| IntroductionRadiation-induced heart disease (RIHD) is severe sequelae of radiation for thoracic cavity and chest wall. RIHD usually may include acute/chronic pericarditis, accelerated atherosclerosis(such as coronary artery disease), conduction abnormalities, valvular changes, and, notably, pericardial and myocardial fibrosis. Radiation fibrosis is chain reacting process of pro-inflammatory factor and pro-fibrosis factor. These factors stimulate the proliferation of fibroblast, promote the startup of collagen gene, so as to result in fibrosis. Nuclear factor-kappaB is a ubiquitous transcription factor that can control and encode cytokines, growth factors, cell adhesion molecules, the chemical activator, a number of acute phase protein gene expression at health and various disease states. It is involved in a variety of inflammatory cytokines, chemotactic factors and fibrogenic cytokines synthesis, cell proliferation, extracellular matrix crosslinking and differentiation process of fibroblasts.Currently NF-kappaB in cardiac injury radiation have not been reported. The objects of this study are Sprague-Dawley rats. The treatment group received X-ray irradiation, while the control group did not receive X-ray irradiation. After 1 month, using the immunohistochemical method to determine the expression of NF-kappaB in radiation induced heart disease, using the computer image analysis system to quantitatively determine the immunohistochemical pigmentation, and investigating the internal relations between NF-kappaB and acute Radiation-induced heart disease, and its pathophysiologic role in the formation of radiation-induced heart disease.Materials and Methods1. Tissue Samples General level SD rats, male and female in half, weights about 180-220g,3 months of age, were purchased from Animal Center of China Medical University.1 month after intervention, rats were killed by chloral hydrate overdose anesthesia and their heart tissue was taken out, stored in-85℃refrigerator.2. ReagentsNF-kappaB polyclonal antibodies were purchased from Santa Cruze company in the USA. The residual immunohistochemical kits were purchased from Beijing Golden Bridge Biotechnology Company Ltd.3. MethodsUse the Sprague-Dawley rats as the study object, the treatment group received X-ray irradiation (irradiated 15Gy group, irradiated 18Gy group), while the control group did not receive X-ray irradiation. After 1 month the expression of NF-kappaB in the Radiation-induced heart disease was determined by immunohistochemical method, using the computer image analysis system to quantitatively determine the immunohistochemical pigmentation. Statistical data were expressed by mean±standard deviation, analyzed by using the SPSS 13.0 software, using ANOVA analysis to compare the two groups, normal data group was analyzed with LSD t-test, nonparametric test was followed when the heterogeneity of variance occur, P<0.05 was statistically significant.ResultsNon-irradiated group had a small amount of NF-kappaB expression, while the groups irradiated 15Gy and 18Gy had an increased expression of NF-kappaB. There was statistical difference of NF-kappaB expression between non-irradiation group and irradiation groups, the p values were 0.004,< 0.001. But there was no significant difference between the two irradiation groups, P> 0.05.Conclusions1. NF-kappaB is an important factor that can cause radiation-induced heart disease. As the radiation doses rise, the expression of NF-kappaB is more significant, the relationship between NF-kappaB and radiation induced heart disease is more closely. It plays an important pathophysiological role in the progress of radiation-induced heart disease.2. However, the NF-kappaB expression in acute radiation-induced heart disease has no significant difference between the two irradiation groups (P> 0.05). It may relate to the small sample size of this experiment (10,9), but may also relate to the length of the observation time and/or the dose of irradiation, but this requires further study and discussion.
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