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 : | Effet du complexe Budésonide-Hydroxypropyl-B-Cyclodextrine sur la réponse inflammatoire de cellules A549. Importance de lhistone désacétylase |
Auteurs : | Sophie SECONDE, Auteur ; Marie-Paule Mingeot-Leclercq, Promoteur |
Type de document : | Travail de fin d'études |
Editeur : | Bruxelles : Institut Paul Lambin, 2020 |
Langues: | Français |
Index. décimale : | TFE - Biologie médicale |
Résumé : |
Chronic obstructive pulmonary disease is a disease that affects the pulmonary and alveolar tracts by creating breathing difficulties. It mainly affects smokers. The inhalation of cigarette smoke causes a massive supply of agents responsible of oxidative and inflammatory stress.
The treatments administered are bronchodilators, anti-inflammatory drugs and secretion fluidizers. Unfortunately, some people develop a form of cortico-resistance. Researchers have hypothesized that this resistance is due to the inhibition of the activity of histone deacetylase (HDAC2), an enzyme capable of preventing the transcription of the coding genes to produce inflammatory proteins. Restoring the activity of HDAC2 would therefore decrease corticosteroid resistance. As a first part of the study, we used HDAC2 inhibitors like trichostatin A to study the role or not of HDAC2 in corticosteroid resistance. IL-8 release was measured. The second part of the study consisted in comparing the effects of the BUD: HPBCD complex and BUD + HPBCD mixture on cells pre-treated or not with increasing concentration of trichostatin A and to TNF-α as inflammatory stressor. We showed that (1) the BUD + HPβCD mixture has a better protective effect as compared to the complex BUD: HPβCD with a greater decrease in the production of IL-8 induced by TNF-α (2) The inhibition of HDAC2 by increasing doses of a pharmacological inhibitor induced a decrease in the effect of the glucocorticoid ( budesonide) on IL-8 release but also on the effect of the complex, BUD: HPβCD or of the mixture BUD + HPβCD. Thus, the results confirm the role of HDAC2 inhibition in the loss of anti-inflammatory effect of budesonide. They question the interest of the BUD complex: HPβCD compared to the BUD + HPβCD mixture. |
Accès : | Identifiez-vous avant d'accéder au document électronique |
Disponible en ligne : | Oui |
Lieu du stage : | Unité de pharmacologie cellulaire et moléculaire (FACM)-Louvain Drug Research Institute (LDRI) |
Département : | Biologie médicale |
Documents numériques (1)
Ce document n'est visible qu'après identification
TFE biologie médicale Adobe Acrobat PDF |