[Effect of tanshinone II A on the calcineurin activity in proliferating vascular smooth muscle cells of rats].
Yong-Jun Pan, Xiaoyong Li, Guangtian Yang
Abstract
Yong-Jun Pan, Xiaoyong Li, Guangtian Yang
Abstract
OBJECTIVE: To study the effect of tanshinone II A (TSN) on angiotensin II (Ang II) induced proliferation of vascular smooth muscle cells (VSMCs). METHODS: VSMCs were cultured by explant attached method, and induced to proliferative cell model with Ang II. The effect of TSN in different concentrations on calcineurin (CaN) activity was detected by enzyme reaction phosphorus measurement; the CaN mRNA expression was detected by RT-PCR; and the expression of proliferating cell nuclear antigen (PCNA) were observed by immunocytochemical method. RESULTS: Compared with the normal control group, Ang II could significantly stimulate the proliferation of VSMCs, showing obviously elevated degree of proliferation activity (P <0. 01). After being treated with TSN, all the indexes, including CaN activity, CaN mRNA expression and PCNA expression, were obviously reduced in a dose-dependent manner (P<0.05, P<0.01). CONCLUSION: VSMCs proliferation can be inhibited by TSN in a dose-dependent manner and the inhibiting mechanism may be related to the down-regulation of CaN activities and the inhibition on CaN mRNA and PCNA expressions.
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OBJECTIVE: To study the effect of tanshinone II A (TSN) on angiotensin II (Ang II) induced proliferation of vascular smooth muscle cells (VSMCs). METHODS: VSMCs were cultured by explant attached method, and induced to proliferative cell model with Ang II. The effect of TSN in different concentrations on calcineurin (CaN) activity was detected by enzyme reaction phosphorus measurement; the CaN mRNA expression was detected by RT-PCR; and the expression of proliferating cell nuclear antigen (PCNA) were observed by immunocytochemical method. RESULTS: Compared with the normal control group, Ang II could significantly stimulate the proliferation of VSMCs, showing obviously elevated degree of proliferation activity (P <0. 01). After being treated with TSN, all the indexes, including CaN activity, CaN mRNA expression and PCNA expression, were obviously reduced in a dose-dependent manner (P<0.05, P<0.01). CONCLUSION: VSMCs proliferation can be inhibited by TSN in a dose-dependent manner and the inhibiting mechanism may be related to the down-regulation of CaN activities and the inhibition on CaN mRNA and PCNA expressions.
Key concepts: Proliferating cell nuclear antigen, Vascular smooth muscle, Calcineurin, Messenger RNA, Cell growth, Angiotensin II, Chemistry, Cell