AIMS:Radiation-induced intestinal injury (RIII) significantly impairs the quality of life in patients with abdominal/pelvic cancer undergoing radiotherapy, often necessitating treatment cessation. The ACE2/Ang-(1-7)/MasR axis, a protective pathway within the renin-angiotensin system, represents a potential anti-inflammatory target. This study explored the role of ACE2 activation in mitigating RIII and the underlying mechanisms. RESULTS:Treatment with diminazene aceturate (DIZE), a selective ACE2 agonist, prior to lethal radiation blocked intestinal stem cell (ISC) death, enhanced crypt regeneration, preserved epithelial barrier integrity, and reduced intestinal inflammation, thereby promoting mice survival. Notably, the radioprotective effect of DIZE was reversed by ACE2 or MasR antagonists, and other ACE2 agonists exhibited similar radioprotective efficacy. DIZE treatment improved the survival of ISCs both in vitro and in vivo postradiation. Mechanistically, DIZE directly targeted intestinal epithelial cells (IECs), preventing the activation of radiation-induced MAPK (p38/JNK) and NF-κB pathways. This effect was abolished by ACE2 knockdown in a human intestinal epithelial cell line (HIECs) in vitro. Intriguingly, DIZE failed to inhibit endothelial cell apoptosis or attenuate MAPK/NF-κB pathway activation in irradiated endothelial cells. Preliminary evidence indicates DIZE did not affect the radiosensitivity of colorectal tumor cells or azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colorectal tumors in mice.Conclusion and Innovation:This study is the first to demonstrate selective ACE2-mediated intestinal protection without compromising tumor radiosensitivity. These findings demonstrate ACE2 activation selectively shields IECs from radiation damage by inhibiting MAPK/NF-κB pathways, offering a novel therapeutic strategy to alleviate RIII without compromising tumor radiosensitivity. Antioxid. Redox Signal. 44, 843-858.

Background and Purpose Radiation-induced ovarian injury (RIOI) compromises the clinical utility of pelvic radiotherapy and reduces fertility in young female patients. Dimethyl sulfoxide (DMSO) exhibits antioxidant property. Hearin, we aimed to explore the protective effect and underlying mechanism of DMSO on RIOI. Materials and Methods C57BL/6J female mice were treated with DMSO prior to undergoing lower abdominal radiation. Intragenerational and transgenerational fertility were assessed by mating experiment. Ovaries were harvested to evaluate follicle count and morphology. Granulosa cells were analyzed by immunohistochemical staining of TUNEL and Ki67. An ovary explant organ culture system was established to evaluate the effect of DMSO. Fluorescent probes were employed to evaluate mitochondrial mass and function. DNA double-strand breaks were detected by immunoblotting of γ-H2AX. Results DMSO preserved the fertility of irradiated mice and even safeguarded the reproductive capacity of their unirradiated female offspring. Histological analyses revealed that DMSO preserves the ovarian follicle reserve, including both primordial and developing follicles. Additionally, DMSO demonstrated radioprotective effects in ex vivo ovarian tissue. Moreover, DMSO reduced apoptosis and enhanced proliferation in granulosa cells. Mechanistically, DMSO alleviated radiation-induced oxidative stress and preserved mitochondrial function, as evidenced by increased mitochondrial mass, reduced oxidant levels, and enhanced mitochondrial membrane potential. Moreover, DMSO reduced the levels of DNA damage accumulation in vivo and in vitro . Conclusion Our data suggest that DMSO may offer a potential pharmacological treatment option for fertility impairment in women undergoing radiotherapy, which warrants further investigation in clinical settings.

PURPOSE:Radiation-induced skin injury is a common complication that seriously affects the follow-up treatment and life quality of tumor patients. Nocardia rubra cell-wall skeleton (N-CWS) has been reported to have pro-angiogenesis effects, and its role on RISI remains unclear. The aim of this study was to investigate its effect on repair of radiation induced skin injury. MATERIALS AND METHODS:After exposure to 45 Gy X-rays, the irradiated areas of SD rats were treated by N-CWS every 3 days. The radioprotective effects of N-CWS were evaluated by body weight changes, skin scores, H&E staining and TUNEL staining. Microvascular monitoring system and immunofluorescence staining of CD31 were performed to assess angiogenic capacity in vivo. In vitro, the activity and apoptosis of HUVECs were measured by CCK8 and flow cytometry. The angiogenic capacity of HUVECs was evaluated by tubule formation assay and Transwell assay. Western blot was performed to verify the possible mechanisms of the protective effect of N-CWS against radiation-induced skin damage. RESULTS:N-CWS was demonstrated to have low toxicity and radioprotective effects, maintained cell activity and attenuated radiation-induced apoptosis. In addition, N-CWS attenuated radiation-induced vascular injury in vivo and in vitro. Furthermore, P38 MAPK was shown to be associated with the radiation protection capability of N-CWS in HUVECs. CONCLUSIONS:N-CWS promoted the repair of radiation-induced skin injury by enhancing angiogenesis, and the mechanism was related to the activation of P38 MAPK.

The phosphatase PTEN is an important molecule for maintaining chromosome stability. PTEN deficiency induces DNA replication stress, confers stress tolerance, and disrupts mitotic spindle architecture, leading to the accumulation of structural and numerical chromosome instability. PTEN has many posttranslational modifications, including phosphorylation, acetylation and methylation; its modification level directly regulates protein levels and functions, thereby affecting the stability of the genome. It has been reported that Plk1, a Ser/Thr kinase, can directly phosphorylate PTEN at S380, impair its interaction with cdh1 and stabilize its association with chromatin. As the phosphorylation of PTEN at the STT motif is associated with the DNA damage response and Plk1 activity is inhibited when DNA damage occurs, it is not clear whether there are other upstream molecules that can regulate S380 phosphorylation, and if so, by what mechanism. We found that the ATM/Chk2 signaling pathway can affect PTEN p-S380 when DNA damage occurs and that PTEN p-S380, which may be regulated by ATM/Chk2, is involved in chromatin decondensation. These results suggest a role for PTEN modification by other kinases and provide a target for improving radiotherapy efficacy.

AIMS:Radiation-induced intestinal injury (RIII) severely compromises the quality of life in patients undergoing abdominal/pelvic radiotherapy and may necessitate treatment discontinuation. To date, there is no approved agent for the prevention or treatment of RIII. This study aims to clarify the protective effects of mannose on RIII and elucidate its mechanisms of action, in order to identify new safe and effective therapeutic agents and potential therapeutic targets for the prevention and treatment of RIII. RESULTS:Here, we report that intraperitoneal administration of mannose, a natural bioactive monosaccharide, at 24, 12, and 2 h prior to lethal irradiation increased the survival rate of mice from 0% to 50%. Specifically, mannose pretreatment significantly blocked crypt cell apoptosis, preserved epithelial barrier integrity, attenuated intestinal inflammation, and enhanced crypt regeneration. Additionally, mannose treatment enhanced the survival of intestinal stem cells both in vitro and in vivo following radiation exposure. We further confirmed that mannose maintains mitochondrial homeostasis and alleviates cellular oxidative stress. Moreover, mannose facilitated the repair of DNA double-strand breaks, thereby inhibiting aberrant mitosis after radiation exposure. Additionally, preliminary evidence indicates that mannose does not affect the radiosensitivity of colorectal tumor cells or azoxymethane/dextran sodium sulfate-induced colorectal tumors in mice.Conclusion and Innovation:Given its low toxicity and wide availability, our findings suggest that mannose represents a promising protective strategy for RIII. Antioxid. Redox Signal. 00, 000-000.

To investigate the functional and molecular mechanisms by which Piezo1regulates HT-22 hippocampal neuronal autophagy, and to explore whether Piezo1 regulates hippocampal neuronal autophagy via the Ca2+/Calpain, CaMKKβ, or Calcineurin pathways. The impacts of Piezo1 inhibition, activation and gene knockdown on the autophagy of HT22 neurons was investigated by Western blotting, PCR and immunofluorescence. The changes of intracellular calcium (Ca2+) concentration were also observed. To pinpoint the specific downstream Ca2+ signaling pathway by which Piezo1 modulates autophagy, the calcium chelator BAPTA-AM, the Calpain inhibitor PD151746, and the CaMKKβ inhibitor STO609 were employed either alone or in combination. Enhanced autophagy was observed when Piezo1 was activated using the agonist Yoda1, manifesting as increased release of autophagic vacuoles, enhanced LC3 II/LC3 I ratio, decreased p62 protein level, and elevated nuclear translocation and expression of the TFEB protein. ATG7 knockdown by ATG7 shRNA mitigated the effects of Yoda1 on LC3 II/LC3 I ratio and p62 protein levels. The Piezo1 inhibitor GsMTx4 partially reversed the autophagy caused by starvation in HT22 neurons while Yoda1 still activated autophagy in the presence of BDNF. Following Piezo1 knockdown, neuronal autophagy was decreased. Piezo1-induced autophagy was accompanied with an increased cytoplasmic concentration of Ca2+. The calcium chelator BAPTA-AM partly reversed Piezo1 activation-induced autophagy, which was also mitigated by blocking calcineurin/TFEB signaling or Calpain signaling. Piezo1 modulates the autophagy of HT-22 neurons by activating Ca2+/Calpain and Calcineurin/TFEB pathways.

BackgroundIonizing radiation (IR), including radiotherapy, can exert lasting harm on living organisms. While liposaccharide (LPS) offers resistance to radiation damage, it also induces toxic responses. Thankfully, an LPS analogue called N-formylmethionine-leucyl-phenylalanine (fMLP) holds the potential to mitigate this toxicity, offering hope for radiation protection.MethodsSurvival of C57BL/6 mice exposed to IR after administration with fMLP/LPS/WR-2721 or saline was recorded. Cell viability and apoptosis assay of bone marrow (BMC), spleen and small intestinal epithelial (HIECs) cells were tested by Cell Counting Kit-8 (CCK-8) and flow cytometry assay. Tissue damage was evaluated by Hematoxilin and Eosin (H&E), Ki-67, and TUNEL staining. RNA sequencing was performed to reveal potential mechanisms of fMLP-mediated radiation protection. Flow cytometry and western blot were performed to verify the radiation protection mechanism of fMLP on the cell cycle.ResultsThe survival rates of C57BL/6 mice exposed to ionizing radiation after administering fMLP increased. fMLP demonstrated low toxicity in vitro and in vivo, maintaining cell viability and mitigating radiation-induced apoptosis. Moreover, it protected against tissue damage in the hematopoietic and intestinal system. RNA sequencing shed light on fMLP's potential mechanism, suggesting its role in modulating innate immunity and cell cycling. This was evidenced by its ability to reverse radiation-induced G2/M phase arrests in HIECs.ConclusionfMLP serves as a promising radioprotective agent, preserving cells and radiosensitive tissues from IR. Through its influence on the cell cycle, particularly reversing radiation-induced arrest in G2/M phases, fMLP offers protection against IR's detrimental effects.

Much effort has been devoted to improving treatment efficiency for osteosarcoma (OS). However, most current approaches result in poor therapeutic responses, thus indicating the need for the development of other therapeutic options. This study developed a multifunctional nanoparticle, PDA-MOF-E-M, an aggregation of OS targeting, programmed death targeting, and near-infrared (NIR)-aided targeting. At the same time, a multifunctional nanoparticle that utilises Fe-MOFs to create a cellular iron-rich environment and erastin as a ferroptosis inducer while ensuring targeted delivery to OS cells through cell membrane encapsulation is presented. The combination of PDA-MOF-E-M and PTT increased intracellular ROS and LPO levels and induced ferroptosis-related protein expression. A PDA-based PTT combined with erastin showed significant synergistic therapeutic improvement in the anti-tumour efficiency of the nanoparticle in vitro and vivo. The multifunctional nanoparticle efficiently prevents the osteoclasia progression of OS xenograft bone tumors in vivo. Finally, this study provides guidance and a point of reference for clinical approaches to treating OS.

Bacterial outer membrane vesicles (OMVs) are potent immuno-stimulating agents and have the potentials to be bioengineered as platforms for antitumor nanomedicine. In this study, OMVs are demonstrated as promising antitumor therapeutics. OMVs can lead to beneficial M2-to-M1 polarization of macrophages and induce pyroptosis to enhance antitumor immunity, but the therapeutic window of OMVs is narrow for its toxicity. We propose a bioengineering strategy to enhance the tumor-targeting ability of OMVs by macrophage-mediated delivery and improve the antitumor efficacy by co-loading of photosensitizer chlorin e6 (Ce6) and chemotherapeutic drug doxorubicin (DOX) into OMVs as a therapeutic platform. We demonstrate that systemic injection of the DOX/Ce6-OMVs@M therapeutic platform, providing combinational photodynamic/chemo-/immunotherapy, eradicates triple-negative breast tumors in mice without side effects. Importantly, this strategy also effectively prevents tumor metastasis to the lung. This OMVs-based strategy with bioengineering may serve as a powerful therapeutic platform for a synergic antitumor therapy.

Abstract We studied 57 patients with cerebral infarction and Fetal-type Posterior cerebral artery (FTP)\, confirmed by MRA and CTA. 26 cases (45.61%) of Complete Fetal-type Posterior cerebral artery (cFTP), 21 cases (36.84%) of Partial Fetal-type Posterior cerebral artery (pFTP), 10 cases (17.54%) of unilateral cFTP.When the ipsilateral internal carotid artery occlusion of cFTP occurs, the bidirectional collateral circulation from the posterior circulation to the posterior communication artery to the anterior circulation cannot be established to compensate, simultaneous infarction of the ipsilateral anterior and posterior circulation can be caused. In the presence of pFTP, since the diameter of P1 was less than that of the posterior communicating artery (PcoA), the collateral circulation of posterior circulation - posterior cerebral artery - middle cerebral artery pia meningeal anastomosis could not be established, anterior circulation infarction was caused by ipsilateral internal carotid artery occlusion. In the presence of bilateral cFTP, the anterior circulation-posterior communication artery-basilar artery could not be established to compensate for the collateral circulation of other branches except bilateral posterior cerebral artery, resulting in bilateral cerebellar and brainstem infarction. FTP changes the cerebral artery circulation and collateral circulation pathways in the normal state.

AIMS:To verify the hypothesis that an enriched environment (EE) alleviates sleep deprivation-induced fear memory impairment by modulating the basal forebrain (BF) PIEZO1/calpain/autophagy pathway.METHODS:Eight-week-old male mice were housed in a closed, isolated environment (CE) or an EE, before 6-h total sleep deprivation. Changes in fear memory after sleep deprivation were observed using an inhibitory avoidance test. Alterations in BF PIEZO1/calpain/autophagy signaling were detected. The PIEZO1 agonist Yoda1 or inhibitor GsMTx4, the calpain inhibitor PD151746, and the autophagy inducer rapamycin or inhibitor 3-MA were injected into the bilateral BF to investigate the pathways involved in the memory-maintaining role of EE in sleep-deprived mice.RESULTS:Mice housed in EE performed better than CE mice in short- and long-term fear memory tests after sleep deprivation. Sleep deprivation resulted in increased PIEZO1 expression, full-length tropomyosin receptor kinase B (TrkB-FL) degradation, and autophagy, as reflected by increased LC3 II/I ratio, enhanced p62 degradation, increased TFEB expression and nuclear translocation, and decreased TFEB phosphorylation. These molecular changes were partially reversed by EE treatment. Microinjection of Yoda1 or rapamycin into the bilateral basal forebrain induced excessive autophagy and eliminated the cognition-protective effects of EE. Bilateral basal forebrain microinjection of GsMTx4, PD151746, or 3-MA mimicked the cognitive protective and autophagy inhibitory effects of EE in sleep-deprived mice.CONCLUSIONS:EE combats sleep deprivation-induced fear memory impairments by inhibiting the BF PIEZO1/calpain/autophagy pathway.

Radiation-induced intestinal injury (RIII) occurs after high doses of radiation exposure. RIII restricts the therapeutic efficacy of radiotherapy in cancer and increases morbidity and mortality in nuclear disasters. Currently, there is no approved agent for the prevention or treatment of RIII. Here, we reported that the disulfiram, an FDA-approved alcohol deterrent, prolonged the survival in mice after lethal irradiation. Pretreatment with disulfiram inhibited proliferation within 24 h after irradiation, but improved crypt regeneration at 3.5 days post-irradiation. Mechanistically, disulfiram promoted Lgr5+ intestinal stem cells (ISCs) survival and maintained their ability to regenerate intestinal epithelium after radiation. Moreover, disulfiram suppresses DNA damage accumulation, thus inhibits aberrant mitosis after radiation. Unexpectedly, disulfiram treatment did not inhibit crypt cell apoptosis 4 h after radiation and the regeneration of crypts from PUMA-deficient mice after irradiation was also promoted by disulfiram. In conclusion, our findings demonstrate that disulfiram regulates the DNA damage response and survival of ISCs through affecting the cell cycle. Given its radioprotective efficacy and decades of application in humans, disulfiram is a promising candidate to prevent RIII in cancer therapy and nuclear accident.

过氧化物酶体增殖物活化受体(peroxisome proliferator activatived receptors,PPARs)是核受体超家族成员,包括PPARα、PPARδ和PPARγ3种亚型,他们在不同组织中表达,其中PPARγ在脂肪组织、心脏、 肠道和免疫细胞中存在,在脂肪合成过程中起着关键作用.PPARγ具有抗氧化作用,通过调控Nrf2信号通路、 内皮型NOS(eNOS)和诱导型NOS(iNOS)表达以及其他相关信号通路发挥作用.辐射诱导的氧化应激是引起细胞水平和全身水平损伤的主要因素,由于PPARγ具有抗氧化应激的能力,有望成为辐射防护和辐射治疗的有效靶点.

Radiotherapy of abdominal and pelvic tumors almost inevitably injures the intestine by oxidative stress and causes inflammation. Regrettably, traditional radioprotective agents for irradiation (IR) induced intestinal injury suffer from challenges such as poor solubility, unsatisfactory bioactivity and undesired adverse reactions, which significantly limit their usefulness. Polydopamine nanoparticles (PDA-NPs) have shown promising potential in scavenging reactive oxygen species (ROS) and suppressing inflammation. In this study, PDA-NPs were prepared by a simple method and their physical properties were characterized. Mice received two doses of PDA-NPs by oral gavage 22 h apart, and were irradiated with X-rays 2 h after the last gavage. The protective effect of PDA-NPs and possible mechanisms of protection against IR-induced intestinal injury were explored. The results showed that PDA-NPs were spherical and well dispersed, with good shape uniformity, compact structure, good colloid dispersion stability, concentration-dependent light absorption, and accurate quantification. Importantly, PDA-NPs reduced mortality and prolonged the average survival time of mice after IR. Furthermore, PDA-NPs protected mice from IR-induced injury to crypt-villus units and maintained intestinal barrier function in the intestine. In particular, PDA-NPs significantly inhibited the depletion of Lgr5+ intestinal stem cells (ISCs) and promoted cell regeneration after IR, which indicated that the regeneration ability of ISCs was maintained and the repair of intestinal structure and function was promoted. Finally, PDA-NPs significantly suppressed the apoptosis, inflammatory pyroptosis and DNA damage of intestinal cells induced by ionizing radiation. Altogether, our study suggested that PDA-NPs may have great potential in protecting the intestines from ionizing radiation damage.

Abstract Background radiation-induced intestinal injury (RIII) is an important cause of death in nuclear accidents and common complication after radiotherapy in patients with pelvic, abdominal, or retroperitoneal tumors. Up to now there is no effective means to prevent or treat RIII due to its complex mechanism, in which the death of intestinal cells is the main reason. Recently, GSDMD-mediated pyroptosis was identified as an important type of cell death and play a role in many diseases. However, the effect of pyroptosis on RIII is still unclear. Method using GSDMD knockout mice, the role of pyroptosis in the RIII was investigated. By detecting the release of LDH, expression of GSDMD, Caspase-11, Caspase-1 and absorption rate of SYTOX Green, the pyroptosis of radiated Mode-k cells was determined, simultaneously the common pyroptosis induced by LPS was conducted as positive control. Further, the upstream of GSDMD were screened by predictive analysis of transcription factors combing RNA-seq. Results we showed that GSDMD-mediated pyroptosis is involved in the process of RIII, and unexpectedly found that radiation induced a delayed pyroptosis that is substantially different from common pyroptosis induced by such as LPS. Further investigation revealed that radiation-induced DNA damage up-regulated the expression of P53, which subsequently transcribes GSDMD. In addition, the up-regulated GSDMD led to pyroptosis simultaneously promoting Ca2+ influx that afterwards enhanced apoptosis induced by radiation. Finally, targeting GSDMD, disulfiram displayed a potential protection for RIII. Conclusion radiation could induce delayed pyroptosis in the intestinal epithelial cell that is greatly different from common pyroptosis. During that process, GSDMD was cleaved and had inducible high expression which was mainly mediated by P53 transcription.

Recently, Toll-like receptors (TLRs) have been extensively studied in radiation damage, but the inherent defects of high toxicity and low efficacy of most TLR ligands limit their further clinical transformation. CRX-527, as a TLR4 ligand, has rarely been reported to protect against radiation. We demonstrated that CRX-527 was safer than LPS at the same dose in vivo and had almost no toxic effect in vitro. Administration of CRX-527 improved the survival rate of total body irradiation (TBI) to 100% in wild-type mice but not in TLR4-/- mice. After TBI, hematopoietic system damage was significantly alleviated, and the recovery period was accelerated in CRX-527-treated mice. Moreover, CRX-527 induced differentiation of HSCs and the stimulation of CRX-527 significantly increased the proportion and number of LSK cells and promoted their differentiation into macrophages, activating immune defense. Furthermore, we proposed an immune defense role for hematopoietic differentiation in the protection against intestinal radiation damage, and confirmed that macrophages invaded the intestines through peripheral blood to protect them from radiation damage. Meanwhile, CRX-527 maintained intestinal function and homeostasis, promoted the regeneration of intestinal stem cells, and protected intestinal injury from lethal dose irradiation. Furthermore, After the use of mice, we found that CRX-527 had no significant protective effect on the hematopoietic and intestinal systems of irradiated TLR4-/- mice. in conclusion, CRX-527 induced differentiation of HSCs protecting the intestinal epithelium from radiation damage.

The testis is susceptible to ionizing radiation, and male infertility and sexual dysfunction are prevalent problems after whole-body or local radiation exposure. Currently, there is no approved agent for the prevention or treatment of radiation-induced testicular injury. Herein, we investigated the radioprotective effect of dimethyl sulfoxide (DMSO), an organosulfur compound that acts as a free radical scavenger, on testicular injury. Treatment of mice with a single dose of DMSO prior to 5 Gy irradiation restored sex hormones and attenuated the reduction in testis weight. Histological analyses revealed that DMSO alleviated the distorted architecture of seminiferous tubules and promoted seminiferous epithelium regeneration following irradiation. Moreover, DMSO provided quantitative and qualitative protection for sperm and preserved spermatogenesis and fertility in male mice. Mechanistically, DMSO treatment enhanced GFRα-1+ spermatogonial stem cell and c-Kit+ spermatogonial survival and regeneration after radiation. DMSO also alleviated radiation-induced oxidative stress and suppressed radiation-induced germ cell apoptosis in vivo and in vitro. Additionally, DMSO efficiently reduced DNA damage accumulation and induced the expression of phosph-BRCA1, BRCA1, and RAD51 proteins, indicating that DMSO facilitates DNA damage repair with a bias toward homologous recombination. In summary, our findings demonstrate the radioprotective efficacy of DMSO on the male reproductive system, which warrants further studies for future application in the preservation of male fertility during conventional radiotherapy and nuclear accidents.

分析当前核应急医学救援人体表面污染控制相关标准,探讨现有标准的不足,提出核应急医学救援人体表面污染控制相关标准应用建议.认为现行标准WS/T 467-2014《核和辐射事故医学响应程序》、GBZ/T 271-2016《核或辐射应急准备与响应通用准则》、T/WSJD 7-2020《核辐射突发事件放射性污染人员洗消流程及技术要求》适用于核应急医学救援人体表面污染控制,其中GBZ/T 271-2016的参考理念较新、可操作性较强,建议任务单位及相关应急力量参考使用.

Bone tumors occur in bone or its accessory tissues. Benign bone tumors are easy to cure and have good prognosis, while malignant bone tumors develop rapidly and have poor and high mortality. So far, there is no satisfactory treatment method. Here, we designed a universal template vector for bone tumor therapy that simultaneously meets the needs of bone targeting, tumor killing, osteoclast suppression, and tumor imaging. The template is composed of a polydopamine (PDA) core and a multifunctional surface. PDA has excellent biosafety and photothermal performance. In this study, alendronate sodium (ALN) is grafted to enable its general bone targeting function. PDA core can carry a variety of chemotherapy drugs, and the rich ALN group can carry a variety of metal ions with an imaging function. Therefore, more personalized treatment plans can be designed for different bone tumor patients. In addition, the PDA core enables photothermal therapy and enhanced chemotherapy. Through template drug Doxorubicin (DOX) and template imaging ion Fe (Ⅱ), we systematically verified the therapeutic effect, imaging effect, and inhibition of bone dissolution of the agent on Osteosarcoma (OS), a primary malignant bone tumor, in vivo. In conclusion, our work provides a more general template carrier for the clinical treatment of bone tumors, through which personalized treatment of bone tumors can be achieved.