In recent years, with the introduction of novel vectors capable of highly efficient transduction ,ribozymes and dexyribozymes have been become an ideal approach to anticancer therapy due to their high efficiency and lack of severe adverse effects. As many high efficiency targets have been found for cancer therapy, targeted therapy using ribozymes and deoxyribozymes may have multiple effects such as induction of tumor apoptosis and inhibition of tumor growth, metastasis, and angiogenesis.

CD+4 CD+25 regulatory T cell (Treg) has immune incompetent and immune suppression functions, and is a kind of suppressor T-cell subsets. It can inhibit the activation and proliferation of CD+4 T cells and CD+8 T cells, so as to effectively suppress the immune system to foreign organ and reduce the graftversus-host disease (GVHD) after hematopoietic stem cell transplantation (HSCT), without affecting the role of graft-versus-leukemia (GVL), which plays an important role in the transplantation immune tolerance.

Objective To explore the effect of proteasome inhibitor bortezomib (BOR) on proliferation inhibition and apoptosis in imatinib-resistant chronic myeloid leukemia cell line K562/G01. Methods MTT assay was used to observe the effect of growth inhibitory of cells; flow cytometry was used to detect cell cycle and apoptosis. Results K562/G01 cells was not sensitive to imatinib,1C50 values of imatinib to K562 and K562/G01 cells was (20.09±1.38) and (0.54±0.13) μmol/L,respectively; BOR could inhibit proliferation in K562/G01 cell,peaked at 48 h,and IC50 value of BOR to K562/G01 was (23.10±2.71) nmol/L. G2/M phase cell cycle arrest and significant apoptosis peak could be seen by flow cytometry with increased in the concentration and action time of BOR. Conclusion BOR can inhibit proliferation and induce apoptosis in imatinib-resistant K562/G01 cell,the mechanism may be related to cell cycle G2/M phase arrest.

Objective To investigate the apoptosis-inducing effect,inhibiting multidrug resistanceassociated protein 1 (MRP-1) and mRNA expression of arsenic trioxide (As2O3) and buthionine sulfoximine (BSO) in multidrug-resistant cell K562/ADM.To compare the effect of As2O3 and the combined group.To determine the effect of intracellular glutathione (GSH) content on the arsenic effect.Methods The arsenic group (0.5 μmol/L,2.0 μmol/L,5.0 μmol/L) solo or combined BSO (100 μmol/L) applied in multidrugresistant cell K562/ADM.The cell proliferating activity was assessed with MTT assay.The cell apoptosis effect was detected by Annexin-V and propidium iodide (PI) staining.Intracellular GSH contents were measured using GSH Assay Kit by spectrophotometry.MRP1 expression was determined by flow cytometry.MRP1 mRNA expression were directed by semi-quantitative RT-PCR.Results With the GSH contents were degraded by the combination of clinic dose arsenic group (0.5 μmol/L,2 μmol/L) and BSO (100 μmol/L),the K562/ADM cell proliferating activity was obviously inhibited and the cell apoptosis-inducing effect was increased in 24 hours.In 72 hours,the rate of apoptosis with arsenic (0.5 μmol/L,2 μmol/L) were (8.32± 2.11) ％,(16.75±3.56) ％.After the GSH contents were degraded,the rates of apoptosis in the combination group (clinic dose arsenic group) were (82.15±9.28) ％ and (92.72±9.41) ％.The fluorescence intensity of MRP1 in 72 hours of the combination group (clinic dose arsenic group) was 8.20±0.92 and 10.40±2.33.The MRP1 attenuated effect of the combination group (clinic dose arsenic group) was obviously stronger than that of the high dose arsenic group (21.30±3.09).Conclusions The intracellular GSH contents closely correlate with the arsenic effect.The cell apoptosis-inducing effect of the combination of clinic dose arsenic and BSO on K562/ADM cell is obvious increased.The combination of clinic dose arsenic and BSO obviously inhibit MRP1 expression and MRP1 mRNA expression in K562/ADM cell.

Objective To investigate the apoptosis-inducing effect , inhibiting MRP-1 and mRNA expression of arsenic trioxide (As2O3) and buthionine sulfoximine (BSO) on multidrug-resistant cell-K562A/DM cell .To compare the effect of As2O3 and the com-bined group .To determine the effect of intracellular GSH content on the arsenic effect .Methods To investigate the effect of the arse-nic group (0.5,2.0,5.0μmol/L)and/or BSO (100μmol/L) on multidrug-resistant cell -K562/ADM cell.To detect the change of the correlated index .⑴Intracellular GSH contents were measured using Glutathione Assay Kit by spectrophotometry .⑵MRP-1 expression were determined by flow cytometry .⑶MRP-1 mRNA expression were directed by semi-quantitative RT-PCR.Results After the GSH contents were degraded by the combination of clinic dose arsenic group (0.5,2μmol/L) and BSO(100μmol/L), in 48 hours and 72 hours, the effect of the combination group ( clinic dose arsenic group ) was obviously stronger than the clinic dose arsenic group and the high dose arsenic group .In 48 hours, the MRP-1 mRNA depressive effect of the combination group ( clinic dose arsenic group ) was obviously stronger than high dose arsenic group .In 72 hours, the MRP-1 depressive effect of the combination group ( clinic dose arsenic group ) was obviously stronger than high dose arsenic group .Conclusions The intracellular GSH contents closely correlated with the arsenic effect .The combination of clinic dose arsenic and BSO inhibit obviously MRP-1 expression and MRP-1 mRNA expres-sion in K562/ADM cell.

Objective To explore the anti-inflammatory mechanisms of three stains. Methods Airpouch induced acute inflammation rat model was developed by subcutaneous injection of carrageenan.Inflammatory invasion and tumor necrosis fator-alpha (TNF-α) expression levels of the inflammed skins were examined by immunohistochemical methods and digital image analysis. The anti-inflammatory action of the 3 different statins was compared. Results Stains could inhibit inflammatory invasion and the expression of TNF-α. Conclusion The statins have demonstrated strong inhibition of inflammation.

To study the effects of Xifeng Capsule, a compound traditional Chinese herbal medicine, combined with carbamazepine on spontaneous epileptic seizure induced by lithium and pilocarpine in rats and the expression level of multidrug resistance-associated protein 1 (MRP1).

ObjectiveTo study the protective effects of Qiqiong(QQJN) on focal cerebral ischemia/reperfusion injury and its mechanism. MethodsMiddle cerebral artery occlusion(MCAO) was used to make focal cerebral ischemia/reperfusion model by intravascular nylon filament occlusion. The protective effects of QQJN were evaluated by investigating neurological function score, percentage of cerebral infarction, pathomorphology of brain, the activity of SOD and the content of MDA in hrain tissue,thrombogenesis and platelet aggregation in vitro. ResultsCompared with model group, QQJN(4.4、8.8g/kg)could decrease the neurological score in 8 and 22h after reperfusion, reduce the percentage of cerebral infauction,improve pathomorphology of brain, decrease the length, wet weight and dry weight of thromb and inhibit platelet aggregation. ConclusionQQJN had protective effects on focal cerebral ischemia/reperfusion injury. The role of anti-injury of free radicals,inhibit thrombogenesis and platelet aggregation should contribute to its neuroprotective effects.

Objective To investigate the relationship between the CD+4 CDHigh25 regulatory T cells and cytokine IL-10 and acute graft-versus-host disease (aGVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Methods Flow cytometric was used to detect the percentage of CD+4 CDHigh25Foxp3High Treg cell and CD+4 CDHigh25 CDLow127 Treg cell in CD+4 T cells and at the same time ELISA was used to test the serum IL-10 levels in corresponding period. Results 13 patients have received hematopoietic function reconstruction. aGVHD group of CD+4 CDHigh25 CDLow127/CD+4 and CD+4 CDHigh25 Foxp3High/CD+4 ratio were significantly lower than non-aGVHD group, the difference was statistically significant (P ＜0.01); Ⅲ-Ⅳ degree of aGVHD subgroup was lower than Ⅰ - Ⅱ degree of aGVHD subgroup, but no statistical significance(P ＞0.05); the same as between-group CD+4 CDHigh25 CDLow127/CD+4 and the CD+4 CDHigh25 Foxp3High/CD+4 has no significant difference;aGVHD group of IL-10 concentration was significantly lower than non-GVHD group, the difference was statistically significant (P ＜0.01). Treg cell and IL-10 changes in correlation, r = 0.557, P ＜0.05. Conclusion The level of Treg cell was closely related to the occurrence of aGVHD after allo-HSCT. So it is very important to monitor the Treg cell level for clinical early diagnosis of aGVHD and predict prognosis of aGVHD and guide the application of immunosuppressant. CD127 can serve as a Treg cell surface-specific marker, to promote the detection of Treg cell and purification. IL-10 was an important negative regulator. Treg cell and IL-10expression in patients with aGVHD was correlation, which may provide some basis for Treg cell immunosuppressive mechanism.