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GW24-e3626 Effects of prescription of Jiashen on TGF-beta/Smads pathway after myocardial infarction in rats
  1. Xiaoli Nan,
  2. Youping Wang,
  3. Shiyang Xie,
  4. Bin Li,
  5. Mingjun Zhu
  1. First Affiliated Hospital, Henan University of Traditional Chinese Medicine

Abstract

Objectives This study was designed to study the effect of PJS on TGF-β/Smads pathway after MI in rats.

Methods Male Sprague-Dawley rats (9-10 weeks) were subjected to sham-MI or MI by ligating the left anterior descending coronary artery for 1 and 4 weeks. The rats were divided into five groups: sham, MI, PJS (3 g/kg/day), PJS (6 g/kg/day), and losartan (an AT1 antagonist, 10 mg/kg/day). The vehicle, PJS, or losartan was given by oral gavage once a day after MI. The expressions of TGF-β1, p-smad2, p-smad3 in the myocardium were assayed using Western-blot at 1 week or 4 weeks after MI.

Results At 1 week after MI, administration of PJS (3 or 6 g/kg/day) attenuated the increases in myocardial expression levels of TGF-β1, p-smad2 and p-smad3 compared with MI group (TGF-β1: 1.21 ± 0.06 or 1.06 ± 0.03 vs.1.37 ± 0.09,p < 0.0 5; p-smad 2: 1.88 ± 0.04 or 1.52 ± 0.11 vs. 2.09 ± 0.24,p < 0.05; p-smad3: 0.83 ± 0.01 or 0.5 ± 0.02 vs. 1.05 ± 0.120, p < 0.05). The greater effect was achieved at a dose of 6 g/kg/day. Losartan treatment also inhibited the increases in myocardial expression levels of TGF-β1, p-smad2 and p-smad3 compared with MI group (TGF-β1: 0.58 ± 0.03 vs. 1.37 ± 0.09, P < 0.05; p-smad2: 1.27 ± 0.02 vs. 2.09 ± 0.24, P < 0.05; p-smad3: 0.23 ± 0.01 vs.1.05 ± 0.12, P < 0.05). At 4 week after MI, administration of PJS (3 or 6 g/kg/day) attenuated the increases in myocardial expression levels of TGF-β1, p-smad2 and p-smad3 compared with MI group (TGF-β: 0.58 ± 0.03 or 0.69 ± 0.02 vs. 0.78 ± 0.01, p < 0.0 5; p-smad 2: 0.57 ± 0.04 or 0.77 ± 0.02 vs. 0.88 ± 0.05, p < 0.05; p-smad3: 0.50 ± 0.01 or 0.65 ± 0.02 vs. 0.78 ± 0.01, p < 0.05). The greater effect was achieved at a dose of 6 g/kg/day. Losartan treatment also inhibited the increases in myocardial expression levels of TGF-β1, p-smad2 and p-smad3 compared with MI group (TGF-β1: 0.42 ± 0.01vs. 0.78 ± 0.01, P < 0.05; p-smad2: 0.24 ± 0.57 vs. 0.88 ± 0.05, P < 0.05; p-smad3: 0.39 ± 1.87 vs. 0.78 ± 0.01, P < 0.05).

Conclusions Our studies showed PJS administered can significantly inhibite TGF-β/Smads pathway after MI in rats. The data indicate that PJS improves cardiac remodelling possibly via inhibiting TGF-β/Smads pathway. The results suggest that PJS may have a promising potential for the prevention and treatment of MI.

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