Objective:To establish a RP-HPLC method with pre-column derivation for determining the content of stilbene glyco-sides in Yening granules. Methods:DNS-Cl was used as the derivation reagent, a Wondasil-C8 column (250 mm × 4. 6 mm, 5 μm) was used as the stationary phase and 30mM ammonium phosphatere gulation (pH 3. 5)-acetonitrile (78∶22) was applied as the mobile phase, a fluorescence detector (λex=370 nm,λem=560 nm) was used, the flow rate was 1. 0 ml·ml-1 , the column temperature was 30℃ and the injection volume was 20 μl. Results: There was no interference from the other substances in the preparation. The linear range of the two stilbene glycosides was 0.071-27.280 mg·ml-1(r=0.999 9). The average recovery was 99.04%(RSD=0. 1%, n= 9). Conclusion:The method is simple, quick, sensitive and accurate, which can be used for the quality control of Ye-ning granules.

Objective:To study the effect of macrophage colony stimulating factor (M-CSF) in the nucleus on the proliferation and invasion ability of cervical cancer cells and its possible mechanisms.Methods:Using the HeLa cell line with stable expression of M-CSF in the nucleus as the model, the proliferation ability of the cells was detected using bromodeoxyuridine (BrdU) labeled deoxyribonucleic acid (DNA) replication analysis, and the invasiveness of the cells was detected using Transwell cells; Western blot was used to detect the expression of nuclear protein transcription factor κB p65 (NF-κB p65) and total cell protein matrix metalloproteinase-2 (MMP-2).Resultsl:The proliferation and invasion ability of HeLa cells stably expressing MCSF in the nucleus were significantly enhanced ( P<0.05, P<0.01), and the expression of NF-κB p65 and MMP-2 was increased (all P<0.05). Conclusions:Intranuclear MCSF can promote the proliferation and invasion ability of cervical cancer cells, and its mechanism is related to the upregulation of NF-κB p65 and MMP-2 expression.

[Objective]To explore how hyperthyroidism induces ventricular remodeling via activating β-catenin/FoxO1 in rat cardiomyocytes.[Methods]Hyperthyroidism-induced ventricular remodeling rat models were established by intraperitoneal injection of levothyroxine(T4)at 0.1 mg/kg for 30 days.β-catenin inhibitor MSAB(14 mg/kg)was admin-istrated for 30 days.We used western blot to detect the expression of myocardial hypertrophy marker ANP,β-catenin and FoxO1;immunofluorescence to examine the expression and intracellular distribution of β-catenin and FoxO1.Hyperthy-roidism-induced cardiomyocyte hypertrophy rat models were established by treatment of triiodothyronine(T3)into cul-tured primary neonatal rat cardiomyocytes for 24 hours.β-catenin siRNA(30 nmol/L)was used to down-regulate β-catenin expression in cardiomyocytes.Western blot and immunofluorescence were used to analyze the effects of β-catenin inhibition on the hyperthyroidism-induced cardiomyocyte hypertrophy.[Results]Following Wnt/β-catenin activation,β-catenin was found increased nuclear expression,to bind to the nuclear transcriptional factors and regulate the gene ex-pression.β-catenin nuclear expression was significantly increased in the hyperthyroidism-induced ventricular remodeling rats,but no change was found in the expression of typical transcriptional factor TCF7l2.Our results revealed that inhibiting β-catenin by MSAB attenuated the hyperthyroidism-induced rat ventricular remodeling.Further analysis indicated that β-catenin/FoxO1 expression was significantly increased in hyperthyroidism-induced myocardial hypertrophy which could be attenuated by suppressing β-catenin/FoxO1 in cardiomyocytes.[Conclusions]β-catenin/FoxO1 is activated in hyperthy-roidism-induced myocardial hypertrophy and β-catenin/FoxO1 inhibition attenuates hyperthyroidism-induced cardiomyo-cyte hypertrophy.