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Bioactive peptides attenuate cardiac apoptosis in spontaneously hypertensive rat hearts through activation of autophagy and mitochondrial biogenesis pathway
Author(s) -
Lin Wan Teng,
Nithiyanantham Srinivasan,
Hsieh Dennis JineYuan,
Chen RayJade,
Day CeciliaHsuan,
Liao Jia Ying,
Kuo ChiaHua,
Mahalakshmi B.,
Kuo WeiWen,
Huang ChihYang
Publication year - 2020
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22916
Subject(s) - mitochondrial biogenesis , autophagy , downregulation and upregulation , apoptosis , microbiology and biotechnology , pi3k/akt/mtor pathway , mitochondrion , ampk , creb , chemistry , tfam , tunel assay , protein kinase b , biology , endocrinology , biochemistry , protein kinase a , phosphorylation , transcription factor , gene
Alcalase potato protein hydrolysate (APPH) might have a very important role in therapeutic effects. This study aims to examine the beneficial effects of bioactive peptides (DIKTNKPVIF [DI] and IF) from APPH supplement in the regulation of cardiac apoptosis, autophagy, and mitochondrial biogenesis pathway in spontaneously hypertensive rats (SHR). We have investigated ejection fraction, fractional shortening, Tunel assay, apoptosis, autophagy, and mitochondrial biogenesis pathway marker expression to show the efficacy of bioactive peptides in an SHR model. Bioactive peptides significantly upregulate ejection fraction and fractional shortening in SHR rats. SHR rats exhibited higher protein expression of apoptotic markers such as BAD, cytochrome c , and caspase 3. Finally, the bioactive peptides upregulate survival proteins (p‐AKT/p‐PI3K), autophagy (Beclin1/LC3B), and mitochondrial biogenesis (p‐AMPKα/SIRT1/PGC1α/p‐Foxo3a/Nrf2/CREB) marker expressions compared with the SHR groups. In summary, the bioactive peptides protect the heart tissues through the activation of autophagy and mitochondrial biogenesis pathway and thereby attenuate cardiac apoptosis in a spontaneously hypertensive rat model.