AIM: To investigate the changes of T cell cycle, the expression of bcl-2 in allergic asthmatic mice and the effects of dexamethasone on them. METHODS: An animal model with asthma was established by means of ovalbumin sensitizing-challenging. CD3 expression in spleen and lymphocytes in bronchoalveolar lavage fluid (BALF), T cell cycle and Bcl-2 expression in spleen were detected by flow cytometry. RESULTS: In BALF lymphocytes and spleen lymphocytes, CD3 expression rate in the asthmatic group was significantly higher than that of control group. In BALF lymphocytes, CD3 expression rate in the asthma plus dexamethasone group was significantly lower than that of the asthmatic group. However, in spleen lymphocytes, CD3 expression rate in the asthma plus dexamethasone group was significantly higher than that of the asthmatic group. In spleen lymphocytes, the cell count in S phase, G 2+M phase and apoptosis rate of T cell from the asthmatic group were significantly higher than that from the control group. Cell count in S phase, G 2+M phase and apoptosis rate of T cell from the asthmaplus dexamethasone group was significantly lower than that from the asthmatic group. The Bcl-2 expression rate of T cell from the asthmatic group was significantly higher than that from the control group. CONCLUSIONS: In the allergic asthmatic mice model, T cell count, proliferation and activation of T cells, apoptosis rate of T cells in spleen lymphocytes increase, meanwhile bcl-2 expression also increases significantly. There was no significant effect of dexamethasone on the bcl-2 expression. The therapeutic effects of dexamethasone on asthma may be not due to the inhibition of the bcl-2 expression in T cells.

This study examined the effects of arsenic trioxide on apoptosis and interleukin4 release in T cells of asthmatic patients in vitro and investigated the role of Bcl2 in the active mechanism. Tcells were isolated from asthmatic patients (n=21) and healthy controls (n=20), and then treated with arsenic trioxide and dexamethasone. Cell apoptosis was measured using fluorescence microscopy, flow cytometry and a cytochrome c ELISA kit. Interleukin4 levels in the serum and in supernatants from T cells were quantified by ELISA. Flow cytometric analysis and immunofluorescence studies were performed to determine Bcl 2 expression. Tcells of the asthmatic patients (I.e. without treatment) exhibited decelerated spontaneous apoptosis after 24 h incubation in vitro when compared to T cells of the healthy controls. With dexamethasone treatment, an increase in apoptosis of Tcells was not significantly different between both groups, irrespective of the method used. Arsenic trioxide treatment, however, significantly increased the apoptosis of T cells of the asthmatic group and showed a slight effect on the control group. In asthmatic patients, elevated levels of interleukin 4 and upregulated Bcl 2 expression were detected. Moreover, in vitro, T cells of asthmatic patients spontaneously released more interleukin4 and exhibited more Bcl 2 expression than T cells from the control group. Arsenic trioxide treatment significantly decreased interleukin4 release and downregulated Bcl 2 expression in asthmatic patients, while it only slightly affected healthy controls. Dexamethasone treatment decreased interleukin4 release in both groups examined. It did not significantly influence Bcl2 expression. These results suggest that arsenic trioxide induces T cell apoptosis and decreases interleukin4 release in T cells of asthmatic patients in vitro and that downregulation of Bcl2 expression may be an important mechanism.

AIM To study the possible mechanism of the treatment of arsenic trioxide on asthma. METHODS T cells isolated from 21 asthmatic patients and 20 healthy controls were treated with arsenic trioxide (0.1 mg·L-1) or dexamethasone (5 mg·L-1),in vitro, for 24 h. Interleukin-4 (IL-4) levels in supernatants from T cells were quantified with ELISA. Cell apoptosis was measured by using fluorescence microscopy, flow cytometry and cytochrome c ELISA kit. RESULTS T cells of asthmatic patients spontaneously released more IL-4 than that of healthy controls. Arsenic trioxide significantly decreased IL-4 release of T cells from asthmatic patients, which was more obvious compared with healthy controls. Dexamethasone decreased IL-4 release in both groups. Apoptosis percentage and cytochrome c content in cytoplasm of T cells from asthmatic patients were lower than those from healthy controls. Arsenic trioxide significantly increased the apoptosis percentage and cytochrome c content in cytoplasm of T cells in the asthmatic group, and had slighter effects on that in healthy controls. Dexamathasone increased the apoptosis percentage and cytochrome c content of T cells in both groups. CONCLUSION The mechanism of the treatment of arsenic trioxide on asthma involves the induction of T cell apoptosis and decrease of IL-4 release in asthmatic patients.

OBJECTIVE: To observe the effects of glycyrrhizin on hydroxyproline(HYP),hyaluronic acid(HA) and laminin(LN) in pulmonary fibrosis model rats.METHODS: A total of 80 SD rats were randomly divided into normal control group,model group,hormone group(prednisone 0.6 mg?kg?d-1),and glycyrrhizin group(10 g?kg?d-1).The latter 3 groups were established into pulmonary fibrosis model with bleomycin,and on the second day after modelling,each group was given corresponding test drugs(the normal group and model group were treated with same amount of normal saline) then the changes of the levels of HYP in lung tissues,and serum levels of HA and LN in every group were observed at 7 and 28 days respectively.RESULTS: In glycyrrhizin group compared with model group,the contents of HYP in lung tissue,HA and LN in serum decreased significantly(P

OBJECTIVE: To explore the effect of glycyrrhizin on eotaxin expression in lung tissue from asthmatic model mice and the mechanism for glycyrrhizin to treat bronchial asthma.METHODS: The mice were randomized to asthma model group,prednisone-treated group and glycyrrhizin-treated group and normal control group.Egg protein asthma mouse model was established before being giving the corresponding drugs.Then the mice were sacrificed after 4 weeks for the counting of eosinophils in bronchoalveolar lavage fluid(BALF) and detection of Eotaxin expression in lung tissues by immunohistochemistry,with the results compared with normal control group.RESULTS: In glycyrrhizin-treated group compared with model group,the counting of eosinophils in BALF were decreased(P

AIM: To explore the effect of liquorice on airway inflammation and Th_1/Th_2 imbalance in chronic asthma. METHODS: The chronic asthma model was established by intraperitoneal ovalbumin. The effect of liquorice on mice model of chronic bronchial asthma was observed, and the levels of serum IFN-? and IL-4 were tested by ELISA. RESULTS: Decreasing inflammatary cells infiltration in pulmonary tissue slices of tiny bronchial wall together with increasing serum IFN-? and decreasing serum IL-4 levels. CONCLUSION: Liquorice can adjust Th_1/Th_2 imbalance and inhibit the airway inflammation.

AIM To investigate the effects of D galactose on bone contents of hydroxyproline(HOP), calcium, microelements and activities of antioxidation in mice. METHODS Twenty female kunming mice at three months of age were used in this study. D galactose at dose of 1 g?kg -1 ?d -1 was given subcutaneous injection daily to the mice for 42 days. The right femurs were collected to determine the bone dry weight, bone hydroxyproline content, bone calcium, and bone microelements. The activities of catalase (CAT), glutathione peroxidase (GSH Px) and superozide dismutases (SOD) in blood, and contents of methylenedioxyamphetamine (MDA) in serum, lipofuscin in liver were determined. RESULTS The bone dry weight, hydroxyproline, calcium of bone decreased significantly in D galactose treaded group(compared with control group, P

Aim To investigate the effects of glycyrrhizin on the proliferation of ASMC stimulated by fetal calf or histamine in rats. Methods Cell culture of rat ASMC, MTT assay, flow cytometry and cell growth counts were used in this study. Results ①In the culture medium containing 100g?L -1 fetal calf serum, Glycyrrhizin at low concentration(6?10 -5 mol?L -1 ) stimulated the increase of A 570 in ASMC. This effect descended with increasing glycyrrhizin concentration and changed to be inhibitory at high concentration (from 384?10 -5 mol?L -1 to 1 536 ?10 -5 mol?L -1 ). In the culture medium containing 10 -2 mol?L -1 histamine, Glycyrrhizin at both low and high concentration inhibited the increase of A 570 in ASMC. ②In the culture medium containing 100 g?L -1 fetal calf, Glycyrrhizin at low concentration(6?10 -5 mol?L -1 ) stimulated the proliferation of ASMC. This effect descended with increasing glycyrrhizin concentration and changed to be inhibitory at high concentration (from 384?10 -5 mol?L -1 to 1 536 ?10 -5 mol?L -1 ). In the culture medium containing 1 g?L -1 histamine, Glycyrrhizin at both low and high concentration inhibited the proliferation of ASMC. ③In the culture medium containing 100 g?L -1 fetal calf or 10 -2 mol?L -1 histamine, with increasing glycyrrhizin concentration, the cell count in G 1 phase increase, the cell count in G 2 and M phase decrease. Conclusion ①Glycyrrhizin accelerated the proliferation of ASMC stimulated by fetal calf at low concentration, inhibited the proliferation at high concentration. ②Glycyrrhizin inhibited the proliferation of ASMC stimulated by histamine at both low concentration and high concentration.

Objective To evaluate the diagnostic efficiency of Q?SPECT, CTPA, Q?SPECT/CT, and Q?SPECT/CTPA for pulmonary embolism (PE) in rabbit models. Methods (1) The PE models were constructed by injecting Gelfoam into the femoral vein of New Zealand rabbits ( n=30) . Q?SPECT, CTPA, Q?SPECT/CT and Q?SPECT/CTPA fusion images were obtained by integrated SPECT/CT. (2) All images were interpreted by two experienced nuclear radiologists who were blind to pathologic findings. The locations and numbers of lung lobes with PE were recorded respectively. ( 3) Serial sectioning of the lungs was per?formed and pathologically determined. (4) Se, Sp and Ac of different methods were compared using McNemar test;PPV and NPV were compared usingχ2 test. Kappa test was used to analyze the consistency between two nuclear radiologists. Kappa values<0.40 were interpreted as poor consistency, 0.40 to 0.75 as moderate con?sistency, >0.75 as good consistency. Results (1) Histologically confirmed emboli were present in a total of 26 pulmonary lobes and absent in 79 lobes. (2)The Se, Sp, Ac, PPV, and NPV of 4 imaging methods were:53.8%(14/26), 93.7%(74/79), 83.8%(88/105), 14/19, 86.0%(74/86) for Q?SPECT;73.1%(19/26), 96.2%(76/79), 90.5%(95/105), 86.4%(19/22), 91.6%(76/83) for CTPA;76.9%(20/26), 93.7%(74/79), 89.5%(94/105), 80.0%(20/25), 92.5%(74/80)for Q?SPECT/CT;88.5%(23/26), 91.1%(72/79), 90.5%(95/105), 76.7%(23/30), 96.0%(72/75) for Q?SPECT/CTPA. (3) McNemar test showed Q?SPECT/CT and Q?SPECT/CTPA had higher diagnostic Se for the detection of PE than Q?SPECT (χ2=4.167, 7.111, both P<0.05) , but without any significant difference with CTPA in diagnostic efficiency (χ2=0-2.250, all P>0.05) . Q?SPECT/CT had higher diagnostic Ac than Q?SPECT (χ2=4.167, P<0.05) . There was no significant difference between Q?SPECT/CT and Q?SPECT/CTPA in diagnostic effi?ciency (χ2=0.001-1.333, all P>0.05). (4)Kappa values of 4 imaging methods for radiologist 1 and 2 were 0.902, 0.915, 0.973, and 0.884. Conclusions Q?SPECT/CT imaging provides good Se and Sp. The diag?nostic efficiency of Q?SPECT/CT is better than that of Q?SPECT and is corresponded roughly to the efficien?cy of CTPA, Q?SPECT/CTPA. The diagnosis of two radiologists on Q?SPECT/CT images has the best con?sistency.

Objective To study the clinical efficacy and safety of iguratimod in the treatment of active rheumatoid arthritis. Methods Ninety patients with rheumatoid arthritis were randomly divided into three groups, with 30 cases in each group. Group A: oral administration of iguratimod, 25 mg two times a day, and oral administration of methotrexate, 10 mg once a week. Group B:oral administration of iguratimod, 25 mg two times a ady. Group C: oral administration of methotrexate, 15 mg once a week. According to the American College of Rheumatology criteria for judging 20%, 50%and 70%(ACR20, ACR 50 and ACR 70) improvement of swollen and tender joint was judged according to the American College Of Rheumatology criteria, and the adverse reactions were observed. Results After the treatment in group A and group B ACR20, ACR50 and ACR70 were higher than those in group C [76.67%(23/30) and 60.00% (18/30) than 40.00% (12/30), 50.00% (15/30) and 33.33% (10/30) than 20.00% (6/30), 23.33%(7/30) and 13.33%(4/30) than 6.67%(2/30)], and in group A was higher than that in group B. The differences were statistically significant (P<0.05). The adverse reaction rate in group A and group B was significantly lower than that in group C:16.67%(5/30) and 13.33%(4/30) than 30.00%(9/30), and the difference was statistically significant (P<0.05); the adverse reaction occurred rate in group A and group B, had no significant difference (P>0.05). Conclusions Monotherapy with iguratimod in the treatment of active rheumatoid arthritis is superior to methotrexate, and has fewer side effects. The combined application of the two drugs is more effective, and can reduce the dose of methotrexate and reduce the incidence of side effects, which is worthy of clinical application.