This study was aimed to screen out an optimal pharmaceutical formulation of Wuji Gastric Floating Sus-tained-release Tablets. With multicomponents of release for index, the extra-floating ability of the tablets was stud-ied with the orthogonal test of four excipients, which were HPMC (K100M), PEG 6000, sodium bicarbonate and se-tanol. The results showed that the combined optimal pharmaceutical formulation was 35% HPMC, 5% PEG 6000, 10% sodium bicarbonate, 15% setanol, 10% MCC and 25% main drug. It was concluded that Wuji Gastric Floating Sustained-release Tablets had the characteristics of slow-release and long floating duration which comply with re-quirements of formulation design. This preparation technique is with good maneuverability.

This article was aimed to study the multicomponent in vivo releasing rules of Zuojin Gastric Floating Sus-tained-release Tablet. Stomach contents of rabbits were collected at different times and then prepared into solutions for the study. The HPLC was used to establish fingerprints of each time and fingerprints of completely dissolved samples. The in vivo releasing rates were calculated. The evaluation was made on releasing behaviors among index components as well as between index components and preparations. The results showed that within 10 h, the f2 of berberine and limonin, rutaecarpine, preparation were 52, 61.5, 66.4, respectively. The f2 of limonin and rutae-carpine, preparation were 70, 46.5, 53.7, respectively. It was concluded that within 10 h, the releasing behavior of berberine and limonin, rutaecarpine, preparation was similar. The releasing behavior of rutaecarpine and limonin, preparation was similar. However, the releasing behavior of limonin and preparation was different.

Objective To explore the effect of noscapine on the biological function of A549 cells and its underlying mechanism. Methods Concentrations of 10 μmol/L and 20 μmol/L of noscapine were used on the A549 cells. The effect of noscapine on their proliferation was observed via the MTT assay. Western blotting and real time PCR were used to detect the effects on Cyclin D1, BCL-2, and MMP2. The Hoechst 33258 staining assay was used to observe the effects of noscapine on the apoptosis of A549 cells. The metastasis of A549 cells was detected by using the Transwell assay. Results The MTT assay showed that the rate of inhibition of cell proliferation after treatment with 10 μmol/L and 20 μmol/L noscapine were (32.98±1.09) ％ and (49.56±3.98) ％, with a significant difference between the values (P ＜ 0.05). Hoechst 33258 staining evinced that noscapine promoted apoptosis, while the Transwell assay displayed that noscapine inhibited A549 cell metastasis. Western blotting and real time PCR indicated that the expression of Cyclin D1, BCL-2, and MMP2 in A549 cells was inhibited by noscapine. Conclusion Noscapine can inhibit the growth and metastasis of the lung cancer cell line A549 and promote the apoptosis of A549 cells. In conclusion, noscapine can potentially be used as a chemotherapeutic drug for lung cancer.

Objective To investigate how microRNA 24 (miR-24) regulates the development of lung cancer. Methods The levels of miR-24 in 30 cases of lung cancer were detected using real-time PCR, and the relationship between miR-24 levels and overall survival was analyzed. After overexpression or silencing of miR-24 in A549 lung cancer cells, the effect on cell proliferation was observed by the MTT assay. Transwell assays were carried out to observe the effect of miR-24 on cell migration. The effects of miR-24 on the expression of cyclin-dependent kinase (CDK) 4/6 and matrix metalloproteinase (MMP) 2 in A549 cells were examined by Western blotting. Results Survival analysis showed that patients with low miR-24 expression had a shorter survival time. The MTT-based viability assay revealed that overexpression of miR-24 inhibited A549 cell proliferation. Cell proliferation was promoted when miR-24 was inhibited. In the Transwell assay, overexpression of miR-24 significantly inhibited the A549 cell migration, and cell migration increased when miR-24 was inhibited.Western blotting analysis revealed that overexpression of miR-24 could inhibit CDK4/6 and MMP2 production in A549 cells. Inhibition of miR-24 was associated with increased production of CDK4/6 and MMP2 in A549 cells. Conclusion miR-24 can inhibit the proliferation and migration of A549 lung cancer cells.