The anti-apoptotic effect of cytoplasmic alpha-fetoprotein in hepatoma cells induced by all-trans retinoic acid involves activation of the PI3K/AKT signaling pathway / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To explore the effect of alpha-fetoprotein (AFP) on transduction of the PI3K/ AKT signal in hepatocellular carcinoma cells and the role played by AFP in resistance to cytotoxicity of all-trans retinoic acid (ATRA).</p><p><b>METHODS</b>The effects of ATRA of human liver cancer cells was assessed using the BEL-7402 cell line with the MTT assay (to evaluate proliferation), microscopy (to evaluate morphology), flow cytometry (to evaluate apoptosis), laser confocal microscopy and coimmunoprecipitation (co-IP; to evaluate co-localization and interaction of AFP with PTEN), Western blotting (to evaluate expression of phosphorylated-protein kinase B (pAKT) and Src, and RNA interference (RNAi)-mediated knockdown of AFP. Finally, application of the PI3K-specific inhibitor Ly294002 was used to monitor the influence of AFP in transduction of the PI3K signal pathway.</p><p><b>RESULTS</b>The human hepatoma cell line BEL-7402 were resistant to ATRA cytotoxicity. PTEN and AFP co-localized in the cytoplasm, and co-IP indicated that AFP interacts with PTEN in BEL-7402 cells.RNAi knockdown of AFP expression led to reduced growth of BEL-7402 cells.BEL-7402 cells transfected with AFP-short interfering (si)RNA vectors showed enhanced sensitivity to ATRA and reduced expression of pAKT(Ser473) and Src; Ly294002 reduced the role of AFP in stimulating expression of pAKT(Ser473) and Src.</p><p><b>CONCLUSION</b>AFP can activate transduction of the PI3K/AKT signal, and expression of AFP in hepatoma cells is a pivotal event for resisting ATRA-induced apoptosis.</p>

Effect of Modified Zhisou Powder on the lung function of chronic obstructive pulmonary disease model rats of northwest China cold dryness syndrome / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe Modified Zhisou Powder (MZP) on the lung function of chronic obstructive pulmonary disease (COPD) model rats of northwest China cold dryness syndrome (NCCDS).</p><p><b>METHODS</b>Totally 90 male Wistar rats were randomly divided into three groups, i.e., the normal control group (n =20), the COPD model group (n =35), and the COPD of NCCDS group (n =35). The COPD model was established by tracheal dripping porcine pancreatic elastase (PEE) in combination with fumigation for 90 days. The COPD of NCCDS model was set up by tracheal dripping PEE +fumigation + cold and dry environmental stress for 90 days. Then rats in the COPD of NCCDS were randomly divided into the MZP intervention group (n =11 )and the normal saline intervention group (n =10).All intervention lasted for 15 successive days. The lung function was detected using Small Animal Lung Function Device at day 90 and day 105. And the lung pathology was also observed.</p><p><b>RESULTS</b>Little amount of sputum sound could be heard in the airway of the COPD model group and the COPD of NCCDS group. Pathological section showed alveolar ectasia, narrowed and broken alveolar septa, forming larger capsular space with infiltration of inflammatory cells. Rats in the COPD of NCCDS group showed chills, increased amount of drinking water, and loose stool. MZP could improve their symptoms. As for lung function test, compared with the normal control group, Te increased in the COPD model group (P <0.01), and EF50 decreased (P<0.05). PEF and EF50 decreased (P <0.01), Ti and Te increased (P <0.01, P <0.05) in the COPD of NCCDS group. Compared with the normal saline intervention group, PEF and EF50 increased (P < 0.01), Ti and Te decreased (P <0.01) in the MZP intervention group.</p><p><b>CONCLUSION</b>MZP could improve the symptoms of COPD rats of NCCDS, and delay the velocity of decreased lung function.</p>

The expressions of TNF-alpha and MMP-9 in serum and MMP-1 mRNA in the bone tissue in chronic obstructive pulmonary disease patients of cold dryness syndrome in northwest China / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the expressions of tumor necrosis factor a (TNF-alpha) and matrix metalloproteinase (MMP-9) in serum and matrix metalloproteinase 1 (MMP-1) mRNA in the bone tissue in chronic obstructive pulmonary disease (COPD) patients of cold dryness syndrome (CDS) in northwest China, thus providing reference for wholism treating COPD of CDS.</p><p><b>METHODS</b>Twenty-one male Wistar rats were randomly divided into three groups, i.e., the normal control group, the COPD model group, and the COPD of CDS group, 7 in each group. The COPD model was established by dripping porcine pancreatic elastase (PEE) in trachea combination with cigarette smoking, and the COPD of CDS model was also set up by dripping PEE in trachea in combination with cigarette smoking and cold-dry environmental stress. Serum contents of TNF-alpha and MMP-9 were determined using ELISA. The MMP-1 mRNA expression in rats' bone tissue was detected using fluorescent quantitative PCR.</p><p><b>RESULTS</b>Compared with the normal control group, the serum MMP-9 level obviously increased in the COPD of CDS group (P < 0.05). The MMP-1 mRNA expression level in the bone tissue of the COPD of CDS group and the COPD model group also obviously increased (P < 0.01, P < 0.05). The MMP-1 mRNA expression level was obviously higher in the COPD of CDS group than in the COPD model group (P < 0.01). There was no statistical difference in the serum TNF-alpha level among the three groups (P > 0.05).</p><p><b>CONCLUSION</b>CDS could increase the serum MMP-9 level and the MMP-1 mRNA expression in the bone tissue, which might be one of reasons for the fact that cold and dry environment causes more bone resorption and bone degradation in COPD.</p>

Role of mucosal immunity in pathogenesis of asthma and allergic rhinitis / 第二军医大学学报

Objective: To explore the role of mucosal immunity in the pathogenesis of asthma and allergic rhinitis and to search for common materials for the two conditions, so as to reveal the relationship of asthma and allergic rhinitis. Methods: A total of 82 patients with acute asthma, including 44 with asthma alone and 38 with asthma complicated with rhinitis, were included in this study. Another 30 patients with allergic rhinitis alone and 30 healthy controls were also included. The saliva, sputum, and nasal secretions (all 2 ml) were collected to observe the secretory immunoglobulin-A (sIgA) by enzyme-linked immunosorbent assay (ELISA). Flow cytometry was employed to observe CD4 -, CD8+ lymphocytes in blood samples (2 ml) obtained from the elbow vein. The levels of eosinophil cationic protein (ECP) and serum total immunoglobulin E (T-IgE) were assessed by fluorescent enzyme immunoassay. Results: Sputum sIgA levels in the asthmatic group, combination group, and rhinitis group were significantly lower than that in the normal control group (P<0. 01); saliva sIgA levels in the asthmatic group and combination group had a decreasing tendency but had no significant difference compared with that in the normal control group. sIgA levels in the nasal secretions in the asthma group and combination group were significantly higher than those in the normal control group (P<0. 05) and rhinitis group (P<0. 01), and there was no significant difference between the rhinitis group and the control group. Blood CD4+ cells in the asthmatic group and combination group were decreased than that in the normal control group (P<0. 05). Blood CD8 + cells were similar in all the groups. CD4+/CD8 + cells in the asthma group was significantly more than those in the normal control group and rhinitis group (P<0. 05). Serum T-IgE-levels in the combination group and rhinitis group were significantly higher than that in the normal control group (P<0. 01). Serum ECP was hardly detected in the normal control group; that in the asthma group was significantly higher than that in the rhinitis group (P<0. 05), and that in the combined group was not significantly different with those in the asthma group or the rhinitis group. ECP and T-IgE levels were positively correlated (r=0. 467, P<0. 05) in the asthma group, and not correlated in other groups. Conclusion: The asthma and allergic rhinitis are both closely related to mucosal immunity, which is the manifestation of asthma and rhinitis in different sites. The sIgA, CD4 +, CD8+, ECP, and T-IgE may be the material bas for mucosal immunity.