Periostin expression induced by oxidative stress contributes to myocardial fibrosis in a rat model of high salt-induced hypertension

Wu,Han; Chen,Liang; Xie,Jun; Li,Ran; Li,Guan‑Nan; Chen,Qin‑Hua; Zhang,Xin‑Lin; Kang,Li‑Na; Xu,Biao

doi:10.3892/mmr.2016.5308

Periostin expression induced by oxidative stress contributes to myocardial fibrosis in a rat model of high salt-induced hypertension

Authors:
- Han Wu
- Liang Chen
- Jun Xie
- Ran Li
- Guan‑Nan Li
- Qin‑Hua Chen
- Xin‑Lin Zhang
- Li‑Na Kang
- Biao Xu
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Affiliations: Department of Cardiology, Drum Tower Hospital, Nanjing University Medical School, Nanjing, Jiangsu 210008, P.R. China, Department of Gynaecology and Obstetrics, Drum Tower Hospital, Nanjing University Medical School, Nanjing, Jiangsu 210008, P.R. China
Published online on: May 19, 2016 https://doi.org/10.3892/mmr.2016.5308
Pages: 776-782
Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Periostin is an extracellular matrix protein involved in fibrosis. The present study investigated the importance of periostin in hypertension‑induced myocardial fibrosis. Rats were randomly divided into either the normal group (0.4% NaCl diet; n=8) or hypertension group (8% NaCl diet; n=8). For 36 weeks, the blood pressure and heart rate of the rats were monitored. At week 36, the hearts were extracted for further analysis. Masson's staining and western blotting were performed to determine the levels of periostin protein expression, oxidative stress and fibrosis. In addition, fibroblasts were isolated from adult rats and cultured in vitro, and following treatment with angiotensin II (Ang II) and N-acetyl-L-cysteine (NAC), western blotting, immunofluorescence and 2',7' dichlorodihydrofluorescin staining were performed to examine reactive oxygen species production, and periostin and α‑smooth muscle actin (α‑SMA) expression levels. The results demonstrated that periostin expression and oxidative stress were increased in hypertensive hearts compared with normal hearts. The in vitro experiments demonstrated that Ang II upregulated the expression levels of periostin and α‑SMA compared with the control, whereas, pretreatment with NAC inhibited oxidative stress, periostin and α‑SMA expression in fibroblasts. In conclusion, the results of the current study suggested that oxidative stress‑induced periostin is involved in myocardial fibrosis and hypertension. The present study demonstrated that periostin inhibition may be a promising approach for the inhibition of hypertension-induced cardiac remodeling.

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