Abstract
Objective To investigate the effect of 7, 8-dihydroxyflavone (7, 8-DHF) on the phenotypic transformation of vascular smooth muscle cells (VSMCs) in spontaneously hypertensive rats (SHR). Methods Western blotting assay was carried out to detect the Wistar-Kyoto rats and SHR′s protein expression of smooth muscle actin (SM-α-actin) and proliferating cell nuclear antigen (PCNA). With the different concentrations of 7, 8-DHF and (or) TrkB specific inhibitor ANA-12, the VSMCs derived from thoracic aortic of SHR were processed and the VSMCs activity was detected by CCK-8 method. Western blotting was used to detect the protein expression levels of SM-α-actin and PCNA after 7, 8-DHF and (or) ANA-12 treated in VSMCs derived from thoracic aortic of SHR. The independent sample t-test and single factor variance analysis were used for statistical comparison. Results Compared with WKY, the expression of SM-α-actin in aorta of SHR decreased significantly [(0.72±0.06), (0.41±0.08), t=6.35, P<0.05], while PCNA increased[(0.51±0.09), (0.99±0.15), t=6.43, P<0.05], and so was the case in VSMCs derived from thoracic aortic of SHR, SM-α-actin decreased [(0.71±0.05), (0.36±0.04), t=11.12, P<0.01] and PCNA increased[(0.69±0.07), (1.05±0.08), t=8.49, P<0.05]. The proliferative activity of VSMCs derived from thoracic aortic of SHR was greatly attenuated by 7, 8-DHF in a concentration-dependent manner(F=17.49, P<0.01), which could be enhanced by ANA-12 [ (0.52±0.08), (0.86±0.14), t=5.13, P<0.01]. ANA-12 can significantly weaken the effect of 7, 8-DHF on the expression of SM-α-actin[(0.85±0.13), (0.35±0.15), t=4.37, P<0.01]and PCNA protein[(0.42±0.13), (0.76±0.10), t=3.54, P<0.05]in VSMCs derived from thoracic aortic of SHR. Conclusion 7, 8-DHF can effectively inhibit the transformation of VSMCs derived from thoracic aortic of SHR from contractile to proliferative type, which may be mediated by TrkB receptor. Key words: 7, 8-dihydroxyflavone; Hypertension; Vascular smooth muscle cell; Phenotype; Receptor, trkB
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