Baicalein attenuates angiotensin II-induced cardiac remodeling via inhibition of AKT/mTOR, ERK1/2, NF-κB, and calcineurin signaling pathways in mice

American Journal of Hypertension

Volumn 28, Issue 4, 2015, Pages 518-526

  Wang, Ai Wu ^a   Song, Lina ^b   Miao, Jie ^c   Wang, Hong Xia ^b   Tian, Cui ^b   Jiang, Xue ^b   Han, Qiu Yue ^b   Yu, Liqing ^d   Liu, Ying ^e   Du, Jie ^b   Xia, Yun Long ^e   Li, Hui Hua ^e  

^a SHANDONG PROVINCIAL HOSPITAL AFFILIATED TO SHANDONG UNIVERSITY   (China)

^b CAPITAL MEDICAL UNIVERSITY   (China)

^c SHANDONG UNIVERSITY OF TRADITIONAL CHINESE MEDICINE   (China)

^d UNIVERSITY OF MARYLAND   (United States)

^e DALIAN MEDICAL UNIVERSITY   (China)

Author keywords

12 15 lipoxygenase; Angiotensin II; Baicalein; Blood pressure; Cardiac remodeling; Hypertension; Signaling pathways

Indexed keywords

1,4 DIAMINO 1,4 BIS(2 AMINOPHENYLTHIO) 2,3 DICYANOBUTADIENE; ANGIOTENSIN II; BAICALEIN; CALCINEURIN; CYCLOSPORIN A; CYTOKINE; EOSIN; HEMATOXYLIN; MALONALDEHYDE; MAMMALIAN TARGET OF RAPAMYCIN; MESSENGER RNA; MITOGEN ACTIVATED PROTEIN KINASE 1; PROTEIN; PROTEIN KINASE B; PYRROLIDINE DITHIOCARBAMATE; SODIUM CHLORIDE; TRANSCRIPTION FACTOR RELA; WHEAT GERM AGGLUTININ; WORTMANNIN; AUTACOID; CALCINEURIN INHIBITOR; FLAVANONE DERIVATIVE; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; LIPOXYGENASE INHIBITOR; MAPK1 PROTEIN, MOUSE; MITOGEN ACTIVATED PROTEIN KINASE 3; MTOR PROTEIN, MOUSE; TARGET OF RAPAMYCIN KINASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIHYPERTENSIVE ACTIVITY; ANTIINFLAMMATORY ACTIVITY; ARTICLE; CONTROLLED STUDY; DISEASE ASSOCIATION; ELEVATED BLOOD PRESSURE; EXPERIMENTAL HYPERTENSION; HEART DISEASE; HEART LEFT VENTRICLE EJECTION FRACTION; HEART MUSCLE CONTRACTILITY; HEART MUSCLE FIBROSIS; HEART PROTECTION; HEART VENTRICLE HYPERTROPHY; HISTOPATHOLOGY; IMMUNOHISTOCHEMISTRY; MACROPHAGE; MALE; MONOTHERAPY; MOUSE; MYOCARDITIS; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN EXPRESSION; REAL TIME POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; STAINING; T LYMPHOCYTE; WESTERN BLOTTING; WILD TYPE; ANIMAL; C57BL MOUSE; CHEMICALLY INDUCED; DISEASE MODEL; DRUG EFFECTS; ENZYME ACTIVATION; ENZYMOLOGY; FIBROSIS; GENE EXPRESSION REGULATION; GENETICS; HEART LEFT VENTRICLE FUNCTION; HEART MUSCLE; HEART VENTRICLE REMODELING; HYPERTENSION; HYPERTROPHY, LEFT VENTRICULAR; METABOLISM; PATHOLOGY; PATHOPHYSIOLOGY; PHOSPHORYLATION; TIME;

ANGIOTENSIN II; ANIMALS; CALCINEURIN INHIBITORS; CYTOKINES; DISEASE MODELS, ANIMAL; ENZYME ACTIVATION; FIBROSIS; FLAVANONES; GENE EXPRESSION REGULATION; HYPERTENSION; HYPERTROPHY, LEFT VENTRICULAR; INFLAMMATION MEDIATORS; LIPOXYGENASE INHIBITORS; MALE; MICE, INBRED C57BL; MITOGEN-ACTIVATED PROTEIN KINASE 1; MITOGEN-ACTIVATED PROTEIN KINASE 3; MYOCARDIUM; NF-KAPPA B; OXIDATIVE STRESS; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION; TIME FACTORS; TOR SERINE-THREONINE KINASES; VENTRICULAR FUNCTION, LEFT; VENTRICULAR REMODELING;

EID: 84926658626     PISSN: 08957061     EISSN: 19417225     Source Type: Journal    
DOI: 10.1093/ajh/hpu194     Document Type: Article

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