Alarin alleviated cardiac fibrosis via attenuating oxidative stress in heart failure rats

Figures

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  Fig. 1. Alarin improved cardiac fibrosis in myocardial infarction (MI) induced heart failure (HF) rats. A alarin alleviated cardiac fibrosis in MI-induced HF rats. B alarin inhibited the increases of collagen I, collagen III, and transforming growth factor (TGF)-β in the heart of MI rats. The results are expressed as mean ± SEM. N = 10 for each group. *p < 0.05 versus the Sham + Saline group; #p < 0.05 versus the MI + Saline group

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  Fig. 2. Effects of alarin and galanin receptor antagonists. A Alarin 6-25 Cys (Ala6-25 Cys), an antagonist of alarin, reversed the attenuating effects of alarin on the increases of collagen I, collagen III and transforming growth factor (TGF)-β in the heart of myocardial infarction (MI) rats. B Galanin receptor antagonist M35 had no effect on the roles of alarin in inhibiting increases of collagen I, collagen III, and TGF-β in the heart of MI rats. C Galanin receptor antagonist C7 had no effect on the roles of alarin in inhibiting increases of collagen I, collagen III, and TGF-β in the heart of MI rats. D Alarin and galanin receptor antagonists alleviated cardiac dysfunction in myocardial infarction (MI) induced HF rats. The results are expressed as mean ± SEM. N = 8 for each group. *p < 0.05 versus the Sham + Saline (A, B and C) or Saline (D) group; #p < 0.05 versus the MI + Saline group; &p < 0.05 versus the MI + Alarin group

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  Fig. 3. Alarin alleviated cardiac fibroblasts (CFs) fibrosis induced by angiotensin (Ang) II. A Low dose had no effect, and middle and high doses of alarin inhibited the increases of collagen I, collagen III and transforming growth factor-β (TGF-β) mRNA levels in CFs induced by Ang II. B Alarin 6-25 Cys (Ala6-25 Cys), an antagonist of alarin, reversed the attenuating effects of alarin on the increases of collagen I, collagen III and transforming growth factor (TGF)-β induced by Ang II in CFs. C alarin attenuated the increases of collagen I, collagen III and TGF-β protein levels in CFs induced by Ang II. The results are expressed as mean ± SEM. *p < 0.05 versus the PBS group; #p < 0.05 versus the Ang II group

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  Fig. 4. Alarin alleviated the oxidative stress in the heart of myocardial infarction (MI) rats and in the cardiac fibroblasts (CFs) induced by angiotensin (Ang) II. A Alarin reversed the increases of NADPH oxidase (Nox) activity, superoxide anions and malondialdehyde (MDA), and the decrease of superoxide dismutase (SOD) activity levels in the heart of MI rats. B Alarin reversed the increases of NADPH (Nox) activity, superoxide anions and malondialdehyde (MDA), and the decrease of superoxide dismutase (SOD) activity levels induced by Ang II in CFs. The results are expressed as mean ± SEM. *p < 0.05 versus the Sham + Saline (A) or PBS (B) group; #p < 0.05 versus the MI + Saline (A) or Ang II (B) group

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  Fig. 5. NADPH oxidase 1 (Nox1) overexpression reversed the effects of alarin on inhibiting cardiac fibrosis. A Alarin inhibited the increase of Nox1 in cardiac fibroblasts (CFs) induced by angiotensin (Ang) II. B Nox1 expression was significantly increased by overexpression. C Nox1 overexpression reversed the effects of alarin on inhibiting the increases of collagen I, collagen III and transforming growth factor-β (TGF-β) mRNA levels in the heart of myocardial infarction (MI) rats. D Nox1 overexpression reversed the effects of alarin on inhibiting Ang II-induced increases of collagen I, collagen III and TGF-β mRNA levels in CFs. The results are expressed as mean ± SEM. *p < 0.05 versus the PBS (A) or Ad-GFP (B, C and D) group; #p < 0.05 versus the Ang II (A and C) or MI (B) group; &p < 0.05 versus the MI + Alarin (B) or Ang II + Alarin (C) group