1.Effects of radiation injury on peripheral blood and liver NO concentration in mice.
Cheng-shan OU ; Li-hong JIANG ; Qing YE ; Mei-juan ZHOU
Journal of Southern Medical University 2008;28(8):1405-1406
OBJECTIVETo study the effect of radiation injury on nitric oxide (NO) concentration in mouse peripheral blood and liver.
METHODSNIH mice were subjected to gamma-ray exposure at 9.0 Gy and transferred immediately in room temperature condition. NO concentrations in the liver and peripheral blood were examined before and at different time points after the exposure.
RESULTSCompared to that before exposure, NO concentration in the peripheral blood and liver significantly increased after gamma-ray exposure. NO concentration in the peripheral blood began to increase 3 h after the exposure, but that in the liver increased till 6 h after the exposure.
CONCLUSIONRadiation can cause the increase of NO concentration in the peripheral blood and liver, but different tissues may exhibit different response intensities to radiation.
Animals ; Gamma Rays ; Liver ; metabolism ; radiation effects ; Male ; Mice ; Nitric Oxide ; blood ; metabolism ; Radiation Injuries, Experimental ; blood ; metabolism ; Time Factors
2.Effects of total body irradiation injury on the participation of dermal fibroblasts in tissue repair.
Ji-Fu QU ; Tian-Min CHENG ; Lin-Shui XU ; Chun-Meng SHI ; Xin-Ze RAN
Acta Physiologica Sinica 2002;54(5):395-399
Wound combined with total body irradiation (TBI) injury results in impairment of tissue repair and delayed processes of healing, so it has been considered as an important and representative model of impaired wound healing, but the mechanism is not fully clarified. Fibroblasts in wound are the most important cells participating in tissue repair, whereas its radiosensitivity is not high. To understand whether TBI injury has direct damaging effects on fibroblasts in wound, fibroblasts in wound combined with TBI injury and in wound of simple incision injury were isolated and cultured, and parameters associated with tissue repair were determined. The results showed that the abilities of proliferation, attachment and adhesion of fibroblasts isolated from wounds combined with TBI injury significantly decreased as compared with those of simple incision injury, nevertheless, apoptotic ratio of fibroblasts isolated from wounds combined with TBI injury increased significantly. These data suggest that TBI injury may cause direct damaging effects on fibroblasts in wounds, which might be one of the dominant reasons for impairment of wound healing when it is combined with TBI injury.
Animals
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Disease Models, Animal
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Fibroblasts
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metabolism
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physiology
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radiation effects
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Radiation Injuries, Experimental
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metabolism
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Rats
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Rats, Wistar
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Skin
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injuries
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Whole-Body Irradiation
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Wound Healing
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physiology
3.beta-irradiation (166Ho patch)-induced skin injury in mini-pigs: effects on NF-kappaB and COX-2 expression in the skin.
Joong Sun KIM ; Kyung Jin RHIM ; Won Seok JANG ; Sun Joo LEE ; Yeonghoon SON ; Seung Sook LEE ; Sunhoo PARK ; Sang Moo LIM
Journal of Veterinary Science 2015;16(1):1-9
In the present study, the detrimental effect of beta-emission on pig skin was evaluated. Skin injury was modeled in mini-pigs by exposing the animals to 50 and 100 Gy of beta-emission delivered by 166Ho patches. Clinicopathological and immunohistochemical changes in exposed skin were monitored for 18 weeks after beta-irradiation. Radiation induced desquamation at 2~4 weeks and gradual repair of this damage was evident 6 weeks after irradiation. Changes in basal cell density and skin depth corresponded to clinically relevant changes. Skin thickness began to decrease 1 week after irradiation, and the skin was thinnest 4 weeks after irradiation. Skin thickness increased transiently during recovery from irradiation-induced skin injury, which was evident 6~8 weeks after irradiation. Epidermal expression of nuclear factor-kappa B (NF-kappaB) differed significantly between the untreated and irradiated areas. One week after irradiation, cyclooxygenase-2 (COX-2) expression was mostly limited to the basal cell layer and scattered among these cells. High levels of COX-2 expression were detected throughout the full depth of the skin 4 weeks after irradiation. These findings suggest that NF-kappaB and COX-2 play roles in epidermal cell regeneration following beta-irradiation of mini-pig skin.
Animals
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Cyclooxygenase 2/genetics/*metabolism
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*Holmium
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Male
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NF-kappa B/genetics/*metabolism
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Radiation Injuries, Experimental/metabolism/*veterinary
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Skin/metabolism/*radiation effects
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Swine
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Swine, Miniature
4.The effects of Ligustrazine on the expression of bFGF and bFGFR in bone marrow in radiation injured mice.
Ning, WU ; Hanying, SUN ; Wenli, LIU ; Huizhen, XU ; Wu, LU
Journal of Huazhong University of Science and Technology (Medical Sciences) 2003;23(4):348-51
To study the expression of the bFGF and its receptor in the mouse bone marrow by treatment with acute radioactive injury and Ligustrazine, 56 mice were divided into 3 groups: normal group, radiation-injured group and Ligustrazine group. After irradiation by 6.0 Gy 60Co gamma-ray, each mouse was orally given 0.1 ml Ligustrazine twice a day for 13 days in Ligustrazine group, and each mouse in radiation injured group was orally given equal amount of saline. On the 3rd, 7th, 14th day after irradiation, bone marrow mono-nuclear cells (BMMNC) were counted, and the expression levels of bPGF and bFGFR in bone marrow were evaluated by immunohistochemistry and flow cytometry analysis respectively. On the 3rd, 7th, 14th day after irradiation, expression of bFGF in bone marrow were significantly lower than in normal group (P<0.05 or P<0.01). Expressions of bFGF and bFGFR were much higher in Ligustrazine treated group than that in the control group (P<0.05 or P<0.01). Ligustrazine potentiate the expression of bFGF and bFGFR in bone marrow MNC to recover the bone marrow hematopoiesis inductive microenvironment, which is one of the mechanisms by which Ligustrazine rebuild the bone marrow hematopoiesis after acute radioactive injury.
Bone Marrow Cells/metabolism
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Fibroblast Growth Factor 2/*biosynthesis
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Hematopoiesis/drug effects
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Pyrazines/*pharmacology
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Radiation Injuries, Experimental/*metabolism
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Radiation-Protective Agents/pharmacology
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Receptors, Fibroblast Growth Factor/*biosynthesis
5.Effect of radiation on the activity and expression of Ca(2+)-Mg(2+)-ATPase in rat masseter muscle.
Zhi-Min LI ; Xu-Chen MA ; Xing-Min QU ; Shou-Ping XU ; Lin MA
Chinese Journal of Stomatology 2009;44(8):479-482
OBJECTIVETo investigate the activity and expression of Ca(2+)-Mg(2+)-ATPase in irradiated rat masseter muscle.
METHODSThe rats were irradiated locally with a single dose of 20 Gy X-ray. The activities of Ca(2+)-Mg(2+)-ATPase were measured with colorimetric method. The protein expression of Ca(2+)-Mg(2+)-ATPase was determined by Western blotting and immunohistochemistry.
RESULTSThe activities of Ca(2+)-Mg(2+)-ATPase in masseter muscle decreased by approximately 20% and 40% in irradiated rats on days 3 and 30 postirradiation. There was significant difference in the expression of Ca(2+)-Mg(2+)-ATPase protein between irradiated and nonirradiated rats on day 30 postirradiation. Ca(2+)-Mg(2+)-ATPase protein was found in the cytoplasm of masseter muscle.
CONCLUSIONSThe decrease of ATPase activity played an important role in the cause of radiation-induced skeletal muscle injury, while there was no significant reduction in the expression of Ca(2+)-Mg(2+)-ATPase protein in irradiated rat masseter muscle.
Animals ; Blotting, Western ; Ca(2+) Mg(2+)-ATPase ; metabolism ; Cytoplasm ; enzymology ; Immunohistochemistry ; Masseter Muscle ; enzymology ; radiation effects ; Radiation Injuries, Experimental ; enzymology ; Rats
6.Expression of alpha-smooth muscle actin on experimental radiation nephropathy.
Dian-Ge LIU ; Bi-Cheng LIU ; Chun-Xia ZHANG
Chinese Journal of Pathology 2005;34(11):743-744
Actins
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metabolism
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Animals
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Creatinine
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blood
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Kidney
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pathology
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Kidney Diseases
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metabolism
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pathology
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Male
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Radiation Injuries, Experimental
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metabolism
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pathology
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Rats
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Rats, Wistar
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Vimentin
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metabolism
7.Protective effects of shikonin on brain injury induced by carbon ion beam irradiation in mice.
Lu GAN ; ; Zhen Hua WANG ; Hong ZHANG ; ; Rong ZHOU ; ; Chao SUN ; ; Yang LIU ; ; Jing SI ; ; Yuan Yuan LIU ; ; Zhen Guo WANG
Biomedical and Environmental Sciences 2015;28(2):148-151
Radiation encephalopathy is the main complication of cranial radiotherapy. It can cause necrosis of brain tissue and cognitive dysfunction. Our previous work had proved that a natural antioxidant shikonin possessed protective effect on cerebral ischemic injury. Here we investigated the effects of shikonin on carbon ion beam induced radiation brain injury in mice. Pretreatment with shikonin significantly increased the SOD and CAT activities and the ratio of GSH/GSSG in mouse brain tissues compared with irradiated group (P<0.01), while obviously reduced the MDA and PCO contents and the ROS levels derived from of the brain mitochondria. The shikonin also noticeably improved the spatial memory deficits caused by carbon ion beam irradiation. All results demonstrated that shikonin could improve the irradiated brain injury which might resulted from its modulation effects on the oxidative stress induced by the 12C6+ ion beam.
Animals
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Antioxidants
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pharmacology
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Brain Injuries
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prevention & control
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Catalase
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metabolism
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Heavy Ion Radiotherapy
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Male
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Malondialdehyde
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metabolism
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Mice
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Naphthoquinones
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pharmacology
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Protein Carbonylation
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Radiation Injuries, Experimental
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prevention & control
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Radiation-Protective Agents
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pharmacology
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Random Allocation
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Specific Pathogen-Free Organisms
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Superoxide Dismutase
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metabolism
8.Manganese superoxide dismutase gene transfection of mouse small intestinal epithelial cells protects them from radiation injury.
Hong-liang GUO ; Hong-wei ZHAO ; Zhong-fa XU ; Heng MA ; Xi-lin SONG ; Jie GUAN ; Zeng-jun LI ; Jin-ming YU
Chinese Journal of Oncology 2005;27(11):672-675
OBJECTIVETo investigate the protective effect of manganese superoxide dismutase (MnSOD) gene transfer to small intestinal epithelial cells from radiation injury.
METHODSHerpes simplex virus (HSV) vector containing both the human MnSOD and GFP genes was introduced into mouse small intestine. Expression of MnSOD by the intestinal villi was confirmed by nested RT-PCR, immunofluorescence and enzyme activity assay. Mice were then given various doses of irradiation over the abdomen. The height of intestinal villi was measured on histopathology sections by SZ-PT optical system before irradiation, 24 h and 72 h post-irradiation. All comparisons were performed by one-way analysis of variance using the SPSS statistical software to analyze the significance between groups.
RESULTSNested RT-PCR, immunofluorescence and enzyme activity assay of MnSOD demonstrated overexpression and increased activity of MnSOD in the inoculated intestine of mice. Control (sham inoculated) irradiated mice showed decreased villi height by 40.1%-59.3% on day 1 and 44.2%-65.1% on day 3 (7.5-15 Gy). Treatment of mice with HSV-MnSOD prior to radiation led to statistically significant radioprotection of the small bowel with mean villi height decreased by only 3.1%-12.4% on day 1 and 6.3%-29.1% on day 3.
CONCLUSIONThe results demonstrate that overexpression of human MnSOD via a replication defective herpes simplex viral vector is an effective method to protect the small intestine from damage caused by ionizing radiation.
Animals ; Epithelial Cells ; metabolism ; Genetic Therapy ; Genetic Vectors ; Intestine, Small ; metabolism ; Mice ; Radiation Injuries, Experimental ; prevention & control ; Simplexvirus ; genetics ; Superoxide Dismutase ; genetics ; Transfection
9.Expression of aquaporin-4 protein in rats with acute radiation-induced cerebral edema.
Jiao-de JIANG ; Zhi-ming MA ; Yu-sheng LIU
Journal of Central South University(Medical Sciences) 2008;33(3):252-256
OBJECTIVE:
To explore the relation between changes in expression of aquaporin-4(AQP4) protein and acute radiation-induced cerebral edema after Gamma knife radiation.
METHODS:
The experimental model was established in rats by radiating 2 mm right to median line in cerebral hemisphere with 50 Gy Gamma knife (the center located at the line of auditory canal). The changes of brain water content were measured by the wet and dry weight method. Immunohistochemistry was used to determine the change of expression of AQP4 protein at different periods after Gamma knife radiation.
RESULTS:
The brain water content and the expression of AQP4 in the target area and the peripheral zone obviously increased at 12 h after Gamma knife radiation, and achieved the peak after 2 d. It was still higher than normal after 14 d. The gray value of expression of aquaporin-4 was negatively related to brain water content (r=-0.9857, P<0.05).
CONCLUSION
AQP4 has a close relationship with acute radiation-induced cerebral edema.
Acute Disease
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Animals
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Aquaporin 4
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biosynthesis
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Brain Edema
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etiology
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metabolism
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Female
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Male
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Radiation Injuries, Experimental
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metabolism
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Radiosurgery
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Random Allocation
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Rats
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Rats, Sprague-Dawley
10.Increased Expression of EMMPRIN and VEGF in the Rat Brain after Gamma Irradiation.
Ming WEI ; Hong LI ; Huiling HUANG ; Desheng XU ; Dashi ZHI ; Dong LIU ; Yipei ZHANG
Journal of Korean Medical Science 2012;27(3):291-299
The extracellular matrix metalloproteinase inducer (EMMPRIN) has been known to play a key regulatory role in pathological angiogenesis. A elevated activation of vascular endothelial growth factor (VEGF) following radiation injury has been shown to mediate blood-brain barrier (BBB) breakdown. However, the roles of EMMPRIN and VEGF in radiation-induced brain injury after gamma knife surgery (GKS) are not clearly understood. In this study, we investigated EMMPRIN changes in a rat model of radiation injury following GKS and examined potential associations between EMMPRIN and VEGF expression. Adult male rats were subjected to cerebral radiation injury by GKS under anesthesia. We found that EMMPRIN and VEGF expression were markedly upregulated in the target area at 8-12 weeks after GKS compared with the control group by western blot, immunohistochemistry, and RT-PCR analysis. Immunofluorescent double staining demonstrated that EMMPRIN signals colocalized with caspase-3 and VEGF-positive cells. Our data also demonstrated that increased EMMPRIN expression was correlated with increased VEGF levels in a temporal manner. This is the first study to show that EMMPRIN and VEGF may play a role in radiation injuries of the central nervous system after GKS.
Animals
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Antigens, CD147/*metabolism
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Brain/blood supply/metabolism/pathology/*radiation effects
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Brain Injuries/metabolism/pathology
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Caspase 3/metabolism
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Gamma Rays/*adverse effects
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Immunohistochemistry
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Male
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Microscopy, Electron, Transmission
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Parietal Lobe/metabolism/pathology/radiation effects
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Radiation Injuries, Experimental/metabolism
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Radiosurgery/adverse effects
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Rats
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Rats, Wistar
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Time Factors
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Vascular Endothelial Growth Factor A/*metabolism