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GABA tea attenuates cardiac apoptosis in spontaneously hypertensive rats (SHR) by enhancing PI3K/Akt‐mediated survival pathway and suppressing Bax/Bak dependent apoptotic pathway.

Authors :
Chen, Bih‐Cheng
Hung, Meng‐Yu
Wang, Hsueh‐Fang
Yeh, Li‐Jen
Pandey, Sudhir
Chen, Ray‐Jade
Chang, Ruey‐Lin
Viswanadha, Vijaya Padma
Lin, Kuan‐Ho
Huang, Chih‐Yang
Source :
Environmental Toxicology; Jul2018, Vol. 33 Issue 7, p789-797, 9p
Publication Year :
2018

Abstract

Abstract: Cardiomyocyte apoptosis is the major risk factor for the development of heart failure (HF). The purpose of this study was to evaluate the effects of Gamma‐aminobutyric acid (GABA) tea on hypertension‐induced cardiac apoptotic pathways in spontaneously hypertensive rats (SHR). In order to reveal the mechanisms, 36 male SHR at eight weeks of age, 200 g were divided into six groups. One group was fed water as a control group. Other rats were administered one of the following treatments: GABA tea at dose 150 and 300 mg/kg/day as low GABA tea (LGT) and high GABA tea (HGT) groups, respectively, pure GABA at dose 150 and 300 mg/kg/day as LG and HG groups, respectively, green tea (GT) as control of LGT and HGT groups. After 12 weeks, cardiac tissues were analyzed by histological analysis, western blotting, and TUNEL assays. GABA tea, GT, and pure GABA decreased hypertension‐induced cardiac abnormalities, including abnormal myocardial architecture. In addition, GABA tea, GT, and pure GABA dramatically increased anti‐apoptotic protein, Bcl2. Furthermore, GABA tea, GT, and pure GABA also decreased activated‐caspase 9 and activated‐caspase 3. Additionally, the survival associated protein IGF‐I and PI3K/Akt were enhanced in cardiac tissues upon treatment. Our results showed an optimistic anti‐apoptotic and pro‐survival effects of GABA tea treatment against hypertensive rat hearts. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15204081
Volume :
33
Issue :
7
Database :
Complementary Index
Journal :
Environmental Toxicology
Publication Type :
Academic Journal
Accession number :
130417986
Full Text :
https://doi.org/10.1002/tox.22565