星形胶质苷IV通过miR-135a-trpm7-tgf-β/smads途径抑制心脏纤维化。
摘要来源：
j et nnopharmacol。 2019年11月15日：112404。 EPUB 2019 11月15日。PMID： 31739105“> 31739105 Feng, Ru Tao, Haonan Xu, Yiqun Tang
Article Affiliation:Yanchun Wei
Abstract:ETHNOPHARMACOLOGICAL RELEVANCE: Cardiac fibrosis is a common characteristic of many cardiac diseases.我们先前的结果表明，TRPM7通道在纤维化过程中起着重要作用。据报道，microRNA-135A参与了纤维化过程。作为黄质膜（Fisch。）Bumge的活性成分之一，已经显示出通过各种机制抑制心脏纤维化的抑制作用，而没有数据表明其与miRNAS调节有关的作用。
研究的目的： 本文的目的是研究黄色盐IV对通过miR-135a-trpm7-tgf-β/smads pathway。和方法： 我们使用异丙肾上腺素（ISO）在体内和体外诱导心脏纤维化。 SD大鼠皮下（S.C.）用ISO（5mg/kg/day）处理14天，并给予ASG（10mg/kg/d）P.O.从建模的第六天开始。 Cardiac fibroblasts (CFs) of neonatal rats were incubated with ISO (10 μM) and treated with ASG (10 μM) simultaneously for 24 h.
RESULTS: The results showed that ASG treatment could significantly decrease the current and protein expression of TRPM7 which was proved as one target of mir-135a。 TGF-β/SMADS途径的激活被抑制，α-SMA和胶原蛋白I是ALS的表达o明显下降。 In addition, we proved that there was a positive feedback between the activation of TGF-β/Smads pathway and the elevation of TRPM7, both of which could promote the development of myocardial fibrosis.
CONCLUSIONS: All these findings suggested that ASG inhibited cardiac fibrosis by targeting the mir-135a-trpm7-tgf-β/smads途径。