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Expression of 8-hydroxy-2-deoxy guanosine, thioredoxin reductase 1 and glutathione peroxidase 1 in myocardium of autopsy patients with Keshan disease / 中国地方病学杂志
Chinese Journal of Endemiology ; (6): 631-634, 2012.
Artículo en Chino | WPRIM | ID: wpr-642867
ABSTRACT
Objective In this study,we investigated the relationship between oxidative stress,selenoproteins level and onset of Keshan disease (KD) through detecting the expression of 8-hydroxy-2-deoxy guanosine (8-OH-dG),thioredoxin reductase 1 (TrxR1) and glutathione peroxidase 1 (GPx1) in myocardial tissue.Methods Myocardium samples of autopsy patients including 8 cases of KD (KD group included 4 acute KD and 4 chronic KD) and 9 cases of non-KD (control group) were immunohistochemically stained for 8-OH-dG,TrxR1 and GPx1.The staining intensities subsequently quantified by using Olympus Image-Pro Plus 6.0 software.Results The positive rate of 8-OH-dG expression in myocardial nuclei was higher in the case group[(68.6 ± 20.4)%] than that of the control group[(2.4 ± 1.5)%,t =8.515,P < 0.05].In addition,the positive rate of 8-OH-dG expression in acute KD[(91.7 ± 3.7)%] was significantly higher than that of chronic KD[(53.2 ± 7.9)%,t =6.409,P<0.05].The distribution of TrxR1 and GPx1 was not associated with the distribution of myocardial damage.The expression of these two selenoproteins in KD group (401340 ± 59865,497590 ± 197082) were both lower than that of control group(2790300 ± 379298,1348400 ±615840; t =-28.493,-6.016,respectively,all P<0.01).Conclusions Oxidative damage is detected in myocardium tissue of KD,and 8-OH-dG expression is associated with the degree of myocardial damage in KD.Selenoproteins,TrxR1 and GPx1,may be closely related to the pathogenesis of KD.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Endemiology Año: 2012 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Endemiology Año: 2012 Tipo del documento: Artículo