Abstract
The aim of this study is to investigate the therapeutic role of Tanshinone II A, a key integrant from salvia miltiorrhiza, against pathological vascular remodeling. Completed ligation of mouse left common carotid arteries animal model and rat smooth muscle cells used to investigate the role of Tanshinone II A in regulating pathological vascular remodeling through hematoxylin and eosin staining, immunohistochemistry staining, immunofluorescence staining, adenovirus infection, real time PCR and western blotting. Our data demonstrated that Tanshinone II A treatment suppresses vascular injury-induced neointima formation. In vitro studies on rat smooth muscle cell indicated that Tanshinone II A treatment attenuates PDGF-BB induced cell growth, and promotes smooth muscle cell differentiated marker genes expression that induced by rapamycin treatment. Tanshinone II A treatment significant inhibits rat smooth muscle cell proliferation and migration. Tanshinone II A promotes KLF4 expression during smooth muscle phenotypic switching. Overexpression of KLF4 exacerbates Tanshinone II A mediated smooth muscle cell growth inhibition. Tanshinone II A plays a pivotal role in regulating pathological vascular remodeling through KLF4 mediated smooth muscle cell phenotypic switching. This study demonstrated that Tanshinone II A is a potential therapeutic agent for vascular diseases.
Highlights
The aim of this study is to investigate the therapeutic role of Tanshinone II A, a key integrant from salvia miltiorrhiza, against pathological vascular remodeling
To determine whether Tanshinone II A plays a critical role in regulating smooth muscle cell phenotypic switching, we pretreated C57BL/6 mice with 5 mg/kg Tanshinone II A by intraperitoneal injection for 3 consecutive days and following left common carotid artery ligation to induce vascular injury (Fig. 1A)
Our results indicated that treatment with Tanshinone II A dramatically suppresses neointima formation (Fig. 1B)
Summary
The aim of this study is to investigate the therapeutic role of Tanshinone II A, a key integrant from salvia miltiorrhiza, against pathological vascular remodeling. Tanshinone II A treatment significant inhibits rat smooth muscle cell proliferation and migration. Tanshinone II A promotes KLF4 expression during smooth muscle phenotypic switching. Tanshinone II A plays a pivotal role in regulating pathological vascular remodeling through KLF4 mediated smooth muscle cell phenotypic switching. Tanshinone II A inhibits proliferation of pulmonary artery smooth muscle cells induced by h ypoxia[11]. Tanshinone II A induces pulmonary artery smooth muscle cell apoptosis through suppressing JAK1/STATS signaling p athway[12]. This study aimed to test hypothesis that Tanshinone II A regulates pathological vascular remodeling through KLF4 mediated smooth muscle cell phenotypic switching
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