Login
Communauté Vinci
Extérieur
Si votre nom d'utilisateur ne se termine pas par @vinci.be ou @student.vinci.be, utilisez le formulaire ci-dessous pour accéder à votre compte de lecteur.
Titre : | The role of mitochondrial oxidative stress for cardiac remodeling in chronic kidney disease |
Auteurs : | Mallaurie WAUMAN, Auteur ; Leticia Prates Roma, Promoteur |
Type de document : | Travail de fin d'études |
Editeur : | Bruxelles : Institut Paul Lambin, 2020 |
Langues: | Français |
Index. décimale : | TFE - Biologie médicale |
Résumé : |
Chronic kidney disease (CKD) is recognized as an important disease in terms of public health. It causes a gradual and irreversible damage to the kidney capacity. The diagnosis is based on proteinuria, albuminuria and estimated glomerular filtration rate (eGFR). According to the eGFR and the ratio albumin/creatinine, kidney diseases can be classified in 5 stages. One of the consequences of CKD is cardiac remodeling. Indeed, some studies have shown that left ventricular hypertrophy and cardiac fibrosis are often present in patients suffering of this disease. This can be caused by several mechanisms but in this study we investigate the role of mitochondrial oxidative stress which is defined by an imbalance between the reactive oxygen species (ROS) and antioxidants. The ROS, such as anion superoxide (O2●-), hydrogen peroxide (H202) can be produced by the mitochondria and more precisely at the level of complexes I and III of the electron transport chain.
The aim of this study is to understand the mechanism behind cardiac remodeling by analysing some biomarkers of oxidative stress, such as Nrf2, Prx3, SOD1 and SOD2, catalase and HO-1. We extracted heart tissue from two types of mice. We performed western blots analysis on SOD1 and HO-1 proteins and quantified the bands before doing a normalization. In preliminary results, we saw that the results in both type of mice from the western blot of catalase were not the same. Indeed, in Sv129 mice, the relative expression of catalase is higher in control mice than the one fed with adenine. For the Bl6N mice, the results are the same in control mice and the one fed with adenine. Regarding the results of SOD2, the relative expression Bl6N mice is higher in adenine mice than control mice. In Sv129 mice, the results are more or less the same. On the one hand, the results of SOD1 in the three experiments were not the same. In the first experiment, SOD1 is weaker in Sv129 mice fed with adenine and it is higher in Bl6N mice fed with adenine. For the second experiment, it was the opposite of the first experiment. In the third experiment, SOD1 was weaker in Sv129 mice fed with adenine. On the other hand, for the results of HO-1, we saw in both types of mice fed with adenine that the relative expression was higher than in the control mice. In conclusion, we can say the expression of HO-1 show a higher expression in mice with CKD. However, because of the lack of results and the opposing results in SOD1, we cannot say we see a real difference between mice with CKD and the others. We need to redo the experiments to confirm all the results. |
Accès : | Identifiez-vous avant d'accéder au document électronique |
Disponible en ligne : | Oui |
Lieu du stage : | Center forIntegrative Physiology and Molecular Medicine (CIPMM) |
Département : | Biologie médicale |
Documents numériques (1)
Ce document n'est visible qu'après identification
TFE biologie médicale Adobe Acrobat PDF |