Ghrelin Ameliorates Angiotensin II-Induced Myocardial Fibrosis by Upregulating Peroxisome Proliferator-Activated Receptor Gamma in Young Male Rats

Autor: Qian Wang, Pei-Yong Ma, Ping Yang, Tao Ding, Yong-Liang Teng, Rui Chen, Xin Sui, Dian-Jun Sui
Rok vydání: 2018
Předmět:
0301 basic medicine
Male
medicine.medical_specialty
Article Subject
medicine.medical_treatment
lcsh:Medicine
Peroxisome proliferator-activated receptor
030204 cardiovascular system & hematology
General Biochemistry
Genetics and Molecular Biology
Rats
Sprague-Dawley
Transforming Growth Factor beta1
03 medical and health sciences
0302 clinical medicine
In vivo
Internal medicine
Renin–angiotensin system
medicine
Animals
Cells
Cultured
chemistry.chemical_classification
General Immunology and Microbiology
Chemistry
Growth factor
Angiotensin II
Myocardium
lcsh:R
digestive
oral
and skin physiology
General Medicine
Fibroblasts
Fibrosis
Ghrelin
Rats
PPAR gamma
030104 developmental biology
Endocrinology
Myocardial fibrosis
hormones
hormone substitutes
and hormone antagonists
Transforming growth factor
Research Article
Zdroj: BioMed Research International
BioMed Research International, Vol 2018 (2018)
ISSN: 2314-6141
Popis: Angiotensin (Ang) II contributes to the formation and development of myocardial fibrosis. Ghrelin, a gut peptide, has demonstrated beneficial effects against cardiovascular disease. In the present study, we explored the effect and related mechanism of Ghrelin on myocardial fibrosis in Ang II-infused rats. Adult Sprague-Dawley (SD) rats were divided into 6 groups: Control, Ang II (200ng/kg/min, microinfusion), Ang II+Ghrelin (100μg/kg, subcutaneously twice daily), Ang II+Ghrelin+GW9662 (a specific PPAR-γinhibitor, 1 mg/kg/d, orally), Ang II+GW9662, and Ghrelin for 4 wks. In vitro, adult rat cardiac fibroblasts (CFs) were pretreated with or without Ghrelin, Ghrelin+GW9662, or anti-Transforming growth factor (TGF)-β1 antibody and then stimulated with or without Ang II (100 nmol/L) for 24 h. Ang II infusion significantly increased myocardial fibrosis, expression of collagen I, collagen III, and TGF-β1, as well as TGF-β1 downstream proteins p-Smad2, p-Smad3, TRAF6, and p-TAK1 (all pγexpressionin vivoandin vitro, and treatment with GW9662 counteracted the effects of Ghrelin. In conclusion, Ghrelin ameliorated Ang II-induced myocardial fibrosis by upregulating PPAR-γand in turn inhibiting TGF-β1signaling.
Databáze: OpenAIRE
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