Enhancement of the NIR Emission of Cr3+-Yb3+ Co-doped La3GaGe5O16 Phosphors by Doping Nd3+ Ions via Efficient Energy Transfer for NIR Spectroscopy Regulation.

The efficient energy transfer in La3GaGe5O16:Cr3+, Yb3+/Nd3+ and La3GaGe5O16:Cr3+, Yb3+, Nd3+ was investigated in detail. In this phosphor, Cr3+ acts as the energy absorber (250-700 nm) to sensitize Yb3+/Nd3+ in La3GaGe5O16. Under excitation at 418 nm, La3GaGe5O16:Cr3+, Yb3+ phosphors exhibited a broad emission band in the near-infrared (NIR) region located at 976 nm (La3GaGe5O16:Cr3+, Nd3+ at 1056 nm), which was attributed to the 2F5/2-2F7/2 transition of the Yb3+ ions (2F3/2 → 4I11/2 transition of Nd3+). Moreover, a Nd3+ ion was introduced into La3GaGe5O16:Cr3+, Yb3+. The analysis of excitation spectra and decay time proves that Nd3+ acts as a bridging ion in the system. This can be used as a new strategy to enhance the energy transfer in Cr3+, Yb3+ co-doped phosphors, and these phosphors have potential applications in NIR spectroscopy regulation.

Insight into degradation mechanism of PCBs from thermal desorption off-gas over iron-based catalysts.

Iron-based catalysts were developed to achieve the hydrodechlorination (HDC)/oxidation of polychlorinated biphenyls (PCBs) from thermal desorption off-gas, and Fe3O4/γ-Al2O3 showed higher dechlorination efficiency than Fe2O3/γ-Al2O3. The optimal Fe loading resulted in 95.5% degradation efficiency and 76.9% toxicity reduction of gaseous PCBs, and the optimal Fe3O4/γ-Al2O3 exhibited excellent stability during a 60-h test. The gas chromatography-mass spectrometry analysis of intermediate products indicated the presence of two competitive degradation pathways, namely, hydrodechlorination and oxidation with Fe3O4/γ-Al2O3 as catalyst. During the first stage (reductive dechlorination), the reductive activity of iron-based catalysts was effectively enhanced in the presence of water, which was confirmed by density functional theory (DFT) calculations. The removal of chlorine atoms was found in the order of meta > para > ortho. During the second stage (oxidation), hydroxyl and superoxide anion radicals were found to attack PCBs on the surface of Fe3O4/γ-Al2O3. This study provides an insight into the HDC and oxidation mechanism of gaseous PCBs over iron-based catalysts.

Insights into the mechanism of low-temperature H2S oxidation over Zn-Cu/Al2O3 catalyst.

Odor pollution caused by toxic chemicals with low human olfactory thresholds, such as hydrogen sulfide (H2S), has become a major cause of environmental grievance world-wide. Although the low-temperature (<180 °C) catalytic oxidation of H2S using metal oxides has received widespread attention, desulfurization performance is not ideal. Herein, a series of Zn-Cu/Al2O3 catalysts were developed using an impregnation method based on the Al2O3 hydrophilicity and the effects of zinc loading on the catalyst physicochemical properties and performance were systematically studied. The catalysts were characterized using inductively coupled plasma-optical emission spectrometry (ICP-OES), N2 adsorption-desorption isotherms, scanning electron microscopy with energy dispersive spectrometry (SEM-EDS), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), Fourier-transform infrared spectroscopy (FTIR) and electron paramagnetic resonance (EPR). It was found that optimization of zinc doping could improve the hydrophilicity of the catalyst, and hence its activity. Catalytic activity was also dependent on operational parameters such as temperature, humidity and space velocity. The Zn3Cu3 catalyst exhibited the highest breakthrough capacity of 353.91 mg/g at 50 °C and at a relative humidity of 50%. The excellent desulfurization performance was attributed to oxygen vacancies contributed by CuO, Cu2O and ZnO, which facilitated the conversion of H2O into hydroxyl radicals. Consequently, a hydroxyl radical-induced desulfurization mechanism over Zn-Cu/Al2O3 is proposed. This work provides a potential green and efficient catalyst for the selective oxidation of H2S.

The Ablation of Envelope Protein Glycosylation Enhances the Neurovirulence of ZIKV and Cell Apoptosis in Newborn Mice.

Zika virus (ZIKV) has attracted the wide global attention due to its causal link to microcephaly. In this study, two amino acid (aa) mutation (E143K and R3394K) were identified at the fourth generation (named ZKC2P4) during the serial passage of ZIKV-Asian lineage ZKC2/2016 strain in the newborn mouse brain, while another seven aa deletions in envelope (E) protein were detected in ZKC2P6. ZKC2P6 is a novel nonglycosylated E protein Asian ZIKV we first identified and provides the first direct supporting evidence that glycosylation motif could be lost during the passage in neonatal mice. To study the impact of E protein glycosylation ablation, we compared the pathogenicity of ZKC2P6 with that of ZKC2P4. The results showed that the loss of E protein glycosylation accelerated the disease progression, as evidenced by an earlier weight loss and death, a thinner cerebral cortex, and more serious tissue lesions and inflammation/necrosis. Furthermore, ZKC2P6 exhibited a greater ability to replicate and caused severer cell apoptosis than that of ZKC2P4. Therefore, the ablation of E glycosylation generally enhances the neurovirulence of ZIKV and cell apoptosis in newborn mice.

Potential role of senescent macrophages in radiation-induced pulmonary fibrosis.

Radiation-induced pulmonary fibrosis (RIPF) is a late toxicity of therapeutic radiation in clinic with poor prognosis and limited therapeutic options. Previous results have shown that senescent cells, such as fibroblast and type II airway epithelial cell, are strongly implicated in pathology of RIPF. However, the role of senescent macrophages in the development RIPF is still unknown. In this study, we report that ionizing radiation (IR) increase cellular senescence with higher expression of senescence-associated ß-galactosidase (SA-ß-Gal) and senescence-specific genes (p16, p21, Bcl-2, and Bcl-xl) in irradiated bone marrow-derived monocytes/macrophages (BMMs). Besides, there's a significant increase in the expression of pro-fibrogenic factors (TGF-ß1 and Arg-1), senescence-associated secretory phenotype (SASP) proinflammatory factors (Il-1α, Il-6, and Tnf-α), SASP chemokines (Ccl2, Cxcl10, and Ccl17), and SASP matrix metalloproteinases (Mmp2, Mmp9 and Mmp12) in BMMs exposed to 10 Gy IR. In addition, the percentages of SA-ß-Gal+ senescent macrophages are significantly increased in the macrophages of murine irradiated lung tissue. Moreover, robustly elevated expression of p16, SASP chemokines (Ccl2, Cxcl10, and Ccl17) and SASP matrix metalloproteinases (Mmp2, Mmp9, and Mmp12) is observed in the macrophages of irradiated lung, which might stimulate a fibrotic phenotype in pulmonary fibroblasts. In summary, irradiation can induce macrophage senescence, and increase the secretion of SASP in senescent macrophages. Our findings provide important evidence that senescent macrophages might be the target for prevention and treatment of RIPF.

Achieving Multimodal Emission in Zn4B6O13:Tb3+,Yb3+ for Information Encryption and Anti-counterfeiting.

With the rapid development of technology, information security has always been considered a major challenge. In this work, the excellent combination of persistent luminescence, photoluminescence, up-conversion luminescence, and thermo-luminescence in a particular material Zn4B6O13:Tb3+,Yb3+ synthesized via a solid-state reaction is reported, which can be used for the information encryption and anti-counterfeiting. Tb3+ ions were chosen as the emitting centers for multimodal emissions, and Yb3+ codoping can be used as electron traps and sensitizer to adjust trap distribution and efficient up-conversion luminescence in rare-earth-doped luminescent materials. Besides, the as-prepared luminescent materials exhibit high thermal stability and excellent water resistance. On the basis of these properties, the samples were used to print luminescent images through a screen printing process on the film and banknote. The luminescent image in a film is showing different patterns and on a banknote is showing green emissions under different stimulations. These multimodal emissions demonstrate that the as-prepared sample is suitable for advanced information encryption and anti-counterfeiting.

In-situ degradation of polybrominated diphenyl ethers from thermal desorption off-gas over structured Fe-based/γ-Al2O3/Al plate-type catalyst.

Thermal desorption was an efficient method for removal of decabromodiphenyl ether (BDE-209) from contaminated soil, but some less brominated diphenyl ethers (tri- to hepta-BDEs) with high toxicity were detected in the effluent gas. Herein, a novel anodic alumina supported Fe-based catalyst was developed and applied for in-situ degradation of gaseous polybrominated diphenyl ethers (PBDEs). The produced Fe/γ-Al2O3/Al catalyst was able to degrade PBDEs in the effluent gas, while a low activity with degradation efficiency of 70.1% was observed. As such, Cu was added into the Fe-based catalyst, and the effects of Cu loading on gaseous PBDEs degradation were systematically examined. A proper copper loading was found to increase the active Fe3O4 sites, thus improving the catalytic activity. Meanwhile, the degradation of gaseous PBDEs by Fe-based catalysts follows a pseudo-first-order model. A 90.2% PBDEs degradation efficiency was achieved at 375 °C on the optimized Fe/Cu/γ-Al2O3/Al catalyst, which demonstrated that the anodic alumina supported Fe and Cu was an excellent catalyst for gaseous PBDEs degradation system. Thus, this study provides a promising method and catalyst to achieve in-situ degradation of gaseous PBDEs.

Near UV-pumped yellow-emitting Ca3TeO6:Dy3+ phosphor for white light-emitting diodes.

A series of Ca3TeO6:xDy3+ (x = 0.01, 0.02, 0.05, 0.10, 0.15, 0.20, and 0.25) tellurate yellow-emitting phosphors were synthesized via the high-temperature solid-state method. The X-ray diffraction patterns of these phosphors revealed that all the samples have a double-perovskite type with monoclinic structure. The Ca3TeO6:Dy3+ phosphor exhibit characteristic emission transitions, 4F9/2-6H15/2 transition and 4F9/2-6H13/2 transition, respectively. The intense yellow light indicates that Dy3+ ion occupies the interstitial Ca site in the Ca3TeO6 host. The optimal Dy3+ ion concentration was determined as 10 mol%. The critical energy transfer distance was calculated as 14 Å. The concentration quenching mechanism of Dy3+ was investigated in details. The temperature effect on photoluminescence was discussed in order to evaluate the thermal stability. The obtained results illustrate Ca3TeO6:Dy3+ was a new kind of yellow-emitting potential phosphor for WLEDs.

Correlation Between Uptake of 18F-FDG During PET/CT and Ki-67 Expression in Patients Newly Diagnosed With Multiple Myeloma Having Extramedullary Involvement.

The aim of this study was to evaluate the relationship of prognosis of patients with multiple myeloma having extramedullary involvement (EMM) with the 18F- fluorodeoxyglucose(18F-FDG) maximum standardized uptake value and the expression of Ki-67 in biopsy samples. Sixty-five patients were newly diagnosed with multiple myeloma presenting with EMM at our hospital from January 2005 to January 2015. Of these 65 patients, 20 were enrolled in this study. Over the last decade, both the maximum standardized uptake value and Ki-67 expression in these extramedullary lesions significantly correlated with progression-free survival, respectively ( P= .039, P =.009). After combining-the maximum standardized uptake value and the Ki-67 expression as an integral-there was a significant correlation between both the overall survival ( P = .027) and progression-free survival ( P= .014). Patients have poor outcomes when EMM is detected at presentation. Both the maximum standardized uptake value and Ki-67 expression could aid in accurately evaluating EMM patient prognosis.

Toxicity of exogenous antimony to the soil-dwelling springtail Folsomia candida.

Antimony (Sb) is a toxic pollutant, but data for Sb toxicity to springtails in soil are limited, and the effects of Sb speciation, soil physiochemical properties, and aging time on Sb toxicity have not been investigated. To address this, the effects of Sb on Folsomia candida were evaluated in laboratory studies. The results demonstrated that compared with Sb(III), no significant change in mortality was observed in Sb(V)-treated soil, but the EC50 value for the reproduction was 28-fold higher than that of Sb(III). Sb(III) toxicity was very different in four soils. The LC50 values for the survival were 2325-5107 mg kg-1 in the acute test and 605-2682 mg kg-1 in the chronic test, and the EC50 values for the reproduction were 293-2317 mg kg-1. The toxicity discrepancies were associated with the variations in oxidation potential and sorption capacity among corresponding soils. Toxicity significantly positively correlated with the clay and amorphous iron content but significantly negatively correlated with pH. Long-term aging markedly decreased Sb(III) toxicity, and the EC50 and LC50 values were unexpectedly higher than the highest test concentration in soil aged for 180 days. Sb(III) toxicity was probably modified more by oxidation than by changes in the available Sb fraction during aging.

Resveratrol Sensitizes Carfilzomib-Induced Apoptosis via Promoting Oxidative Stress in Multiple Myeloma Cells.

The proteasome inhibitor is a target therapy for multiple myeloma (MM) patients, which has increased the overall survival rate of multiple myeloma in clinic. However, relapse and toxicity are major challenges for almost all MM patients. Thus, there is an urgent need for an effective and less toxic combination therapy. Here, we demonstrated that a natural compound, resveratrol (RSV) displayed anti-proliferative activity in a dose- and time-dependent manner in a panel of MM cell lines. More importantly, a low concentration of RSV was synergistic with a low dose of the proteasome inhibitor carfilzomib (CFZ) to induce apoptosis in myeloma cells. Further studies showed that mitochondria was a key regulatory site after RSV/CFZ combination treatment. RSV induced the release of second mitochondria-derived activator of caspase (Smac) in a dose-dependent manner and kept the Smac in a high level after combination with CFZ. Also, RSV was additive with CFZ to increase reactive oxygen species (ROS) production. Moreover, a stress sensor SIRT1, with deacetylase enzyme activity, was remarkably downregulated after RSV/CFZ combination, thereby significantly decreasing its target protein, survivin in MM cells. Simultaneously, autophagy was invoked after RSV/CFZ combination treatment in myeloma cells. Further inhibition of autophagy could increase more ROS production and apoptosis, indicating a close linkage between autophagy and proteasome to modulate the oxidative stress. Together, these findings suggest that induction of multiple stress responses after RSV/CFZ combination is a major mechanism to synergistically inhibit MM cell growth and reduce the toxicity of CFZ in MM cells. This study also provides an important rationale for the clinic to consider an autophagy inhibitor for the combination therapy in MM patients.

The Wnt inhibitor LGK-974 enhances radiosensitivity of HepG2 cells by modulating Nrf2 signaling.

Nuclear factor (erythroid-derived 2)-like 2 (NRF2) is a master regulator of antioxidant and detoxification activities that can eliminate reactive oxygen species (ROS) produced via irradiation. However, Nrf2 overexpression in liver cancer cells may cause both radioresistance and chemoresistance. Reducing Nrf2 levels can enhance the radiosensitivity of HepG2 cells. Wingless/int-3A (Wnt3A) is a Wnt family protein that mainly activates the canonical Wnt signaling pathway. Recent studies showed that the Axin1-GSK-3ß protein complex, a component of the canonical Wnt signaling pathway, can capture Nrf2 and facilitate its ubiquitination and proteasomal degradation in the cytoplasm. This protein complex is degraded upon activation of the Wnt signaling pathway. In the present study, we treated HepG2 cells with the Wnt3A inhibitor LGK-974, an effective and specific PORCN inhibitor that can prevent the formation of a proper folding of the Wnt protein in the endoplasmic reticulum. We found that HepG2 cells became more sensitive to radiation with increasing LGK-974 concentrations. Upon 2 Gy or 4 Gy irradiation, the cells treated with LGK-974 more frequently underwent apoptosis and grew less rapidly. PCR and western blot results showed that inhibiting the secretion of Wnt3A blocked the Wnt signaling pathway and prevented Nrf2 signaling. Notably, the Wnt inhibitor may serve as a radiosensitizing drug.

Mesenchymal stem cells stimulate intestinal stem cells to repair radiation-induced intestinal injury.

The loss of stem cells residing in the base of the intestinal crypt has a key role in radiation-induced intestinal injury. In particular, Lgr5+ intestinal stem cells (ISCs) are indispensable for intestinal regeneration following exposure to radiation. Mesenchymal stem cells (MSCs) have previously been shown to improve intestinal epithelial repair in a mouse model of radiation injury, and, therefore, it was hypothesized that this protective effect is related to Lgr5+ ISCs. In this study, it was found that, following exposure to radiation, transplantation of MSCs improved the survival of the mice, ameliorated intestinal injury and increased the number of regenerating crypts. Furthermore, there was a significant increase in Lgr5+ ISCs and their daughter cells, including Ki67+ transient amplifying cells, Vil1+ enterocytes and lysozyme+ Paneth cells, in response to treatment with MSCs. Crypts isolated from mice treated with MSCs formed a higher number of and larger enteroids than those from the PBS group. MSC transplantation also reduced the number of apoptotic cells within the small intestine at 6 h post-radiation. Interestingly, Wnt3a and active ß-catenin protein levels were increased in the small intestines of MSC-treated mice. In addition, intravenous delivery of recombinant mouse Wnt3a after radiation reduced damage in the small intestine and was radioprotective, although not to the same degree as MSC treatment. Our results show that MSCs support the growth of endogenous Lgr5+ ISCs, thus promoting repair of the small intestine following exposure to radiation. The molecular mechanism of action mediating this was found to be related to increased activation of the Wnt/ß-catenin signaling pathway.

The Protective Effects of 5-Methoxytryptamine-α-lipoic Acid on Ionizing Radiation-Induced Hematopoietic Injury.

Antioxidants are prospective radioprotectors because of their ability to scavenge radiation-induced reactive oxygen species (ROS). The hematopoietic system is widely studied in radiation research because of its high radiosensitivity. In the present study, we describe the beneficial effects of 5-methoxytryptamine-α-lipoic acid (MLA), which was synthesized from melatonin and α-lipoic acid, against radiation-induced hematopoietic injury. MLA administration significantly enhanced the survival rate of mice after 7.2 Gy total body irradiation. The results showed that MLA not only markedly increased the numbers and clonogenic potential of hematopoietic cells but also decreased DNA damage, as determined by flow cytometric analysis of histone H2AX phosphorylation. In addition, MLA decreased the levels of ROS in hematopoietic cells by inhibiting NOX4 expression. These data demonstrate that MLA prevents radiation-induced hematopoietic syndrome by increasing the number and function of and by inhibiting DNA damage and ROS production in hematopoietic cells. These data suggest MLA is beneficial for the protection of radiation injuries.

Eight-year follow-up study of three individuals accidentally exposed to (60)Co radiation: Chromosome aberration and micronucleus analysis.

We assessed dose levels and the persistence of chromosomal aberrations and micronuclei in three individuals in the 8 year following accidental (60)Co radiation exposure. Venous blood samples were collected and used for analyses: traditional chromosome aberration (CA) measurement, G-banding, and the cytokinesis-block micronucleus (CBMN) assay. For CA analysis, we scored dicentric chromosomes (dic) and rings (r) in peripheral blood lymphocytes. The radiation doses (Gy) suffered by the individuals were estimated as: 1.79-2.43 (A), 2.36-2.86 (B), 1.58-1.82 (C), based on CA analysis; and 1.8-2.34 (A), 2.52-2.98 (B), 1.53-1.77 (C), based on CBMN frequencies. G-banding analysis was used to record translocations (t), inversions (inv), and deletions (del). Following the accident, unstable CAs reduced gradually, but stable aberrations persisted. Unstable CAs and CBMN may be valuable biomarkers for dose estimation shortly after high-dose radiation accidents, while stable aberrations may be more useful for assessing long-term effects.

A Fusion Protein of RGD4C and ß-Lactamase Has a Favorable Targeting Effect in Its Use in Antibody Directed Enzyme Prodrug Therapy.

Antibody directed enzyme prodrug therapy (ADEPT) utilizing ß-lactamase is a promising treatment strategy to enhance the therapeutic effect and safety of cytotoxic agents. In this method, a conjugate (antibody-ß-lactamase fusion protein) is employed to precisely activate nontoxic cephalosporin prodrugs at the tumor site. A major obstacle to the clinical translation of this method, however, is the low catalytic activity and high immunogenicity of the wild-type enzymes. To overcome this challenge, we fused a cyclic decapeptide (RGD4C) targeting to the integrin with a ß-lactamase variant with reduced immunogenicity which retains acceptable catalytic activity for prodrug hydrolysis. Here, we made a further investigation on its targeting effect and pharmacokinetic properties, the results demonstrated that the fusion protein retains a targeting effect on integrin positive cells and has acceptable pharmacokinetic characteristics, which benefits its use in ADEPT.

N-acetylcysteine relieves oxidative stress and protects hippocampus of rat from radiation-induced apoptosis by inhibiting caspase-3.

It has been recognized that radiation-induced effects remain a significant risk. An accumulation of reactive oxygen species (ROS) is considered to be one factor that contributes to neurodegenerative changes. The aim of our study was to investigate the potential radioprotective effects of NAC. Male Sprague-Dawley rats underwent radiation. Irradiation was performed at room temperature with a 4-Gy dose of radiation. A dose of N-acetylcysteine (NAC) was performed 15 min prior to irradiation intraperitoneally. The methods of immunohistochemistry, TUNEL staining, Nissl staining, qRT-PCR, analysis of reactive oxygen species and Western blot were performed. In conclusion, our results demonstrate that NAC inhibits apoptosis induced by irradiation via the inhibition of caspase-3. We demonstrated a decrease in caspase-3 mRNA that was present at 24h of NAC treatment. Such mRNA decrease was accompanied by a decrease of protein. In the present study, NAC effectively antagonized oxidation induced by irradiation. These results provide evidence that the neural protective effect and the antioxidant effect of NAC contribute to metabolic activity.

AP-2α downregulation by cigarette smoke condensate is counteracted by p53 in human lung cancer cells.

Cumulative findings have demonstrated that the dysregulation of tumor suppressor genes may be implicated in cigarette smoke-induced carcinogenesis. Activating enhancer-binding protein 2 (AP-2) is a eukaryotic transcriptional factor that plays a significant role in embryonic development and tumorigenesis. The vertebrate AP-2 family consists of AP-2α, AP-2ß, AP-2γ, AP-2δ and AP-2ε. Previous studies have suggested that cigarette smoking disrupts AP-2 regulation. In the present study, we investigated the effects of cigarette smoke condensate (CSC) on AP-2α expression in human lung cancer cell lines (NCI-H1299, NCI-H446 and A549), as well as the potential mechanisms involved. Using RT-qPCR, we found that CSC decreased AP-2α expression by suppressing its transcription in human lung cancer cell lines, particularly in p53-deficient NCI-H1299 cells. Western blotting and luciferase assays were implemented and we found that the restoration of p53 expression rescued the NCI-H1299 cells from CSC-induced AP-2α loss, while the silencing of p53 resulted in increased AP-2α loss induced by CSC, suggesting an antagonizing role of p53 in the regulation of AP-2α by CSC. Our results indicate that AP-2α downregulation may be involved in smoke-induced lung carcinogenesis.

Nested PCR for mtDNA-4977-bp deletion and comet assay for DNA damage - a combined method for radiosensitivity evaluation of tumor cells.

To identify an effective method of evaluating the radiosensitivity of human tumor cell lines in vitro, the present study adopted mtDNA-4977-bp deletion coupled with comet assay. The three human tumor cell lines applied were HepG2, EC-9706 and MCF-7. The surviving fraction (SF), ratio of the mtDNA-4977-bp deletion and DNA damage were detected by MTT assay, nested polymerase chain reaction (PCR) technique and comet assay, respectively. Clearly, lower SFs were found for the HepG2 and EC-9706 cells as compared with the MCF-7 cells following irradiation at doses of 2, 4 and 8 Gy, indicating a higher radiosensitivity for the HepG2 and EC-9706 cells. Additionally, no significant differences were identified in the mtDNA-4977-bp deletions found among HepG2, EC-9706 and MCF-7 cells by PCR following 1- or 4-Gy γ-ray irradiation, while increased deletion ratios of mtDNA-4977 bp were observed in HepG2 and EC-9706 cells following 8-Gy irradiation, in contrast to decreases in MCF-7 cells. The most notable differences among these three tumor cell lines were observed by comet assay following 8-Gy γ-ray irradiation. A combined method of nested PCR and comet assay, therefore, is the most effective and accurate method in evaluating the radiosensitivity of tumor cells.

Radioprotective effect of a pan-caspase inhibitor in a novel model of radiation injury to the nucleus of the abducens nerve.

There is increasing evidence that neuronal cell death occurs via extrinsic (death receptors) and intrinsic (mitochondria) pathways. Radiation induces caspase activation fundamentally via the mitochondrial pathway. Caspases are the key regulators of apoptosis. Healthy male Sprague­Dawley rats were used in the present study to examine the radioprotective effect of a type of pan-caspase inhibitor, z-VAD-fmk, following radiation, to investigate the effects of caspase blockade in a model of the nucleus of the abducens nerve. z-VAD-fmk was injected intracerebroventricularly as a bolus injection (0.2 µg/h for 1 h) into rats prior to exposure to radiation. Irradiation was conducted at room temperature at a dose of radiation of 4 Gy. The present study performed immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and western blot analysis and identified no significant changes in the expression of the X-linked inhibitor of apoptosis protein (XIAP) following radiation (P>0.05). As compared with the radiation alone group, the quantification of TUNEL-positive neurons was reduced in z-VAD­fmk-treated animals following radiation (P<0.01). Inhibition of caspase induced by z-VAD­fmk reduced the expression and activation of caspase-3, -8 and -9 (P<0.01). z-VAD-fmk effectively prevented radiation-induced apoptosis and this caspase inhibitor may be a potential therapeutic target in the treatment of brain radiation injury. The nucleus of the abducens nerve may be used as a radiation injury model, providing visual information and data on the apoptotic morphology of the abducens nucleus.