Effects of polysaccharide of radix ranunculi ternati on immunomodulation and anti-oxidation / 中国中药杂志

<p><b>OBJECTIVE</b>To study effects of polysaccharide of Radix Ranunculi Ternati (PRT) on immunological function and anti-oxidation activity of mouse.</p><p><b>METHOD</b>Cell proliferations of splenocyte, thymocyte and peritoneal macrophage were measured by MTT colorimetry. The phagocytic function of peritoneal macrophage was measured by neutral red colorimetric method. The disoxidation power of PRT was measured by Prussian blue method. The clearing effect of PRT on hydroxyl radical was measured by salicylic acid capture method. The clearing effect of PRT on superoxide anion free radical was measured by pyrogallol auto oxidation method.</p><p><b>RESULT</b>PRT among 25-400 mg x L(-1) could enhance thymocytes and spleen lymphocyte proliferation and macrophage phagocytosis. PRT(200 mg x L(-1)) has the strongest macrophage proliferation. PRT in different concentration has shown some disoxidation effects. PRT in 8 g x L(-1) has nearly the same ability of clearing x OH by Vit C with the same concentration. The clearance rate of PRT on O2*- is 95.39%.</p><p><b>CONCLUSION</b>PRT can enhance the cell proliferation capability of thymocytes, spleen lymphocytes and peritoneal macrophages. PRT can enhance macrophage phagocytosis in a dose-response relationship. PRT has saome disoxidation power and strong ability of clearing x OH and O2*-.</p>

In vitro arsenic trioxide induces apoptosis in T cells of asthmatic patients by a Bcl-2 related mechanism / 药学学报

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.

Effects of arsenic trioxide on apoptosis and interleukin-4 release of peripheral T cells from asthmatic patients in vitro / 中国药理学与毒理学杂志

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.

Effect of Glycyrrhizin on Eotaxin Expression in Lung Tissue in Asthmatic Model Mice / 中国药房

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

Interventional Effect of Glycyrrhizin on Hydroxyproline,Hyaluronic Acid,and Laminin in Pulmonary Fibrosis Model Rats / 中国药房

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

Effects of glycyrrhizin on the proliferation of ASMC induced by fetal calf or histamine in rats / 中国药理学通报

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.

The effect of D-galactose on bone metabolism in mice and its mechanism / 中国药理学通报

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

Effect of liquorice on airway inflammation and TH_1/TH_2 imbalance in mouse model / 中国临床药理学与治疗学

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.

Determination of T cell cycle and the expression of bcl-2 in asthmatic mice and its significance / 中国病理生理杂志

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.