Objective To investigate the impact of Atractylodin on lung tissue damage in young asthmatic rats by regulating the CXC chemokine ligand 12(CXCL12)/CXC chemokine receptor 4(CXCR4)signaling pathway.Methods Twelve young SD rats were randomly selected from 60 rats as the control group(CON group),while the remaining 48 rats were used to construct asthma models using ovalbumin(OVA).Successfully modeled asthma rats were randomly separated into Model group,Atractylodin group(50 mg/kg Atractylodin),and CXCL-12 group(5 μ g/kg recombinant CXCL-12 protein)and Atractylodin+CXCL-12 group(50 mg/kg Atractylodin+5 μ g/kg recombinant CXCL-12 protein),with 12 in each group,continuously administered for 14 days.The CON and Model groups were given equal amounts of physiological saline.The percentages of neutrophils and eosinophils in bron-choalveolar lavage fluid(BALF)were detected.ELISA method was applied to detect cytokine levels in serum and BALF fluid;HE staining was applied to detect pathological changes in lung tissue;Western blot was applied to detect the levels of CXCL12/CXCR4 pathway related proteins.Results Compared with the CON group,the pathological score of lung tissue,percentage of neutrophils,percentage of eosinophils,the levels of IL-17,IL-4,IL-5,IL-13,IgE,OVA sIgE,and the protein levels of CXCL12 and CXCR4 in Model group were obviously increased(P<0.05);compared with the Model group,the pathological score of lung tissue,percentage of neutro-phils,percentage of eosinophils,the levels of IL-17,IL-4,IL-5,IL-13,IgE,OVA sIgE,and the protein levels of CXCL12 and CXCR4 in the Atractylodin group were obviously reduced(P<0.05),the results in the CXCL-12 group were opposite to those in the Atractylodes group;CXCL-12 eliminated the improvement effect of atractylodes on asthma rats.Conclusion Atractylodin may improve lung tissue damage in asthmatic rats by down-regulating the CXCL12/CXCR4 signaling pathway.

Objective To determine vascular endothelial growth factor(VEGF)-460 gene polymorphism in Uyghurs and its relationship to urolithiasis in south Xinjiang. Methods Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP),gene sequencing and genetic analysis methods were used in 200 urolithiasis patients of Uyghurs, and 200 healthy Uyghurs. Results The distribution of genotype and allele had no significant difference between urolithiasis patients and normal controls (P＞0. 05). The frequencies for the CC,TT and CT genotypes in patients with urolithiasis and normal controls were 1.5 %, 29.0 %, 69.5 % and 0. 5 %, 27.5 %, 72.0 %, respectively. The frequencies for C and T allele were 36.2%,63.7% and 36.9% ,63.1%, respectively. Conclusions The results of VEGF-460 gene polymorphisms indicate no significant relationship between patients with turolithiasis and normal controls in Uyghurs in south Xinjiang,which may not be urolithiasis susceptibility genetic locus.

Objective: To explore the effect of hypoxia inducible factor 1α(HIF-1α)on tamoxifen resistance in breast cancer MCF-7,and to established a human breast cancer cell line(MCF-7/TR)with 4-hydroxy tamoxifen(4-OHT)resistance. Methods: 4-OHT was an active form of tamoxifenin vivo, resistant breast cancer cells MCF-7/TR were establishedin vitrousing 4-OHT. MTT assay was used to detect the effect of 4-OHT on the MCF-7 and MCF-7/TR cells, and the drug resistance multiple was detected. Western blot was used to detect the expression level of HIF-1α protein in MCF-7 and MCF-7/TR cells. The effects of HIF-1α inhibitor(LW6) or siRNA HIF-1α on MCF-7/TR cells and 4-OHT on MCF-7 cells treated with HIF-1α stabilizer(FG-4592) were detected by MTT and flow cytometry AV/PI staining. Results: The results showed that the MCF-7/TR was successfully constructed, and the drug resistance ratio was(5.56±0.80). Compared with MCF-7 cells, MCF-7/TR cells had higher expression of HIF-1α protein and it was up-regulated after tamoxifen treatment. After giving LW6 or silencing the expression of HIF-1α,the down-regulation of HIF-1α expression enhanced the inhibitory effect of 4-OHT on MCF-7/TR cells. After treatment of FG-4592, the expression level of HIF-1α in breast cancer cells MCF-7 was up-regulated, and hindered the inhibition effect of tamoxifen on MCF-7 cells. Conclusion The above results indicate that HIF-1α plays an important role in 4-OHT resistant breast cancer, and targeting HIF-1α may be an effective way to increase the sensitivity of MCF7/TR cells to tamoxifen.