[Effects of resveratrol on the proliferation and CaN of vascular smooth muscle cell induced by angiotensin II].
Qingqing Wang, Jiao Jin-ju, Weihong Li, Qin Qu
Abstract
Qingqing Wang, Jiao Jin-ju, Weihong Li, Qin Qu
Abstract
AIM: To investigate the effects of resveratrol (Res) on the proliferation of VSMCs induced by Ang I and the expression of calmodulin (CaM) and calcineurin (CaN) in the proliferation of VSMCs treated by Ang 1 and to discuss the mechanism. METHODS: Rabbit arterial VSMCs were cultured in vitro and VSMCs were identified with the method of immunocytochemistry. A cell proliferating model of VSMCs induced by AngII was established. VSMCs were cultured for 4-8 passages. The experiments were randomly divided into control group, AngII group (0.1 micromol/L) and AngII + Res groups with different concentrations(20, 40, 80, 160) micromol/L. VSMCs proliferation was determined with MTT colorimetric method. CaM was detected with Coomassie brilliant blue method and CaN was determined by enzyme reaction phosphorus measurement. RESULTS: Rabbit VSMCs were cultured successfully and could be passaged. After immunocytochemistry staining, all the cells cytoplasm were stained and positive. Cell proliferation, CaM and CaN activities were increased significantly in VSMCs proliferation induced by AngII (P <0.05, P < 0.01). The index of AngII + Res groups were obviously reduced compared with AngII group ( P < 0.01). CONCLUSION: The VSMCs proliferation induced by AngII can be inhibited by Res significantly, and the inhibiting mechanism of Res may be related to inhibiting CaM and CaN activities then restraining the proliferation of VSMCs in a dose dependent manner.
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AIM: To investigate the effects of resveratrol (Res) on the proliferation of VSMCs induced by Ang I and the expression of calmodulin (CaM) and calcineurin (CaN) in the proliferation of VSMCs treated by Ang 1 and to discuss the mechanism. METHODS: Rabbit arterial VSMCs were cultured in vitro and VSMCs were identified with the method of immunocytochemistry. A cell proliferating model of VSMCs induced by AngII was established. VSMCs were cultured for 4-8 passages. The experiments were randomly divided into control group, AngII group (0.1 micromol/L) and AngII + Res groups with different concentrations(20, 40, 80, 160) micromol/L. VSMCs proliferation was determined with MTT colorimetric method. CaM was detected with Coomassie brilliant blue method and CaN was determined by enzyme reaction phosphorus measurement. RESULTS: Rabbit VSMCs were cultured successfully and could be passaged. After immunocytochemistry staining, all the cells cytoplasm were stained and positive. Cell proliferation, CaM and CaN activities were increased significantly in VSMCs proliferation induced by AngII (P <0.05, P < 0.01). The index of AngII + Res groups were obviously reduced compared with AngII group ( P < 0.01). CONCLUSION: The VSMCs proliferation induced by AngII can be inhibited by Res significantly, and the inhibiting mechanism of Res may be related to inhibiting CaM and CaN activities then restraining the proliferation of VSMCs in a dose dependent manner.
Key concepts: Vascular smooth muscle, Immunocytochemistry, Angiotensin II, Cell growth, Resveratrol, Cell, MTT assay, Chemistry