| Backgrounds: Qiliqiangxin（QL）, a traditional Chinese medicine, hadlong been used to treat chronic heart failure. Recent studies revealed thatdifferentiation of cardiac fibroblasts（CFs）into myofibroblasts played animportant role in cardiac remodeling and development of heart failure,however little was known about whether QL ameliorates myocardialremodeling via regulating CFs differentiation.Aims: The present study aimed to investigate the effects of QL onangiotensin II（AngII）-induced CFs transdifferentiation and the underlyingmechanism.Methods: Study was performed in in vitro cultured CFs fromSprague-Dawley rats. Cells were stimulated by AngII（100nmol/L）for24h inthe presence and absence of pretreatment with QL（0.5mg/ml）or Olmesartan（OLM10nmol/L）. SiRNA was used to knockdown interleukin-6（IL-6）.CFs transdifferentiation was examined by the expression of transforminggrowth factor-β1（TGF-β1）, α-smooth muscle actin（α-SMA）, IL-6, collagentype I and type III.Results：Ang II induced significant increases of TGF-β1and α-SMA inCFs, which could be attenuated by QL, or by blocking AT1receptor withOLM. In addition, Ang II-induced the mRNA level of IL-6was reduced byQL, and knocking down of IL-6in CFs also suppressed the expression ofAngII-induced TGF-β1and α-SMA. This results suggesting QL-mediateddownregulation of IL-6might be centrally involved in Ang II-induced CFs transdifferentiation. Further data showed that enhanced type I and type IIIcollagens in response to Ang II were inhibited by QL, OLM or IL-6siRNA.Conclusion: These data provided evidence that CFs transdifferentiationcould be reversed by QL through regulating IL-6signaling. |
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