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AIM To establish an HPLC method for the simultaneous content determination of six constituents in Jiaotai Pills (Coptidis Rhizoma and Cinnamomi Cortex).METHODS The analysis of 30% methanol of this drug was performed on a 30 ℃ Agilent ZORBAX SB-C1s column (4.6 mm ×250 mm,5 μm),with the mobile phase comprising of acetonitrile-KH2PO4flowing at 0.8 mL/min in a gradient elution manner,and the detection wavelength was set at 276 nm.RESULTS Epiberberine,jatrorrhizine hydrochloride,coptisine hydrochloride,palmatine chloride,berberine hydrochloride and cinnamaldehyde showed good linear relationships within the ranges of 0.64-41.24 μg/mL (R2 =0.999 9),0.65-43.76 μg/mL (R2 =1.000 0),0.82-52.65 μg/mL (R2 =0.999 9),0.79-50.70 μg/mL (R2 =0.999 9),3.08-197.20 μg/mL (R2=0.999 8) and 0.65-41.65 μg/mL (R2 =0.999 9),whose average recoveries were 98.06%,102.76%,99.27%,99.75%,96.74% and 101.33% with the RSDs of 0.56%,0.54%,0.39%,0.55%,0.48% and 2.14%,respectively.CONCLUSION This accurate,sensitive,stable and reproducible method can be used for the quality control of Jiaotai Pills.
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Objective To investigate the effects of apigenin on the migration of vascular smooth muscle cells (VSMC) induced by platelet derived growth factor (PDGF)-BB and the possible molecular mechanism. Methods VSMCs were isolated from thoracic aortas of male Sprague-Dawley rats using enzyme digestion method. Migration of VSMCs was determined by transwell assay. Western blotting was carried out to evaluate phosphorylation of c-jun N-terminal kinase (JNK). Results Treatment with PDGF-BB (20 ng·mL-1 ) significantly promote VSMC migration,the number of migrated cells was 2. 46 times than that of control group. However,after 12. 5 μmol·L-1 apigenin pretreatment,the number of migrated cells was 46. 5% of the PDGF-BB group. Various dose of apigenin can significantly inhibit VSMC migration induced by PDGF-BB,12. 5 μmol · L-1 apigenin treatment significantly inhibited PDGF-BB phosphorylation of JNK. Conclusion Apigenin can suppress the migration of VSMC induced by PDGF-BB. These beneficial effects on VSMC were at least partly mediated by the inhibition of activity of JNK.