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Objective To investigate the effect of rats'injuries and its mechanism caused by specific dose of radiation combined with decompression exposure.Methods 81 male SD rats were randomly divided into control group(n=9),radiation group(n=18),radiation+low-load decompression group(n=18),radiation+medium-load decompression group(n=18),and radiation+high-load decompression group(n=18).In addition to control group,the rats were irradiated with 60Co γ rays at 4 Gy and then underwent rapid escape experiments.The high-pressure exposure schemes were to stay underwater 57 m for 30 min,45 min or 60 min and reduce to normal pressure within(30±5)s,respectively.The high-pressure exposure was not carried out in radiation group.The behavior and death of rats in each group were observed 0.5 h after leaving the cabin.Blood(abdominal aorta)and lung tissues were collected at 3 h and 72 h,respectively.The changes of lung wet-dry weight ratio(W/D),lung pathology and serum levels of interleukin(IL)-1β,IL-6,tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD),malondialdehyde(MDA),nitric oxide(NO),intercellular adhesion molecule-1(ICAM-1)and thromboxane B2(TXB2)were analyzed.Results Compared with control group and radiation group,radiation+low-load decompression group showed no significant difference in the injury and death rate of rats(P>0.05),while radiation+medium-load decompression group and radiation+high-load decompression group showed significantly increase of the injury and death rate of rats(P<0.05).Compared with control group,other groups showed no significant change in pulmonary W/D at 3 h(P>0.05),and increased at 72 h(P<0.05).HE staining showed that compared with control group,radiation group showed mild lung interstitial edema,while radiation+low-load decompression group showed obvious pulmonary tissue edema and a small number of red blood cells exudated in the alveolar cavity.The edema,congestion and inflammatory cell infiltration of lung tissue were more serious in radiation+medium-load decompression group and radiation+high-load decompression group.Compared with control group and radiation group,all radiation+decompression groups showed an increase in serum levels of IL-1β,IL-6,TNF-α,MDA,NO,ICAM-1 and TXB2(P<0.05),and a decrease in SOD activity(P<0.05).Compared with radiation+low-load decompression group,radiation+medium-load decompression group and radiation+high-load decompression group showed increase in serum levels of IL-1β,IL-6,MDA,ICAM-1 and TXB2(P<0.05),and decrease in activity of SOD(P<0.05).Except for control group,serum levels of IL-1β,IL-6,TNF-α,MDA,NO,ICAM-1 and TXB2 were decreased at 72 h compared with 3 h(P<0.05),and SOD activity was increased at 72 h in all groups(P<0.05).Conclusions High-load decompression can increase the injury and death rate of rats exposed to radiation and high pressure.The potential mechanism of the combined injury effect of radiation and decompression was related to inflammation,immune stress,oxidative damage,vasomotor activity and coagulation mechanism.
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Objective To investigate the characteristic volatile organic compounds(VOCs)in exhaled breath and their diagnostic value in mice with early stage radiation injury.Methods The thermal desorption gas chromatography-mass spectrometry(TD-GC/MS)technique was used to analyze VOCs in exhaled breath of irradiated mice by 60Coγ-ray with 800 cGy.The characteristic VOCs in the early stage of radiation injury were identified,and a diagnostic model was established.Results The 30-day survival rate of mice was 4.2%.There were significant differences in characteristic VOCs at 7 hours after radiation injury,and thirty characteristic VOCs related to early-stage radiation injury were identified.The diagnostic value of differential metabolites in mice after irradiation was evaluated via the ROC curve,and the area under the ROC curve(AUC)of a single compound exceeded 0.8.The diagnostic model was constructed by screening 9 potential biomarkers of exhalation through Fisher discriminant analysis,and its sensitivity and specificity were close to 100%.Conclusion Analysis of VOCs in exhaled breath is expected to provide a non-invasive diagnostic method for early screening and diagnosis of radiation injury.
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OBJECTIVE To explore the protective mechanism of amifostine on acute radiation injury mice. METHODS Thirty C57BL/6J mice were randomly divided into normal control group, model group and amifostine group (150 mg/kg), with 10 mice in each group. Thirty minutes before irradiation, the mice in the amifostine group were intraperitoneally injected with amifostine; normal control group and model group were given constant volume of normal saline intraperitoneally; then acute radiation injury was induced by 4 Gy X-ray radiation in both model group and amifostine group. The white blood cell count (WBC), platelet count and red blood cell (RBC) count in mice were detected 2 hours before irradiation and on days 1, 4, 7, 10 and 14 after irradiation; the changes in the proportion of WBC (neutrophils, lymphocytes and monocytes) on the 7th day after irradiation were analyzed. The 16S rRNA high-throughput sequencing was used to analyze the structure of gut microbiota in mice feces on the 7th day after irradiation, then its correlation with WBC was analyzed. RESULTS The counts of WBC on the 1st, 4th, 7th and 10th day after irradiation, platelet count on the 10th day after irradiation and RBC count on the 1st day after irradiation in the amifostine group were significantly higher than those in model group (P<0.05). Compared with normal control group,β diversity of gut microbiome showed significant change, relative abundance of Firmicutes increased and that of Bacteroidetes decreased in model group. Amifostine could reverse the change in β diversity of gut microbiome, and the relative abundance of Bacteroidetes and Firmicutes. The model group consisted of four distinct species, namely Allobaculum, Erysipelotrichia, Erysipelotrichales and Erysipelotrichaceae, which were significantly negatively correlated with the proportion of peripheral blood lymphocytes (P<0.01); amifostine group consisted of two distinct species, namely Lactobacillus murinus and L. crispatus, which were significantly negatively correlated with the proportion of neutrophils (P<0.05). CONCLUSIONS Amifostine significantly improves irradiation-induced injury by regulating dysbiosis of LY201816) gut microbiota.
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Aim To investigate the protective effect of dimethyl fumarate on spleen injury induced by gamma radiation in mice and the related mechanism. Methods C57BL/6 mice were randomly divided into the blank control group, radiation model group and DMF administration group, which were administered once at 12 h before irradiation and once at 0. 5 h, 12 h, 24 h and 48 h after irradiation. The 30-day survival rate, body weight and pathological injury of spleen were measured after a one-time total body irradiation of Co 7 rays (8 Gy). TUNEL staining was used to detect apoptosis of spleen cells. Enzyme-linked immunoassay ( ELISA) was applied to detect the contents of TNF-a, IL-1 p, IL-6, IL-18, NLRP3 and AIM2 in spleen. Western blot test and immunofluorescence staining test was employed to verify the changes of NLRP3 and AIM2 contents in spleen tissue after irradiation. Results DMF could obviously improve the survival rate of irradiated mice, improve the weight loss of irradiated mice, re-duce the pathological injury of spleen, and inhibit the apoptosis of spleen cells after irradiation. ELISA results showed that DMF could significantly inhibit the increase of spleen inflammatory cytokines TNF-a, IL-lp, IL-6, IL-18 and inflammasome components NL-RP3 and AIM2 induced by irradiation. Western blot and tissue immunofluorescence staining also confirmed that DMF could inhibit the increase of NLRP3 and AIM2 inflammasome protein levels caused by irradiation. Meanwhile, NLRP3 agonist and AIM2 agonist could antagonize the radiation protection effect of DMF on spleen cells. Conclusion DMF can ameliorate spleen injury of Co 7-ray injured mice, and its mechanism is closely related to NLRP3/AIM2 inflamma-somes, which can be used as a potential protective drug for radiation injury.
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Objective To investigate the protective effect of berberine (BBR) against ionizing radiation injury in rats and its mechanism of action. Methods Sprague-Dawley rats were divided into seven groups: normal control group, 1-Gy radiation group, 1-Gy radiation plus low-dose BBR (50 mg/kg) group, 1-Gy radiation plus high-dose BBR (150 mg/kg) group, 3-Gy radiation group, 3-Gy radiation plus low-dose BBR (50 mg/kg) group, and 3-Gy radiation plus high-dose BBR (150 mg/kg) group. All the groups except the normal control group were exposed to external irradiation with a medical electron linear accelerator, followed by BBR administration by gavage for consecutive ten days. The serum levels of superoxide dismutase (SOD), reduced glutathione (GSH), and malondialdehyde (MDA) were measured by using the micromethod. The pathological changes of the bone marrow and small intestine were observed with HE staining. Results Compared with the normal control group, the radiation groups showed significantly increased MDA levels (P < 0.05), significantly decreased SOD and GSH levels (P < 0.05), and more severe pathological damage of the bone marrow and small intestine. Compared with the radiation groups, the BBR groups showed significantly decreased MDA levels (P < 0.05), significantly increased SOD and GSH levels (P < 0.05), and reduced pathological damage to the bone marrow and small intestine, which were more marked in the high-dose BBR group. Conclusion BBR has a certain protective effect against radiation injury in rats, which may be through increasing the activity of antioxidant substances, enhancing free radical clearance, and thereby alleviating free radicals-caused oxidative damage.
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Ionizing radiation can cause damage to biological macromolecules such as DNA and protein, resulting in a series of biological changes such as carcinogenesis, apoptosis and aging. However, after radiation injury, the lack of effective prevention and treatment targets leads to the limited variety of available therapeutic drugs. Recent studies suggest that mitochondria play an important role in radiation injury and are expected to become a new prevention and treatment target. This paper reviewed the effects of ionizing radiation on mitochondria, especially the occurrence of oxidative stress, and the role of mitochondria in radiation-induced biological effects, in order to discuss the feasibility of mitochondria as a potential target for radiation damage prevention and treatment.
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Pyroptosis is an inflammatory programmed cell death. Unlike apoptosis, pyroptosis is always accompanied by inflammation. It has been found that cell pyroptosis is closely related to the occurrence and development of many diseases. Pyroptosis also plays an important role in radiation injury caused by radiotherapy. Ionizing radiation breaks DNA in cells and induces oxygen free radicals, which are good inducers of pyroptosis. Therefore, this paper reviewed the research progress on the mechanism of cell pyroptosis in radiation injury from the perspective of relative signaling pathways, in order to provide new ideas for weakening or blocking radiation injury.
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Antecedentes: Las células madres intestinales generan las distintas estirpes celulares a dicho nivel. Estas se regulan por interacciones entre el epitelio y las células del nicho celular anexo. Estas se pueden ver dañadas en tratamientos con radiación, generando el síndrome gastrointestinal inducido por radiación. Se ha visto que células madre mesenquimales (MSC) y macrófagos de médula ósea (BMM) tienen propiedades de regeneración tisular. Objetivos: Evaluar la expresión génica de IL-4, Wnt6, VEGF y bFGF, a partir de cultivos celulares primarios independientes de MSC derivadas de tejido adiposo y BMM de ratones C57BL/6, por medio de PCR en tiempo real (qRT-PCR). Diseño experimental: A partir de un análisis in silico, se confeccionaron primers para evaluar la expresión génica de las moléculas propuestas, en los cultivos primarios por medio de qRT-PCR y electroforesis. Resultados y proyecciones: IL-4 y Wnt6 no son expresadas en las muestras de BMM y MSC. VEGF y bFGF son expresadas por diferentes células, dando expresión diferenciada. A futuro, se deben evaluar las mismas estirpes celulares en un ambiente inflamatorio y su efecto en la expresión génica, en especial VEGF y bFGF. Limitaciones: El número de moléculas en estudio es limitado y la expresión se evalúo solo a nivel genético.
Background: Intestinal stem cell generates diferents cellular types in their niche. They're regulated by interactions between epithelium and niche's cells, and can be damaged by medical radiation treatments causing radiation-induced gastrointestinal syndrome. It has seen that mesenchymal stem cells (MSC) d and bone marrow-derived macrophages (BMM) have propierties of tissular regeneration. Objectives: Determinated genetic expression of IL-4, Wnt6, VEGF and bFGF, in primary cellular cultures of MSC derivated of adipose tissue and BMM of C57BL/6 mice, through real time PCR (qRT-PCR). Methods: By an in silico analysis, we created primers to evaluate the proposed molecules in the primary cellular cultives, with qRT-PCR and electrophoresis. Results and projections: IL-4 and Wnt6 were not expressed in the MSC and BMM samples. VEGF and bFGF were expressed by different cells, giving differential expression. In the future, the same samples should be analyzed in an inflammatory environment, especially VEGF and bFGF. Limitations: The number of molecules are limited and the expression of them is only in a genetic level.
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Animals , Mice , Radiation Injuries , Biological Factors/genetics , Interleukin-4/genetics , Vascular Endothelial Growth Factor A/genetics , Wnt Proteins/genetics , Mesenchymal Stem Cells/radiation effects , Stem Cells/radiation effectsABSTRACT
Oral squamous cell carcinoma (OSCC) is the most frequent tumour in head and neck malignant. The current treatment is mainly based on surgery therapy, radiation therapy and chemical therapy. Meanwhile, there are many a defect in the treatment. For example, there are many defects in radiotherapy. Radioactive salivatitis is the most common. In addition, there are a series of changes such as dry mouth, oral mucositis, rampant dental caries, and radioactive osteomyelitis of jaw, which cause swallowing, chewing problems, and taste dysfunction. Currently, the research on radioactive salivatitis is progressing rapidly, but its mechanism is more complication. This paper review aims to summarize the research progress in this field.
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Humans , Carcinoma, Squamous Cell , Dental Caries , Head and Neck Neoplasms/radiotherapy , Mouth Neoplasms , Radiation Injuries , Salivary Glands , Xerostomia/etiologyABSTRACT
Nuclear energy is widely used in various fields such as military, medicine, scientific research, industry and agriculture.Nuclear accident may lead to radiation damage to the bodyofpractitioners. At present, the treatment of severe bone marrow radiation sickness is still not ideal.Exosomes are small vesicles with a size of 30-130 nm secreted by living cells and carry a variety of active substances including protein, RNA, DNA, which isimportant medium of intercellular communication.The contents of exosomes can be used not only as biomarkers of radiation damage, but also for the treatment of radiation damage. This article reviewsthe research progress of the application of exosomes in radiological medicine and underlying mechanisms.
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Objective:To study the effect of fasting on 137Cs γ-ray radiation-induced intestinal injury in mice, and to explore the effect of fasting on fecal metabolites of mice through non-targeted metabolomics. Methods:C57BL/6 mice were divided into healthy control group, 9 Gy γ-ray whole body irradiation (WBI)/ 15 Gy γ-ray whole abdominal irradiation (WAI) group, fasting (24 h, 48 h, 72 h)+ 9 Gy WBI/ 15 Gy WAI group. After irradiation, the survival rate, spleen index and thymus index were calculated. C57BL/6 mice in non-target metabolism experiment were randomly divided into four groups: control group, fasting 24 h group, 15 Gy γ-ray WAI group, fasting 24 h + 15 Gy γ-ray WAI group, 6 mice in each group. After 15 Gy WAI, the feces of mice in each group were collected at 3.5 days for non-targeted metabolomics detection.Results:The median survival time of mice with 48 h and 24 h fasting before 9 Gy γ-ray irradiation was increased by 1 day and 4 days, and the survival rates of mice treated with 48 h and 24 h fasting before 15 Gy WAI were 16.67% and 25%, respectively. 15 Gy γ-ray WAI on mice with fasting for 24 h before irradiation could increase the body weight ( t=2.338, P=0.042) and spleen index ( t=2.289, P=0.045) at 3.5 days after irradiation. Through non-targeted metabonomic analysis, it was found that there were 30 differentially expressed metabolites in fecal samples of fasting and non-fasting mice subjected to WAI, and metabolic pathway enrichment analysis showed that there was an imbalance in the metabolic pathway of steroid biosynthesis. Conclusions:Fasting before irradiation can improve the survival rate of mice with intestinal radiation injury and change their intestinal metabolites, suggesting that pre-irradiation fasting or short-term dietary nutrition changes are involved in the regulation of intestinal radiation damage.
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Objective:To investigate the effect of ionizing radiation on the N 6-methyladenine (m 6A) modification profile of circular RNA (circRNA) in mouse bone marrow cells and provide scientific basis for revealing the relationship between RNA epigenetic modification and hematopoietic radiation injury. Methods:A total of twenty four C57BL/6 J mice were randomly divided into two groups: the healthy control group ( n=12), and ionizing radiation group ( n=12) irradiated in total body with 4 Gy of 137Cs γ-rays. At 5 min after irradiation, mice were killed and bone marrow cells were collected from the femur. Total RNAs were extracted and the changes in circRNA m6A modification profiles were investigated by RNA immunoprecipitation-high-throughput sequencing (MeRIP-Seq) technology and bioinformatics analysis. The representative alterations of m 6A peaks were validated by MeRIP-PCR assay. Results:325 and 455 m 6A sites were identified on circRNAs in the healthy control group and ionizing radiation group (178 common sites, 147 specific sites in the healthy control group and 277 specific sites in ionizing radiation group), respectively. 1 275 and 1 017 deriving genes of m 6A-circRNAs were identified in the healthy control group and ionizing radiation group (767 common genes, 508 specific genes in the healthy control group and 250 specific genes in ionizing radiation group), respectively. Compared with the control healthy group, 414 (178) m 6A peaks was significantly up- (down-) regulated in the ionizing radiation group( P < 10 -10; fold-change cut-off > 5). Moreover, Gene Ontology (GO) assay revealed that the deriving genes of circRNAs with differentially methylated m 6A sites between two groups involves various functions including chromatin regulation, ciliary transition fiber and poly (A)-specific ribonuclease activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) assay revealed that the deriving genes of circRNAs with differentially methylated m 6A sites between two groups included numerous pathways such as platelet activation, Fc γ R-mediated phagocytosis and B cell receptor signaling pathway. Conclusions:Ionizing radiation triggers rapid alterations in the m 6A modification profile of circRNA in mouse bone marrow cells. The deriving genes of differentially methylated circRNAs are associated with a variety of functions and signaling pathways of hematopoietic radiobiology.
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Objective:To retrospectively analyze the long-term survival (10-15 years) and late toxicity of nasopharyngeal carcinoma (NPC) patients after intensity-modulated radiotherapy (IMRT), aiming to provide reference for the optimal treatment of NPC.Methods:132 patients with NPC who were treated with IMRT in Sichuan Cancer Hospital from 2003 to 2009 were recruited. Among them, 3 patients were classified as stage Ⅰ, 22 cases of grade Ⅱ, 61 cases of grade Ⅲ, 43 cases of Ⅳ A and 3 cases of Ⅳ B, respectively. The median dose was 73.37Gy (66 to 85Gy), divided into 33 times. Twenty patients received radiotherapy alone, 112 cases of concurrent radiochemotherapy. The survival rate was calculated by Kaplan-Meier method and log- rank test. Univariate prognostic analysis was performed. Cox model was used to conduct multivariate prognostic analysis. The late radiation toxicity was evaluated by RTOG/EORTC criteria. Results:The median follow-up duration was 128 months (range, 3 to 191 months). The 10-and 15-year local control rates of NPC patients were 86.0% and 79.9%. The disease-free survival rates were 72.5% and 63.2%, and the overall survival (OS) rates were 65.2% and 57.1%. The local recurrence rate was 12.1%, and the distant metastasis rate was 16.7%. A total of 53 patients died, of whom 15 patients died of local recurrence, 20 patients died of distant metastasis and 18 patients died of other diseases (pneumonia, intracranial hemorrhage and accident, etc.). The 10-and 15-year non-tumor-related mortality rates were 11.3% and 13.6%. Univariate analysis showed that age, smoking habit, lactate dehydrogenase (LDH), T stage and clinical stage were the independent prognostic factors of OS in NPC patients. Multivariate analysis demonstrated that LDH, T stage and synchronous chemotherapy were the prognostic factors of OS in NPC patients. The incidence of gradeⅠ-Ⅱ late radiation injury (hearing impairment, dysphagia, dental caries and xerostomia) was 90.4%, and 8.5% for grade Ⅲ-Ⅳ late radiation injury (skin fibrosis, hearing impairment and radiation brain injury).Conclusions:The 10-and 15-year OS of NPC patients treated with IMRT is relatively high. With the prolongation of survival, the non-tumor-related mortality rate is increased. Distant metastasis is the main cause of treatment failure. The main late injuries include grade Ⅰ/Ⅱ hearing impairment, dysphagia, dental caries and xerostomia.
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Objective: The objective of the study was to investigate the radiation damage to125 I seeds implanted in canine gastric wall tissue. Materials and Methods: Eight beagles were randomly assigned to either the treatment or control group, with four beagles per group. For each beagle in the treatment group, six125 I seeds were implanted in the gastric wall in two rows, spaced at 1.0 cm, with a seed activity of 0.5 mCi and a half-life of 60.2 d. For each beagle in the control group, six 125 I seeds were similarly implanted as a cold source. After implantation, the beagles were scanned by computed tomography (CT) (slice thickness: 2 mm), the region of interest was labeled along the seed boundaries, and postoperative doses were verified. One beagle per group was sacrificed at the 1, 2, 3, and 4 half-lives to be used as gross specimens for observing histological and ultrastructural changes using light microscopy and electron microscopy, respectively. Results: Beagles from the treatment group who had125 I radioactive seeds implanted in their stomach walls had the most radiation damage after two half-lives, damage repair began after three half-lives, and the damage was stabilized and further repaired after four half-lives. In the control group, only mild inflammatory reactions were observed around the seeds. Conclusion: Appropriate and well-planned implantation of125 I radioactive seeds in beagle stomach walls is safe and reliable
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BACKGROUND: Radiation therapy is currently one of the main treatments for head and neck cancer. Radiation therapy can kill cancer cells, but it can also damage normal cells or tissues. OBJECTIVE: To summarize the research progress of the changed structure of radioactive salivary glands and repair in recent years. METHODS: PubMed database, Wanfang database and China Full-Text Journal Database were searched. The search terms were “salivary glands; radiation injury; histological change; cell therapy” in English and Chinese. The time range was from 1991 to 2020. By reading the title, abstract and full text, repetitive studies were excluded. Finally, 57 articles were summarized. RESULTS AND CONCLUSION: In the treatment of head and neck cancer patients, xerostomia caused by radioactive damage to salivary gland tissue is its typical chronic side effect. At present, it is believed that radiation will mainly affect the structure of salivary gland tissues and lead to the decline of its function, including changes in the structure of salivary glands and ducts, as well as changes in saliva secretion and excretion after blood vessel and nerve injury. However, the mechanism of radiation damage has not been pointed out. Studies have shown that stem cells derived from fat, bone marrow and human amniotic membrane epithelium can treat radiation-induced salivary gland damage, improve salivary secretion, and the transplanted cells can form secretory alveoli and duct structures in the body.
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Radioactive enteritis(RE)is one of the most serious and common complications of intestinal tract caused by radiotherapy for malignant tumors in abdominal cavity,pelvic cavity,or retroperitoneum.Involved intestinal diseases are widespread,complex,and persistent,which make treatment difficult and ineffective.Short bowel syndrome can develop in some serious cases.Gut flora is the largest and most complex micro-ecosystem in human body and has a wide range of functions.Studies have shown that intestinal flora plays an important role in radiation-induced RE.This article summarizes recent research advances in the relationship between RE and gut flora.
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Humans , Ecosystem , Enteritis , Gastrointestinal Microbiome , Neoplasms , Probiotics , Radiation InjuriesABSTRACT
OBJECTIVE@#To explore the protective effect of vitamin E (VE) against radiation injury of hippocampal neurons in mice and explore the possible mechanism.@*METHODS@#Cultured HT-22 and U251 cells with or without exposure to 8 Gy irradiation were treated with VE (200 μmol/L for 24 h), ferroptosis inhibitor (ferrostatin-1, 5 μmol/L for 24 h), apoptosis inhibitor (ZVAD-FMK, 2 μmol/L), or necroptosis inhibitor (100 μmol/L). MTT assay was used to evaluate the cell viability after the treatments, and reduced glutathione (GSH), malondialdehyde (MDA), lipid reactive oxygen species (lipid ROS), and intracellular iron ion levels were detected for assessment of ferroptosis. The mice exposed to 16 Gy irradiation with or without vitamin E (500 U/kg) treatment for 6 weeks were assessed for behavioral changes and cognitive functions using Morris water maze test.@*RESULTS@#Treatment with VE significantly promoted the cell survival following irradiation in HT-22 cells ( < 0.05) but not in U251 cells ( > 0.05). Ferrostatin-1, but not ZVAD or the necroptosis inhibitor, promoted the survival of HT-22 cells following the irradiation. Exposure to irradiation significantly increased ferroptosis-related oxidative stress level in HT-22 cells, manifested by decreased GSH level and increased MDA, lipid ROS and intracellular iron ion levels ( < 0.05); treatment with VE and ferrostatin-1 both obviously reversed radiation-induced ferroptosis-related oxidative stress in the cells ( < 0.05). In Morris water maze test, the mice with radiation exposure showed obviously increased exploration time and distance ( < 0.05), which were significantly decreased after treatment with VE ( < 0.05).@*CONCLUSIONS@#Vitamin E reduces radiation injury by inhibiting ferroptosis in the hippocampal neurons in mice.
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Animals , Mice , Ferroptosis , Hippocampus , Neurons , Radiation Injuries , Vitamin EABSTRACT
@#Gamma ray sources containing the iridium-192 isotope are widely used for industrial radiologic imaging. Irradiation causes biological damages and tissue injuries by the interaction of molecules in the body. The injury is correlated with the amount of energy absorbed. Peripheral nerves are more resistant to radiation injuries than other tissues because of their protected positions, low metabolic rates and low reproductive capabilities. We present here a 17-year-old male who had sciatic nerve denervation after handling a radioactive metal piece containing iridium-192 isotope that dropped accidentally from an industrial radiography machine. Although there are previous case reports of radiation injury after handling gamma ray projector inadvertently, this is the first case with sciatic nerve injury.
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Objective To analyze the effect of epigallocatechin-3-gallate (EGCG) in radiation induced esophagitis of model rabbit.Methods Thirty male New Zealand rabbits were randomly divided into EGCG group,saline group,blank group.The rabbits in EGCG and saline groups were irradiated with 6 MV X-rays.The blank group did not receive radiation.After irradiation,rabbits were given with 440 μmol/L EGCG or saline three times a day in continuous 5 days.The scores of pathological changes of esophagus were observed by optical microscope.The serum levels of interleukine-1 beta (IL-1β),interleukine-6 (IL-6),transforming growth factor-β (TGF-β) and tumor necrosis factor-α (TNF-α) were detected by enzyme linked immunosorbent assay.The expression levels of 67KD laminin receptor (67LR)was detected by immunohistochemistry.Results After treatment,the scores of pathological changes of esophagus in blank group,saline group,EGCG group were 0,3.9± 1.10 and 2.80±0.92,respectively.At different time points after drug treatment,the levels of serum inflammatory factors among three groups were significantly different (F=23.66-236.32,P<0.05).The expressions of 67LR in esophageal tissue of 3 groups were also significantly different (F=585.38,P<0.05).Conclusions EGCG reduced radiationinduced esophagitis in rabbits by decreasing the levels of serum inflammatory factors,which may be related to the expression of 67LR protein.
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Objective@#To analyze the effect of epigallocatechin-3-gallate (EGCG) in radiation induced esophagitis of model rabbit.@*Methods@#Thirty male New Zealand rabbits were randomly divided into EGCG group, saline group, blank group. The rabbits in EGCG and saline groups were irradiated with 6 MV X-rays. The blank group did not receive radiation. After irradiation, rabbits were given with 440 μmol/L EGCG or saline three times a day in continuous 5 days. The scores of pathological changes of esophagus were observed by optical microscope.The serum levels of interleukine-1 beta (IL-1β), interleukine-6 (IL-6), transforming growth factor-β (TGF-β) and tumor necrosis factor-α (TNF-α) were detected by enzyme linked immunosorbent assay. The expression levels of 67KD laminin receptor (67LR) was detected by immunohistochemistry.@*Results@#After treatment, the scores of pathological changes of esophagus in blank group, saline group, EGCG group were 0, 3.9±1.10 and 2.80±0.92, respectively. At different time points after drug treatment, the levels of serum inflammatory factors among three groups were significantly different (F=23.66-236.32, P<0.05). The expressions of 67LR in esophageal tissue of 3 groups were also significantly different (F=585.38, P<0.05).@*Conclusions@#EGCG reduced radiation-induced esophagitis in rabbits by decreasing the levels of serum inflammatory factors, which may be related to the expression of 67LR protein.