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

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.

β-catenin/LEF1/IGF-IIR Signaling Axis Galvanizes the Angiotensin-II- induced Cardiac Hypertrophy

“…Spontaneously hypertensive rats (SHR) 8-week-old (approx. 200 g), were acquired from the National Laboratory Animal Center (Taipei, Taiwan) and sustained following our previous protocol [10]. All animal experiments were performed in accordance with the Guide for the Care and Use of Laboratory Animals (National Institutes of Health Publication No.…”

Bioactive peptides attenuate cardiac apoptosis in spontaneously hypertensive rat hearts through activation of autophagy and mitochondrial biogenesis pathway

“…Previous findings reported that PDCD5 and Tadalafil protect from the cardiac remodeling in mice model . Besides, the Tunel assay revealed that the SHR group showed higher apoptotic cells . To determine the molecular mechanism, we examined the protein markers for apoptosis, antiapoptosis, cell survival, autophagy, and mitochondrial biogenesis.…”

“…In this study, SHR group showed upregulated caspase 3 and cytochrome c protein expression. Furthermore, the bioactive peptide‐treated SHR groups attenuated cardiac apoptosis through the enhancement of survival protein expressions (PI3K/Akt) …”

Potential mechanisms of Guizhi decoction against hypertension based on network pharmacology and Dahl salt-sensitive rat model

“…HIF-1 is the chief hypoxia-regulated transcription factor that can regulate cellular responses under hypoxic and ischemic conditions [55,56]. The PI3K/AKT pathway plays a seminal role in regulating multiple biological effects, including cell growth and proliferation, apoptosis, and angiogenesis [57]. The PI3K/AKT pathway The protein expression levels of IL-6, CCL2, and IL-1β in the left ventricle were evaluated by western blot analysis.…”