Τόμος 24 (2006) – Τεύχος 1 – Άρθρο 1 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Ελληνική Έκδοση – Volume 24 (2006) – Issue 1 – Article 1 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-Greek Edition

Από | | Άρθρο - Article, Β. Α. Κόκκας,Β.Α. Κokkas, Γεωργία Τσίντα, Georgia Tsinta, Κωνσταντίνος Λ. Παπαδόπουλος - Constantine L. Papadopoulos, Πλήρες Κείμενο στα Ελληνικά - Full Text in Greek
Τίτλος – Title

Σχέσεις Φλεγμονωδών και Αθηρωματικών Μηχανισμών. Ο Ρόλος των Υποδοχέων των Ενεργοποιούμενων από τον Πολλαπλασιαστή Υπεροξειδίων  (PPARs)

PPAR-Receptors and Inflammation
Συγγραφέας – Author

Βασίλης A. Κόκκας, Γεωργία Τσίντα και Κωνσταντίνος Λ. Παπαδόπουλος

Εργαστήριο Φαρμακολογίας και Β΄ Καρδιολογική Κλινική, Τμήμα Ιατρικής, Αριστοτέλειο Πανεπιστήμιο, Θεσσαλονίκη, Ελλάς

B.A. Kokkas, G. Tsinta and C.L. Papadopoulos

Departments of Pharmacology and 2nd Cardiol­ogy, Medical Scholl, Aristotle University, Thes­saloniki, Greece
Παραπομπή – Citation
Κόκκας,Β.Α., Τσίντα,Γ., Παπαδόπουλος,Κ.Λ. : Σχέσεις Φλεγμονωδών και Αθηρωματικών Μηχανισμών. Ο Ρόλος των Υποδοχέων των Ενεργοποιούμενων από τον Πολλαπλασιαστή Υπεροξειδίων  (PPARs), Επιθεώρηση Κλιν. Φαρμακολ. Φαρμακοκινητ. 24: 5-24 (2006)
Kokkas,B.Α., Tsinta,G., Papadopoulos,C.L. : PPAR-Receptors and Inflammation, Epitheorese Klin. Farmakol. Farmakokinet. 24: 5-24 (2006)
Ημερομηνία Δημοσιευσης – Publication Date
2006 – 2006
Γλώσσα Πλήρους Κειμένου –
Full Text Language

Ελληνικά – Greek
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Λέξεις κλειδιά – Keywords
Φλεγμονή, αθηρωμάτωση, μηχανισμοί, υποδοχείς ενεργοποιούμενοι από τον πολλαπλασιαστή υπεροξειδίων (PPARs)
Inflammation, atheromatosis, mechanisms, peroxisome proliferator-acti­vated receptors (PPARs)
Λοιποί Όροι – Other Terms

Άρθρο

Article
Περίληψη – Summary

Η αθηρωματώδης διαδικασία έχει σχεδόν όλα τα χαρακτηριστικά κλασσικής φλεγμονώδους αντίδρασης με όλες τις ανοσιακές απαντήσεις που συνοδεύουν αυτή. Στις αθηρωματικές αλλοιώσεις απαντούν πολλά δυνητικά αντιγόνα μεταξύ των οποίων περιλαμβάνονται μικροβιακά και ιικά τοιαύτα, καθώς και ενδογενείς πρωτεΐνες. Κυρίαρχη θέση ανάμεσα σε αυτά έχει η οξειδωθείσα LDL μαζί με πολλά επιτόπιά της. Οι πυρηνικοί υποδοχείς οι ενεργοποιούμενοι από τον πολλαπλασιαστή υπεροξειδίων (PPARs) τροποποιούν τις κυριώτερες μεταβολικές διαταραχές που προδιαθέτουν στην εμφάνιση και στην εξέλιξη της αθηρωμάτωσης, όπως δυσλιπιδαιμία και αντίσταση στην ινσουκλίνη που συνδυάζεται με την παχυσαρκία και τον σακχαρώδη διαβήτη τύπου ΙΙ. Ως εκ τούτου, οι υποδοχείς αυτοί παίζουν βασικό ρόλο παρεμβαλλόμενοι στους μηχανισμούς που έχουν σχέση με τους παράγοντες αυτούς. Αντιλιπιδαιμικά φάρμακα, όπως οι φιβράτες και φάρμακα που δρουν ενάντια στην αντίσταση στην ινσουλίνη, όπως οι γλιταζόνες, είναι γνωστό ότι ασκούν τις ενέργειες αυτές διεγείροντας τους PPARα και  PPARγ αντίστοιχα. Σύμφωνα με νεώτερα δεδομένα, οι PPARs ελέγχουν κυτταρικές λειτουργίες μέσω της ρύθμισης της έκφρασης γονιδίων σε διάφορα κύτταρα που εμπλέκονται στην αθηρωμάτωση, όπως είναι τα μονοκύτταρα, τα μακροφάγα και τα αφρώδη κύτταρα. Ως εκ τούτου, η φαρμακολογική τροποίηση της έκφρασης των γονιδίων αυτών στα ανωτέρω κύτταρα αποτελεί πολύ ενδιαφέρουσα στρατηγική η οποία αποσκοπεί τόσο στην προστασία όσο και στη θεραπεία των διαφόρων φλεγμονωδών παθήσεων, συμπεριλαμβανόμενης και της αθηρωμάτωσης.

Atherosclerotic process has nearly all of the characteristics of a classic inflammatory response with its attendant immune responses. Many potential antigens exist in the atherosclerotic lesion including bacterial and viral ones as well as endogenous proteins. Chief among such antigens is oxidized LDL with its many neoepitopes. PPARs modulate the major metabolic disorders predis­posing to atherosclerosis like dislipidemia and in­sulin resistance associated with obesity and type II diabetes and thus play a major protective role by interfering with mechanisms related to the above factors. Antilipidemic drugs like fibrates and drugs that are used against insulin resistance like glita­zones is known that exert their actions by stimu­lating PPARα and PPARγ correspondingly. Recent data suggest that PPARs activated receptors con­trol cellular functions by regulating gene expres­sion in different cell types implicated in atheroscle­rosis including monocytes, macrophages and foam cells. Pharmacological modulation of these cells gene expression therefore represents an important strategy for the prevention and treatment of in­flammatory related diseases such as atherosclero­sis.
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