Anti-osteoporotic activity of puerarin 6"-O-xyloside on ovariectomized mice and its potential mechanism.

CONTEXT: Osteoporosis is one of the most common bone diseases, and radix of Pueraria lobata (Willd.) Ohwi possesses an obvious therapeutical effect on postmenopausal osteoporosis. OBJECTIVE: This study investigates the anti-osteoporotic activity of the puerarin 6"-O-xyloside (PXY) on ovariectomized mice and its related mechanism. MATERIALS AND METHODS: Osteoporotic mice model was established by ovariectomy (OVX). A total of 50 mice were divided into five groups (n = 10): sham, OVX group, PXY treatment groups (20, 40, and 60 mg/kg/d, i.p.). After 12 weeks' treatment, body weights were recorded. Then, mice were sacrificed, and serum samples were collected to determine the blood calcium, blood phosphorus, alkaline phosphatase (ALP), and osteoprotegerin (OPG) concentrations and uterine index was assayed. The thigh-bones of mice were collected to evaluate histopathological changes. In the in vitro experiment, the effect of PXY on osteoblasts' proliferation was evaluated and western blotting was performed to determine expressions of OPG and the receptor activators of NF-κB ligand (RANKL), as well as the ratio of OPG/RANKL. RESULTS: PXY (40 and 60 mg/kg/d, i.p.) obviously decreased body weights and increased uterine index of OVX (p < 0.05), and improved osteoporotic syndromes of OVX mice; PXY also significantly increased the concentrations of blood calcium, blood phosphorus, ALP, and OPG of OVX mice (p < 0.05); moreover, PXY obviously up-regulated the ratio of OPG/RANKL (p < 0.05). CONCLUSION: Our results demonstrated that the puerarin 6"-O-xyloside possesses significant anti-osteoporotic activity on ovariectomy mice.

Inhibitory effects of emodin, baicalin, schizandrin and berberine on hefA gene: treatment of Helicobacter pylori-induced multidrug resistance.

AIM: To investigate the inhibitory effects of emodin, baicalin, etc. on the hefA gene of multidrug resistance (MDR) in Helicobacter pylori (H. pylori). METHODS: The double dilution method was used to screen MDR H. pylori strains and determine the minimum inhibitory concentrations (MICs) of emodin, baicalin, schizandrin, berberine, clarithromycin, metronidazole, tetracycline, amoxicillin and levofloxacin against H. pylori strains. After the screened MDR stains were treated with emodin, baicalin, schizandrin or berberine at a 1/2 MIC concentration for 48 h, changes in MICs of amoxicillin, tetracycline, levofloxacin, metronidazole and clarithromycin were determined. MDR strains with reduced MICs of amoxicillin were selected to detect the hefA mRNA expression by real-time quantitative PCR. RESULTS: A total of four MDR H. pylori strains were screened. Treatment with emodin, baicalin, schizandrin and berberine significantly decreased the MICs of amoxicillin and tetracycline against some strains, decreased by 1 to 2 times, but did not significantly change the MICs of clarithromycin, levofloxacin, and metronidazole against MDR strains. In the majority of strains with reduced MICs of amoxicillin, hefA mRNA expression was decreased; one-way ANOVA (SPSS 12.0) used for comparative analysis, P < 0.05. CONCLUSION: Emodin, baicalin, schizandrin and berberine significantly decreased the MICs of amoxicillin and tetracycline against some H. pylori strains, possibly by mechanisms associated with decreasing hefA mRNA expression.

Helicobacter pylori isolates from ethnic minority patients in Guangxi: resistance rates, mechanisms, and genotype.

AIM: To investigate the rate of Helicobacter pylori (H. pylori) resistance to clarithromycin among ethnic minority patients in Guangxi, explore the underlying mechanisms, and analyze factors influencing genotype distribution of H. pylori isolates. METHODS: H. pylori strains were isolated, cultured and subjected to drug sensitivity testing. The 23S rRNA gene of H. pylori isolates was amplified by PCR and analyzed by PCR-RFLP and direct sequencing to detect point mutations. REP-PCR was used for genotyping of H. pylori isolates, and NTsys_2 software was used for clustering analysis based on REP-PCR DNA fingerprints. Factors potentially influencing genotype distribution of H. pylori isolates were analyzed. RESULTS: The rate of clarithromycin resistance was 31.3%. A2143G and A2144G mutations were detected in the 23S rRNA gene of all clarithromycin-resistant H. pylori isolates. At a genetic distance of 78%, clarithromycin-resistant H. pylori isolates could be divided into six groups. Significant clustering was noted among H. pylori isolates from patients with peptic ulcer or gastritis. CONCLUSION: The rate of clarithromycin resistance is relatively high in ethnic minority patients in Guangxi. Main mechanisms of clarithromycin resistance are A2143G and A2144G mutations in the 23S rRNA gene. Clarithromycin-resistant H. pylori isolates can be divided into six groups based on REP-PCR DNA fingerprints. Several factors such as disease type may influence the genotype distribution of H. pylori isolates.