Severe ionizing radiation (IR) causes the acute lethal damage of hematopoietic system and gastrointestinal tract. By establishing a radiation injury model, we found that Diprovocim, a TLR2 agonist, protected mice against the lethal damage of hematopoietic system and gastrointestinal tract. Diprovocim inhibited the IR-induced damage, promoted erythrocyte differentiation and elevated the proportion of hematopoietic stem cells (HSCs) in irradiated mice, and promoted the proliferation and differentiation of intestinal stem cells (ISCs). In addition, the RNA seq results suggested that Diprovocim significantly upregulated the TLR2 signaling pathway, and Diprovocim had no radioprotective effect on TLR2 KO mice, suggesting that Diprovocim activated TLR2 signaling pathway to exert its radioprotective function. The RNA sequencing results also suggested that Diprovocim significantly up-regulated the expression of SOX9. Diprovocim had no radioprotective effect after SOX9 knockdown. In conclusion, we demonstrated that Diprovocim protected the radiation-induced damage and upregulated targeting TLR2-SOX9 axis and that Diprovocim might be a potential high-efficiency selective agent.

Background: Ulcerative colitis (UC) is an intestinal disorder marked by chronic, recurring inflammation, yet its underlying mechanisms have not been fully elucidated. Methods: The current research dealt with examining the biological impacts of toll-like receptor 2 (TLR2) on dextran sulfate sodium (DSS)-triggered inflammation in the intestines of wild-type (WT) and TLR2-knockout (TLR2-KO) colitis mouse models. To elucidate the protective function of TLR2 in DSS-triggered colitis, RNA-sequencing (RNA-Seq) was carried out to compare the global gene expression data in the gut of WT and TLR2-KO mice. Further, 16S rRNA gene sequencing revealed notable variations in gut microbiota composition between WT and TLR2-KO colitis mice. Results: It was revealed that TLR2-KO mice exhibited increased susceptibility to DSS-triggered colitis. RNA-Seq results demonstrated that cell cycle pathway-related genes were notably downregulated in TLR2-KO colitis mice (enrichment score = 30, p < 0.001). 16S rRNA gene sequencing revealed that in comparison to the WT colitis mice, the relative abundance of Marinifilacea (p = 0.006), Rikenellacea (p = 0.005), Desulfovibrionaceae (p = 0.045), Tannerellaceae (p = 0.038), Ruminococcaceae (p = 0.003), Clostridia (p = 0.027), and Mycoplasmataceae (p = 0.0009) was significantly increased at the family level in the gut of TLR2-KO colitis mice. In addition, microbiome diversity-transcriptome collaboration analysis highlighted that the relative abundance of Marinifilaceae was negatively linked to the expression of cell cycle signaling-related genes (p values were all less than 0.001). Conclusion: Based on these findings, we concluded that TLR2-KO exacerbates DSS-triggered intestinal injury by mitigating cell cycle signaling in a Marinifilaceae-dependent manner.

The lung is one of the most sensitive tissues to ionizing radiation, thus, radiation-induced lung injury (RILI) stays a key dose-limiting factor of thoracic radiotherapy. However, there is still little progress in the effective treatment of RILI. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatases involved in oxidative stress and apoptosis. Thus, Rac1 may be an important molecule that mediates radiation damage, inhibition of which may produce a protective effect on RILI. By establishing a mouse model of radiation-induced lung injury and orthotopic lung tumor-bearing mouse model, we detected the role of Rac1 inhibition in the protection of RILI and suppression of lung tumor. The results showed that ionizing radiation induces the nuclear translocation of Rac1, the latter then promotes nuclear translocation of P53 and prolongs the residence time of p53 in the nucleus, thereby promoting the transcription of Trp53inp1 which mediates p53-dependent apoptosis. Inhibition of Rac1 significantly reduce the apoptosis of normal lung epithelial cells, thereby effectively alleviating RILI. On the other hand, inhibition of Rac1 could also significantly inhibit the growth of lung tumor, increase the radiation sensitivity of tumor cells. These differential effects of Rac1 inhibition were related to the mutation and overexpression of Rac1 in tumor cells.

Ionizing radiation is one of the common environmental carcinogens. miRNAs play critical roles in the processes of tumor occurrence, development, metastasis. However, the relationship between radiation-induced carcinogenesis and miRNA rarely reported. This study is aimed to investigate the effect of miRNAs on radiation-induced carcinogenesis. In this study we established the radiation-induced thymic lymphoma mice model. By using miRNA array of RTL tissue and predicting for miRNAs target genes, a miRNA-mRNA crosstalk network was established. Based on this network, we identified a critical miRNA, miR-486, which was the most down-regulated in the radiation-induced carcinogenesis. Then the function of miR-486 was confirmed by using knockout mice and cellular experiments. As a result, miR-486 could inhibit proliferation of mouse lymphoma cells by targeting IGF2BP3 mRNA. The adenovirus over-expression miR-486 vector reduced tumorigenesis in vivo . MiR-486 knockout mice have a strong tendency of radiation-induced carcinogenesis. In conclusion, miR-486 inhibits the proliferation of lymphoma cells and tumorigenesis induced by radiation through targeting IGF2BP3.

Backgrounds: There is still little progress in the effective treatment of radiation-induced lung injury (RILI), a key dose-limiting factor for thoracic radiotherapy. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatase involved in various mechanisms of radiation-induced damage and is over-expressed/mutated in various tumors. The gain-of-function mutation of Rac1 mediates tumor cells’ resistance to radiotherapy. Therefore, inhibiting Rac1 has the potential of protecting normal tissues from radiation-induced injury, and at the same time, sensitizing tumor to radiation therapy, which makes it a promising ideal target for radiation protection. To investigate the protective effects and mechanisms of Rac1 inhibition on RILI, and explore the possible mechanisms that mediate the differential effects of Rac1 inhibition on normal lung tissue and tumor cells. Methods: 60 Co radioactive source was used for ionizing radiation (IR). RILI mouse model was constructed. Influence of Rac1 inhibition which was achieved by Rac1-specific inhibitor, NSC23766, on RILI were studied by H & E and Masson staining, and immunohistochemical staining of vimentin, TGF-βand γ-H 2 AX. Normal mouse lung epithelial cell line, MLE-12, and mouse lung cancer cell line, LLC, were used to study the effects of Rac1 inhibition on the cellular level. RNA-seq analysis was used for screening differential gene expression caused by Rac1 knockdown. The molecular mechanisms of Rac1 inhibition were studied at the cellular level. Subcutaneous tumor-bearing nude mouse model and orthotopic lung tumor-bearing mouse model were constructed to verify the bidirectional effects of Rac1 inhibition in vivo. Results: RILI of mouse was alleviated by intraperitoneal injection of NSC23766. Rac1 inhibition/knockdown reduced the radiation-induced damage of MLE-12 while aggravated that of LLC. Rac1 translocated from cytoplasm to nucleus after radiation. Tumor protein p53-inducible nuclear protein 1, Trp53inp1, was down-regulated by Rac1 knockdown. In vivo study further proved the differential effects of Rac1 inhibition. Rac1 was over-expressed and mutated in LLC cells, and the expression level of Trp53inp1 significantly lower, compared with that of MLE-12. Conclusion: Rac1 inhibition reduced the radiation-induced damage of normal lung epithelial cells, thereby alleviating RILI of mouse. These effects were partially mediated by down-regulating the expression of Trp53inp1. However, Rac1 inhibition significantly increased the sensitivity of LLC to radiation damage and inhibited its growth. The over-expression and mutation of Rac1, and the significant low expression of Trp53inp1 in LLC, may be the fundamental reasons mediating the differential effects of Rac1 inhibition.

Endotoxin damage is an acute, multi-organ disease, the most typical symptoms of which are liver injury and inflammatory cytokine storm. Endotoxin tolerance is described as the pretreatment of lipopolysaccharides (LPS) before the toxin invasion, which is consistent with the adaptive response induced by low-dose radiation (LDR). In this study, we verified that LDR could resist the endotoxin damage by suppressing the increase of inflammatory cytokines, including interleukin 6, tumor necrosis factor, and NO, to improve the survival and relieve the inflammatory cell infiltration, in which low dose of LPS performed consistently with LDR.

[摘要] 目的 探讨分子氢对雄性小鼠生殖系统高水平小剂量电离辐射损伤的防护作用及机制。方法 将小鼠 精原细胞系 GC-1 spg 细胞分为对照组、加氢组、4 Gy 照射组、4 Gy 照射加氢组,在各组细胞处理后 24 h 时采用流 式细胞术检测细胞凋亡率。将 72 只雄性 BALB/c 小鼠分为对照组、加氢组、0.25 Gy 照射组、0.25 Gy 照射加氢组、 0.5 Gy 照射组、0.5 Gy 照射加氢组,每组 12 只。小鼠加氢处理采用饮用富氢水联合呼吸高浓度氢气法。各组小鼠 经相应处理后 24 h 分离睾丸组织进行 H-E 染色,并于内眦静脉取血,采用 ELISA 试剂盒检测促性腺激素释放激素 (GnRH)、血清卵泡刺激素(FSH)、黄体生成素(LH)、睾酮含量。照射后 4 周分离小鼠双侧附睾制备精子悬 液,以精子彗星电泳实验检测精子 DNA 损伤情况。结果 4 Gy 照射加氢组 GC-1 spg 细胞的 24 h 凋亡率低于 4 Gy 照射组,差异有统计学意义(t=7.186,P<0.01)。加氢处理缓解了 0.5 Gy 照射导致的小鼠睾丸组织损伤,纠正 了 0.25 Gy、0.5 Gy 照射诱发的 FSH 水平升高(t0.25 Gy=3.195 8,P0.25 Gy=0.019;t0.5 Gy=10.723 4,P0.5 Gy<0.05),并 减轻了 0.25 Gy、0.5 Gy 照射后 4 周小鼠精子 DNA 彗星拖尾程度和 DNA 损伤情况(尾部面积:t0.25 Gy=16.592 3, t0.5 Gy=15.891 5;尾部 DNA 含量:t0.25 Gy=11.296 5,t0.5 Gy=13.785 0;尾部 DNA 百分含量:t0.25 Gy=26.834 0,t0.5 Gy= 10.325 7;尾长:t0.25 Gy=16.865 4,t0.5 Gy=15.441 2;尾矩:t0.25 Gy=26.979 4,t0.5 Gy=13.174 2;Olive 尾矩:t0.25 Gy= 24.752 4,t0.5 Gy=6.896 1;P 均<0.05)。结论 分子氢通过降低精原细胞凋亡、调节激素紊乱、减轻精子 DNA 损 伤等方式对雄性小鼠生殖系统高水平小剂量辐射损伤发挥防护作用。 [关键词] 分子氢;辐射防护;精原细胞;细胞凋亡;雄激素类 [中图分类号] R 135.98 [文献标志码] A [文章编号] 0258-879X(2018)11-1188-08

Pulmonary fibrosis is a serious adverse effect of radiotherapy for thoracic tumor, which is believed to be a process that is tightly regulated by the phenotype of the developing Th response after radiation. Here, we will investigate whether CpG-oligodeoxynucleotides (ODN) prevent radiation-induced pulmonary fibrosis by shifting the imbalance of Th1 and Th2 response and summarizes the possible mechanism. In this study, female C57BL/6 mice were chosen to preform pulmonary fibrosis model, the whole-thorax of mice was exposed to a single radiation dose of 15 Gy. When irradiated mice were administrated with CpG-ODN, forming of pulmonary fibrosis was significantly prevented. Th2-related cytokines (IL-4 and IL-13) expression decreased, Th1 related-cytokine (IFN-gamma and IL-12) expression increased. Alveolar macrophage accumulation was reduced in irradiated tissue. Profibrotic cytokine TGF-beta 1 expression stayed at lower level. In TGF-beta 1-Smad-dependent pathways, TGF-beta 1, T beta R and phosphor-Smad 2/3 were down regulated, and Smad 7 was up regulated. These suggested that CpG-ODN prevented pulmonary fibrosis after radiation. The mechanism might be associated with reduction of alveolar macrophages accumulation and profibrogenic cytokines secretion TGF-beta 1 through stimulating the combination of Th1-promoting and Th2-limiting responses after radiation, and finally inhibited the fibrosis-related downstream TGF-beta 1-Smad-dependent pathway.

It proved that Zymosan‐A protected the haematopoietic system from radiation‐induced damage via Toll‐Like Receptor2 in our previous study. In this study, we investigated the potential mechanism for the radioprotective effects of Zymosan‐A. The mice were treated with Zymosan‐A (50 mg/kg, dissolved in NS) via peritoneal injection 24 and 2 hours before ionizing radiation. Apoptosis of bone marrow cells and the levels of IL‐6, IL‐12, G‐CSF and GM‐CSF were evaluated by flow cytometry assay. DNA damage was determined by γ‐H2AX foci assay. In addition, RNA sequencing was performed to identify differentially expressed genes (DEGs). Zymosan‐A protected bone marrow cells from radiation‐induced apoptosis, up‐regulated IL‐6, IL‐12, G‐CSF and GM‐CSF in bone marrow cells. Zymosan‐A also protected cells from radiation‐induced DNA damage. Moreover, RNA sequencing analysis revealed that Zymosan‐A induced 131 DEGs involved in the regulation of immune system process and inflammatory response. The DEGs were mainly clustered in 18 KEGG pathways which were also associated with immune system processes. Zymosan‐A protected bone marrow cells from radiation‐induced apoptosis and up‐regulated IL‐6, IL‐12, G‐CSF and GM‐CSF. Moreover, Zymosan‐A might also exhibit radioprotective effects through regulating immune system process and inflammatory response. These results provided new knowledge regarding the radioprotective effect of Zymosan‐A.

Background Ionizing radiation often causes severe injuries to radiosensitive tissues, especially haematopoietic system. Novel radioprotective drugs with low toxicity and high effectiveness are required. Prolyl hydroxylases domain (PHD) inhibitors have been reported to protect against radiation-induced gastrointestinal toxicity. In this study, we demonstrated the protective effects of a PHD inhibitor, roxadustat (FG-4592), against radiation-induced haematopoietic injuries in vitro and in vivo. Methods Tissue injuries were evaluated by Haematoxilin-Eosin (HE) staining assay. HSCs were determined by flow cytometry with the Lin(-)Sca-1(+)c-Kit(+) (LSK) phenotype. Cell apoptosis was determined by Annexin V/PI staining assay. Immunofluorescence was performed to measure radiation-induced DNA damage. A western blot assay was used to detect the changes of proteins related to apoptosis. Results We found that FG-4592 pretreatment increased survival rate of irradiated mice and protected bone marrow and spleen from damages. Number of bone marrow cells (BMCs) and LSK cells were also increased both in irradiated mice and recipients after bone marrow transplantation (BMT). FG-4592 also protected cells against radiation-induced apoptosis and double strand break of DNA. Conclusions Our data showed that FG-4592 exhibited radioprotective properties in haematopoietic system both in vivo and in vitro through up-regulating HIF-1 alpha, indicating a potential role of FG-4592 as a novel radioprotector.

BACKGROUND/AIMS:Polymyxin B (PMB) is a cyclic cationic polypeptide antibiotic widely used to counteract the effects of endotoxin contamination, both in vitro and in vivo. Lipopolysaccharide (LPS) is an endotoxin that acts as a radiation protection factor. In this study, we focus on the role of PMB in LPS-induced and radiation-induced mortality in mice.METHODS:Mice received total-body radiation or were pretreated by LPS or PMB, and the survival of mice was recorded. Elisa were used to detect the cytokines levels.RESULTS:PMB decreased LPS-induced, but increased radiation-induced mortality in mice. Moreover, PMB could block the LPS-induced radioprotective effect. The ELISA and gene knock-out experiments indicated that PMB reduces TNF-α level to block LPS-induced mortality in mice, and inhibits IL-6, G-CSF and IL-10 to increase radiation-induced mortality via the TLR4-Myd88-IL-6 pathway.CONCLUSIONS:Our study revealed a role of PMB in LPS-induced endotoxemia and radiation exposure. We infer that the TLR4-Myd88-IL-6 pathway may play a crucial role in the process.

Background/Aims: The hematopoietic system is vulnerable to ionizing radiation and is often severely damaged by radiation. Molecules affecting radioresistance include Toll-like receptor 2. We investigated whether Zymosan-A, a novel TLR2 agonist, can protect the hematopoietic system from radiation-induced damage after total body irradiation. Methods: Mice were exposed to total body radiation after treatment with Zymosan-A or normal saline, and their survival was recorded. Tissue damage was evaluated by hematoxylin–eosin staining. The number of nucleated cells in bone marrow was determined by flow cytometry. Cell viability and apoptosis assay were determined by CCK-8 assay and flow cytometry assay. Enzyme-linked immunosorbent assay was used to detect the level of cytokines. Results: Zymosan-A protected mice from radiation-induced death and prevented radiation-induced hematopoietic system damage. Zymosan-A also promoted cell viability and inhibited cell apoptosis caused by radiation, induced radioprotective effects via TLR2, upregulated IL-6, IL-11, IL-12, and TNF-α in vivo. Conclusion: Zymosan-A can provide protection against radiation-induced hematopoietic system damage by targeting the TLR2 signaling pathway. Thus, Zymosan-A can be potentially effective radioprotectant.

Background: Acute radiation-induced liver injury is a limitation for hepatoma radiotherapy. Come so far the clinical treatments are insufficient. The effective, specific, low toxicity and novel drugs are in powerful need. Glibenclamide is a common hypoglycemic. Some studies have revealed its relation with intracellular reactive oxygen species, the crucial mediator to radiation injury. This study is aimed to investigate if glibenclamide could act on the acute radiation-induced liver injury.Results: Glibenclamide mitigated acute radiation-induced liver injury of mice, indicating as regression of hepatocellular edema, reduction of hepatic sinusoid, decline in serum ALP level and reduction of hepatocellular apoptosis. Pretreatment of glibenclamide reduced the radiosensitivity of NCTC-1469 cells. In mechanism, glibenclamide elevated cells membrane potential to up-regulate intracellular reactive oxygen species. The increased reactive oxygen species subsequently activated AktNF-kappa B pathway to promote survival of irradiated cells.Methods: BALB/C male mice were intraperitoneal injected with glibenclamide 1 hour before hepatic irradiation. At designed time points the livers were taken to make histological study and bloods were collected to measure serum transaminase. With/ without glibenclamide pretreatment the irradiated NCTC-1469 cells were tested apoptosis, viability and proliferation. By western blotting the involved molecules were detected.Conclusions: Glibenclamide, prevents acute radiation-induced liver injury of mice via up-regulating intracellular reactive oxygen species and subsequently activating Akt-NF-kappa B pathway.

MicroRNA-143 has been implicated in tumor metastasis by directly targeting Bcl-2, and microRNA-143 expression is decreased in several human tumors. However, the expression and targets of miR-143 in radiation carcinogenesis remain unclear. We found that the expression of miR-143 is down-regulated and the expression of B7H1 (Pdcd1) is up-regulated in radiation-induced thymic lymphoma model in BALB/c mice. Additionally, overexpression of miR-143 strongly inhibited cell proliferation and increased cell apoptosis and its down-regulation promoted cell proliferation and reduced cell apoptosis. We also determined that there is an inverse correlation between miR-143 expression and B7H1 protein expression in radiation-induced thymic lymphoma samples, and miR-143 targets B7H1 in a 3'UTR-dependent manner. In addition, we found that adenovirus overexpression of pre-miR-143 reduced tumorigenesis in vivo. Finally, we conclude that down-regulated expression of miR-143 and up-regulation of its direct target B7H1 may indicate a novel therapeutic method for radiation-induced thymic lymphoma by increased expression of miR-143 or inhibition of B7H1.

Radiation‐induced lung injury (RILI) is one of the most common and fatal complications of thoracic radiotherapy. It is characterized with two main features including early radiation pneumonitis and fibrosis in later phase. This study was to investigate the potential radioprotective effects of polydatin (PD), which was shown to exert anti‐inflammation and anti‐oxidative capacities in other diseases. In this study, we demonstrated that PD‐mitigated acute inflammation and late fibrosis caused by irradiation. PD treatment inhibited TGF‐β1‐Smad3 signalling pathway and epithelial–mesenchymal transition. Moreover, radiation‐induced imbalance of Th1/Th2 was also alleviated by PD treatment. Besides its free radical scavenging capacity, PD induced a huge increase of Sirt3 in culture cells and lung tissues. The level of Nrf2 and PGC1α in lung tissues was also elevated. In conclusion, our data showed that PD attenuated radiation‐induced lung injury through inhibiting epithelial–mesenchymal transition and increased the expression of Sirt3, suggesting PD as a novel potential radioprotector for RILI.

目的 探讨虾青素对小鼠放射性肺纤维化的防治作用及其机制.方法 60只雌性C57BL/6小鼠随机分为正常组、照射组、照射+虾青素组(25mg/kg),每组20只.除正常组外,其余各组均以60Co γ射线单次16 Gy全胸照射,照射+虾青素组在照射前后每天1次灌胃各7d.照射后1、4、8、16周处死小鼠,取肺组织进行Masson染色,检测肺组织中超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量和羟脯氨酸(hydroxyproline,Hyp)含量,测定血清中转化生长因子β1(transforming growth factor-beta 1,TGF-β1)含量.结果 小鼠受照射后肺纤维化严重程度随照后时间延长而加重,用虾青素处理后可明显减轻小鼠肺纤维化严重程度,提高肺组织SOD活力(P＜0.05或P＜0.01)并减少脂质过氧化产物MDA含量(P＜0.05或P＜0.01);抑制小鼠肺组织Hyp和血清中TGF-β1含量的升高(P＜0.05或P＜0.01).结论 虾青素能够有效地减轻放射性肺纤维化,其机制可能与虾青素能够提高机体的抗氧化能力、下调促纤维化因子TGF-β1表达有关.

Background/Aims: As a major complication after thoracic radiotherapy, radiation-induced lung injury (RILI) has great impact on long term quality of life and could result in fatal respiratory insufficiency The present study was aimed to evaluate the effects of Myrtol standardized on RILI, and to investigate the underlying mechanism. Methods: A mouse model of radiation-induced lung injury was generated by using thoracic irradiation with a single dose of 16Gy. Mice were orally administrated with Myrtol (25 mg/kg/day) for 4 weeks after irradiation, while prednisone (5 mg/kg/day) was used as a positive control. After then, the body weight and lung coefficient were calculated. The severity of fibrosis was evaluated by observing pulmonary sections after radiation and collagen content in lung tissues was calculated following the hydroxyproline (HYP) assay. Pathological changes were observed in all the groups by using HE staining and Masson staining. The serum levels of TGF-β1, TNF-α, IL-1β, IL-6, and PGE2 were also measured with an ELISA assay. Western blot assay was used to measure the impact of Myrtol on AKT and its downstream signaling pathway, including MMP-2 and MMP-9. The levels of Vimentin and α-SMA were evaluated with an immunofluorescence assay. Results: Treatment with Myrtol standardized, but not prednisone, reduced lung coefficient and collagen deposition in lung tissues, while attenuated histological damages induced by irradiation. Myrtol standardized also reduced the production of MDA, while increased the level of SOD. It was also observed that Myrtol standardized inhibited TGF-β1 and a series of pro-inflammatory cytokines including TNF-α, IL-1β, IL-6, PGE2. While in prednisone group, even though the early pneumonitis was ameliorated, the collagen disposition remained unchanged in latter times. Immunofluorescence analysis also revealed elevation of vimentin and α-SMA in the alveoli after a single dose of 16Gy. Conclusion: The present results suggest Myrtol standardized as an effective agent for attenuating the lung injury induced by irradiation.

Molecular hydrogen (H2) has been previously reported playing an important role in ameliorating damage caused by acute radiation. In this study, we investigated the effects ofH2on the alterations induced by low-dose long-term radiation (LDLTR). All the mice in hydrogen-treated or radiation-only groups received 0.1 Gy, 0.5 Gy, 1.0 Gy, and 2.0 Gy whole-body gamma radiation, respectively. After the last time of radiation exposure, all the mice were employed for the determination of the body mass (BM) observation, forced swim test (FST), the open field test (OFT), the chromosome aberration (CA), the peripheral blood cells parameters analysis, the sperm abnormality (SA), the lymphocyte transformation test (LTT), and the histopathological studies. And significant differences between the treatment group and the radiation-only groups were observed, showing thatH2could diminish the detriment induced by LDLTR and suggesting the protective efficacy ofH2in multiple systems in mice against LDLTR.

We have demonstrated that grape seed proanthocyanidins (GSPs) could effectively scavenge hydroxyl radical (•OH) in a dose-dependent manner. Since most of the ionizing radiation- (IR-) induced injuries were caused by •OH, this study was to investigate whether GSPs would mitigate IR-induced injuries in vitro and in vivo. We demonstrated that GSPs could significantly reduce IR-induced DNA strand breaks (DSBs) and apoptosis of human lymphocyte AHH-1 cells. This study also showed that GSPs could protect white blood cells (WBC) from IR-induced injuries, speed up the weight of mice back, and decrease plasma malondialdehyde (MDA), thus improving the survival rates of mice after ionizing radiation. It is suggested that GSPs have a potential as an effective and safe radioprotective agent.