Objective: To observe the effect of Radix Astragali on the transmission time of small intestine(TTSI).Methods: TTSI and the peak value of lactose absorption were determined by hydrogen breath test in 40 healthy subjects a week before and after administration of Radix Astragali. Results: TTSI was 116.48+ 24.57 min and 102.38+ 13.44 min respectively before and after administration (P 0.05).Conclusion: Oral administration of Radix Astragali for one week has no effect on the absorption of the lactose by small intestine,but can promote the movement of small intestine.

Objective To elucidate the expression of gankyrin in human gastric cancer cells and it's role in nimesulide induced apoptosis. Methods Four human gastric cancer cell lines including MKN28 (well differentiated), AGS (poorly differentiated), MKN45 (poorly differentiated), and SGC7901(moderately differentiated) were cultured and treated with nimesulide. Nimesulide induced growth inhibition and apoptosis of the cells were detected by methyl thiazolyl tetrazolium assay, and confirmed by flow cytometry. The expressions of gankyrin gene and protein were further assessed by real-time PCR and Western blotting. Results Gankyrin mRNA and protein were detected in all four human gastric cancer cell lines. The proliferations of AGS and SGC7901 cell lines were significantly suppressed by nimesulide in a time-dose dependent manner. When treated with 400 μmol/L of nimesulide for 48 hours, the significant apoptosis was found in AGS cells (23.30%±2.50%) and SGC7901 cells (16.80%±1.55% ) in comparison with controls (0.57%±0.19% and 0.88%± 0.17%, respectively, all P values <0.01). Apoptosis of AGS cells induced by nimesulide was accompanied by a considerably decreased gankyrin expression that was more significant at 24 hours (0.0035±0.0014) and 36 hours (0.0980±0.0160) in comparison with controls (0.4690±0.1190, all P values<0.01). Conclusion Gankyrin expresses in human gastric cancer cell lines and may be involved in nimesulide induced apoptosis of AGS cells.

Objective To elucidate the effect of clavulanic acid (CLA) in suppressing the antibiotic resistance of Helicobacter pylori (Hp) to metronidazole (MZ) and its mechanism. Methods All Hp strains were isolated from biopsy specimens taken endoscopically and random amplified polymorphic DNA assay (RAPD) was used to certificate the distinct origin of these strains. The minimum inhibitory concentration (MIC) of CLA and MZ aganst Hp were determined by using agar dilution procedure and Epailometer test (E-test). The effect of CLA on the morphology of Hp was examined by transmission electron microscopy. Fluorescein-C6-aminopenicillanic acid (FLU-C6-APA) competition assay was used to detect the binding between CLA and penicillin-binding proteins (PBPs). Results Eleven strains were isolated. In vitro CLA could decrease the MIC of MZ resistant(1.442±0.459 vs 0.376±0.288, P=0.0077), but not affect the MIC for MZ sensitive strains significantly (P>0.05). Exposure to CLA resulted in morphological changes of Hp, including cell wall disintegration and cell lysis. Furthermore, CLA inhibited the binding of FLU-C6-APA to PBPs(30.5-33.5×103). Conclusions CLA suppresses the antibiotic resistance of Hp to MZ through its binding with PBPs which results in the morphology changes of Hp.