Modified Liangfu granule exhibits anti-cancer effects in gastric cancer by regulating apoptosis-related proteins and genes

Objective:To investigate the anti-cancer effects and mechanism of modified Liangfu granule(MLFG)in BGC-823 gastric cancer cells.Methods:The drug serum was extracted from abdominal aorta of Wistar rats treated by cyclophosphamide,dioscin,MLFG(high-,medium-,and low-dose),respectively.MTS assay was performed to detect the effect of different concentrations of MLFG and dioscin on cell growth.The effect of MLFG on cellular apoptosis was detected by flow cytometry.Western blot was used to examine Bcl-2 and Akt in BGC-823 cells treated with MLFG.Quantitative real-time polymerase chain reaction assay was performed to determine the expression level of caspase-3,E2F1 and E2F3 genes in cells treated by MLFG-and dioscin-containing serum.Results:MLFG-and dioscin-containing serum inhibited the cell proliferation of BGC-823 cells.MLFG induced gastric carcinoma cell apoptosis and inhibited the expression of Bcl-2 and Akt in a dosedependent manner.MLFG also significantly induced the gene expression of caspase-3 and downregulated E2F1 and E2F3 gene expression.Conclusion:The effect of MLFG and dioscin on inhibiting cell proliferation and induction of apoptosis of gastric cancer cells might be related to the regulation of Bcl-2 and Akt proteins and the expression of caspase-3,E2F1 and E2F3 genes.

Hemostatic mechanism of the effect of Jianpi Yiqi Shexue decoction on vascular factors in immune thrombocytopenia model mice

Objective: To explore the hemostatic mechanism of Jianpi Yiqi Shexue decoction(JYSD) by regulating vascular factors in an immune thrombocytopenia(ITP) mouse model.Methods: An ITP mouse model was established by the passive-immune modeling method, and interventional drugs used were prednisone tablets and JYSD. The platelet count;vascular activity-related factors v WF, VCAM-1, and TM;and VEGF and b FGF were used as observational indicators.Results: On the 8th day of administration, compared with the model group, platelet counts in the prednisone and JYSD groups increased(both P <.001). Compared with the control group, the levels of v WF, VCAM-1, and TM in the other groups were lower(all P <.05). The VCAM-1 level in the JYSD group was higher than that in the prednisone group(P =.012), but without significant difference compared with the model group(P =.051). The TM level in the JYSD group was the lowest(vs. the model group,P =.047;vs. the prednisone group, P =.006). Compared with the control group, the IOD values of VEGF and b FGF in the other three groups were lower(all P <.01). The IOD values of VEGF in the prednisone and JYSD groups were both higher than those in the model group(P =.002 and P <.001, respectively). The IOD values of b FGF among the model, prednisone, and JYSD groups were not statistically significant(P >.05).Conclusion: A vascular factor disorder is involved in the pathogenesis of ITP. JYSD can increase the platelet count, upregulate VEGF expression, and reduce the TM level. JYSD has the same effect as prednisone tablets in regulating platelet, v WF, VEGF, and b FGF, with a stronger effect in normalizing VCAM-1 and TM levels. The hemostatic mechanism of JYSD is closely related to the effective balance of vascular factors.