AIM: To establish a simple and repeatable orthotopic animal model of the A549 cell line.METHODS: A549 cells in matrigel were inoculated into left lung or right flank of nude mouse. The growth pattern of A549 tumors and the chemotherapeutic efficacy of carboplatinum were studied. RESULTS: Tumors generated and dispersed widespreadly to contralateral lung. Tumors in lung were less susceptible to carboplatinum than those growing in flank. CONCLUSION: A simple and repeatable orthotopic animal model of the A549 cell line was presented, this allows researchers to evaluate novel compounds and new drugs for treatment of human lung cancer.KEY WORDS A549 cell line; orthotopic model; nude mice

The proliferation of vascular smooth muscle cells plays an important role in the initiation and aggravation in cardiovascular diseases such as hypertension, arteriosclerosis, restenosis. This article reviewed the progress in the studies on extracellular influencing factors, intracellular signal transduction, cell cycle of vascular smooth muscle cells and the relative drug research and development.

AIM: To investigate the apoptosis of a vascular smooth muscle cell line A10 caused by mild K+ depolarization. METHODS: Apoptosis was evaluated by nuclear staining, DNA fragmentation gel electrophoresis and propidium iodide-stained flow cytometry. Mitochondrial transmembrane potential (Δψm) was measured by flow cytometry. RESULTS: K+ depolarization caused dose correlated A10 cells apoptosis; nifedipine, BAPTA/AM, ryanodine inhibited the cytotoxic effect of K+ completely.The combination use of nifedipine and cyclosporin A made it clear that mitochondria was involved in the apoptosis of A10 cells,and Δψm measurement further confirmed this speculation; A10 apoptosis caused by K+ depolarization was not influenced by heparin or Zn2+,a effective capacitative calcium entry(CCE) blocker. CONCLUSION: Ca2+ entry through voltage-dependent ca channels increases intracytoplasm Ca2+, then triggers further Ca2+ release from endoplasmic reticulum via ryanodine receptor, and the microdomains of elevated intracytoplasm Ca2+ are sensed by adjacent mitochondria, which ultimately lead to cell apoptosis.

AIM: To study the effect of Lomerizine on the activity of P-glycorprotein (P-gp) in primary cultured rat brain microvessel endothelial cells (RBMECs). METHODS: Flow cytometry was used to study the efflux of rhodamine123 (Rh123) and expression of P-gp in RBMECs. RT-PCR was used to measure the expression in mRNA level of mdr1 gene in RBMECs. Transwell model was used to detect the influence of Lomerizine on the transport of Rh123 through RBMECs monolayer. RESULTS: Lomerizine inhibited the efflux of Rh123 in RBMECs. No changes of P-gp and mdr1 gene mRNA expression were detected in RBMECs after the treatment with 30 μmol·L-1 Lomerizine for 72 h. In the study of Transwell model, Lomerizine increased significantly the transport of Rh123 through RBMECs monolayer from upper compartments to lower compartments, and inhibited obviously the transport in reverse direction. CONCLUTION: The effect of Lomerizine on the activity of P-gp was mainly via its direct inhibitory effect on the function of P-gp in RBMECs and the transport of P-gp substrates in BBB may be affected by lomerizine.

Objective To investigate the changes of CD4 + CD25 + Foxp3 + regulatory T cell (Treg) and relative cell factors in peripheral blood of steroid-resistant allergic rhinitis (AR) patients,and to study their functions in occurrence of steroid-resistant AR.Methods The CD4 + CD25 + Foxp3 + Treg cell in 30 cases general physical examination (The control group),30 cases steroid-sensitive AR patients (steroidsensitive group) and 30 cases steroid-resistant AR patients (steroid-resistant group) were detected by flow cytometry.The levels of serum interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1) in the three groups were detected by enzyme-linked immunoadsorbent assay (ELISA).Results Compare to the control group,proportion of CD4 + CD25 + Foxp3 + Treg cell and the levels of serum IL-10,TGF-β1 in steroid-sensitive group and steroid-resistant group were significantly reduced (P ＜ 0.01).The proportion of CD4 + CD25 + Foxp3 + Treg cell and the levels of serum IL-10,TGF-β1 in steroid-resistant group were decreased significantly than steroid-sensitive group (P ＜ 0.01).The proportion of CD4 + CD25 + Foxp3 + Treg cell were positively correlated with the serum IL-10,and TGF-β1 (P ＜ 0.01).Conclusions The reduced proportion of CD4 + CD25 + Foxp3 + Treg cell and lower serum IL-10,TGF-β1 play an important role in the occurrence of steroid-resistant AR patients.

Objective To investigate the function of activator protein-1(AP-1)and nuclear factor-κB(NF-κB)on the treatment of montelukast sodium tables for patients with steroid-resistant allergic rhinitis (AR). Methods A random-ized study was carried out in 50 patients with steroid-resistant AR. 25 cases were treated with montelukast sodium ta-bles(montelukast sodium group), and the others by ATP tables(placebo group). Score system was used to compare the therapeutic effect of these two drugs on clinical symptoms and signs on 21th day after therapy. The DNA binding activ-ities of Ap-1 and NF-κB were measured by electrophoretic mobility shift assay(EMSA). The expression of IL-4, IL-5 and IL-10 were determined by enzyme-linked immunoadsorbent assay (ELISA). Results The therapeutic effect rate in montelukast sodium group was significantly higher than that in placebo group at 21 days after treatment begining (P<0.01). Compared with placebo group, the DNA binding activities of Ap-1 and NF-κB were significantly reduced in montelukast sodium group (P<0.01). The score reduce index (SRI)of the clinical symptoms and signs was negatively correlated with the DNA binding activities in montelukast sodium group (P<0.05), but there was any correlation be-tween them in placebo group(P>0.05).The expression of IL-4 and IL-5 in montelukast sodium group were significantly lower and IL-10 was higher than those in placebo group (P<0.01). Conclusion The treatment effect of montelukast sodium tables for steroid-resistant AR may be aroused by suppressing the Ap-1 and NF-κB DNA binding activities, and effecting the expression of IL-4, IL-5 and IL-10.