Inhibition of cardiac hypertrophy by probiotic-fermented purple sweet             potato yogurt in spontaneously hypertensive rat hearts.
Cardiovascular hypertrophy is a common feature of hypertension and an important risk factor for heart damage. The regression of cardiovascular hypertrophy is currently considered an important therapeutic target in reducing the omplications of hypertension. The aim of this study was to investigate the inhibition of cardiac hypertrophy by probiotic-fermented purple sweet potato yogurt (PSPY) with high γ-aminobutyric acid (GABA) content in spontaneously hypertensive rat (SHR) hearts. Six-week-old male SHRs were separated randomly and equally into 4 experimental groups: sterile water, captopril and 2 PSPY groups with different doses (10 and 100%) for 8 weeks. The changes in myocardial architecture and key molecules of the hypertrophy-related pathway in the excised left ventricle from these rats were determined by histopathological analysis, hematoxylin and eosin staining and western blot analysis. Abnormal myocardial architecture and enlarged interstitial spaces observed in the SHRs were significantly decreased in the captopril and PSPY groups compared with the sterile water group. Moreover, the increases in atrial natriuretic peptide, B-type natriuretic peptide, phosphorilated protein kinase Cα and calmodulin-dependent protein kinase II levels in the left ventricle were accompanied by hypertension and increases in phosphorylated extracellular signal-regulated kinase 5 activities with enhanced cardiac hypertrophy. However, the protein levels of the hypertrophic-related pathways were completely reversed by the administration of PSPY. PSPY may repress the activation of ANP and BNP which subsequently inhibit the dephosphorylation of the nuclear factor of activated T-cells, cytoplasmic 3 and ultimately prevent the progression of cardiac hypertrophy.
Department of Food and Nutrition, Providence University, Taichung,                     Taiwan, R.O.C.
Pei-Pei
PP
Lin
You-Miin
YM
Hsieh
Wei-Wen
WW
Kuo
Chien-Chung
CC
Lin
Fuu-Jen
FJ
Tsai
Chang-Hai
CH
Tsai
Chih-Yang
CY
Huang
Cheng-Chih
CC
Tsai
D000818:Animals; D000959:Antihypertensive Agents / Q000008:administration & dosage*; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D019703:Calcineurin / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism; D002216:Captopril / Q000008:administration & dosage; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006973:Hypertension / Q000150:complications / Q000178:diet therapy*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000517:prevention & control*; D007335:Insulin-Like Growth Factor II / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D027723:Ipomoea batatas / Q000737:chemistry*; D008297:Male; D048054:Mitogen-Activated Protein Kinase 7 / Q000378:metabolism; D050778:NFATC Transcription Factors / Q000378:metabolism; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D009929:Organ Size; D051571:Protein Kinase C-alpha / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D015014:Yogurt / Q000382:microbiology; D005680:gamma-Aminobutyric Acid / Q000008:administration & dosage
D000959:Antihypertensive Agents; D015850:Interleukin-6; D050778:NFATC Transcription Factors; D020097:Natriuretic Peptide, Brain; D005680:gamma-Aminobutyric Acid; D007335:Insulin-Like Growth Factor II; D009320:Atrial Natriuretic Factor; D002216:Captopril; D051571:Protein Kinase C-alpha; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D048054:Mitogen-Activated Protein Kinase 7; D019703:Calcineurin