title: [Effect of quercetin on proteasome activity in the aorta and heart tissues of spontaneously hypertensive rats].
abstract: To determine the role of proteasome proteolysis in the pathogenesis of hypertension, we have studied the proteolytic activity of the proteasome in the aorta and heart tissues of rats with spontaneous hypertension (line SHR), and used quercetin, the drug that can inhibit the activity of this multicatalytic complex. In the aorta of SHR, the activities of the proteasome were not significantly different from that observed in Wistar rats. At the same time, in the heart tissues the trypsin-like (at 40%, P > 0.05), and chymotrypsin-like (by 1.7 times, P < 0.03) activities were significantly less in SHR. Significant morphological changes (fibrosis of the left ventricle was 4.7%, aorta intima width was increased and heart weight index was higher by 21.6% (3.7 +/- 0.6 mg/g) compared with Wistar rats (2.9 +/- 0,4 mg/g, P < 0.004) were observed in these animals functional disorders (reduced stroke volume by 3 times (P < 0.0001), ejection fraction by 2.5 times (P < 0.0001), increased end diastolic pressure by 6.5 times (P < 0.005), end systolic pressure by 15% (P < 0.004)) were revealed. Pharmacological drug "Qvercetin" effectively inhibited trypsin-like and chymotrypsin-like proteasome activities in the aorta (2.7-fold (P < 0.005) and 2-fold (P < 0.003), correspondingly) and trypsin-like, and peptidyl-glutamyl peptide-hydrolyzing-like activities (2.4-fold, P > 0.05 and 9.3-fold, P < 0.02, correspondingly) activities in the heart, leading to a significant improvement of morphological and functional parameters of the heart. Whereas the drug "Qvercetin" that is widely used in clinical practice (especially in therapy of acute myocardial infarction) it could be recommended for the use in prevention of cardiac remodeling with high level of blood pressure.
authors.forename: S V
authors.initials: SV
authors.lastname: Honcharov
authors.forename: H V
authors.initials: HV
authors.lastname: Portnichenko
authors.forename: L V
authors.initials: LV
authors.lastname: Tumanovs'ka
authors.forename: D O
authors.initials: DO
authors.lastname: Pashevin
authors.forename: M O
authors.initials: MO
authors.lastname: Kuz'menko
authors.forename: O O
authors.initials: OO
authors.lastname: Moĭbenko
authors.forename: V Ie
authors.initials: VIe
authors.lastname: Dosenko
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D002918:Chymotrypsin / Q000037:antagonists & inhibitors / Q000378:metabolism; D005355:Fibrosis; D006352:Heart Ventricles / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D008297:Male; D046988:Proteasome Endopeptidase Complex / Q000187:drug effects* / Q000378:metabolism; D011794:Quercetin / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D013318:Stroke Volume / Q000187:drug effects; D014357:Trypsin / Q000378:metabolism
chemical_list: D000975:Antioxidants; D011794:Quercetin; D002918:Chymotrypsin; D014357:Trypsin; D046988:Proteasome Endopeptidase Complex