Oral administration of alcalase potato protein hydrolysate‐APPH attenuates high fat diet‐induced cardiac complications via TGF‐β/GSN axis in aging rats

Consumption of high fat diet (HFD) is associated with increased cardiovascular risk factors among elderly people. Aging and obesity induced‐cardiac remodeling includes hypertrophy and fibrosis. Gelsolin (GSN) induces cardiac hypertrophy and TGF‐β, a key cytokine, which induces fibrosis. The relation...

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Published in:Environmental toxicology 2019-01, Vol.34 (1), p.5-12
Main Authors: Hu, Wei Syun, Ting, Wei Jen, Tamilselvi, Shanmugam, Day, Cecilia Hsuan, Wang, Ting, Chiang, Wen‐Dee, Viswanadha, Vijaya Padma, Yeh, Yu Lan, Lin, Wan Teng, Huang, Chih Yang
Format: Article
Language:English
Subjects:
Ageing
Aging
Aging (artificial)
cardiac hypertrophy
Cardiovascular diseases
Cells
Diet
Fibrosis
Gelsolin
Geriatrics
Heart
High fat diet
High protein diet
Hypertrophy
Obesity
Older people
Oral administration
Potatoes
Proteins
Rats
Risk analysis
Risk factors
Serum
Subtilisin
TGF‐β
Therapeutic applications
Western blotting
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Summary:Consumption of high fat diet (HFD) is associated with increased cardiovascular risk factors among elderly people. Aging and obesity induced‐cardiac remodeling includes hypertrophy and fibrosis. Gelsolin (GSN) induces cardiac hypertrophy and TGF‐β, a key cytokine, which induces fibrosis. The relationship between TGF‐β and GSN in aging induced cardiac remodeling is still unknown. We evaluated the expressions of TGF‐β and GSN in HFD fed 22 months old aging SD rats, followed by the administration of either probucol or alcalase potato protein hydrolysate (APPH). Western blotting and Masson trichrome staining showed that APPH (45 and 75 mg/kg/day) and probucol (500 mg/kg/day) treatments significantly reduced the aging and HFD‐induced hypertrophy and fibrosis. Echocardiograph showed that the performance of the hearts was improved in APPH, and probucol treated HFD aging rats. Serum from all rats was collected and H9c2 cells were cultured with collected serums separately. The GSN dependent hypertrophy was inhibited with an exogenous TGF‐β in H9c2 cells cultured in HFD+ APPH treated serum. Thus, we propose that along with its role in cardiac fibrosis, TGF‐β also acts as an upstream activator of GSN dependent hypertrophy. Hence, TGF‐β in serum could be a promising therapeutic target for cardiac remodeling in aging and/or obese subjects.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22651