0.94，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：机制驱动的辐射损伤与防护纳米药物：氧化还原稳态、DNA 损伤应答与菌群策略
- 英文标题：Mechanism-Driven Nanomedicine for Radiation Injury and Protection: Redox Homeostasis, the DNA Damage Response, and Microbiome-Based Strategies.
- 期刊与标识：International journal of nanomedicine · PMID 42974519 · DOI 10.2147/IJN.S650755 · PMC PMC13726714