Objectives To explore the expression of macrophage inflammatory protein-1beta (MIP-1β) in patients with none-small cell lung cancer (NSCLC) of different pathological types and its association with cancer clinical stages and metastasis of lymph nodes.Methods MIP-1β mRNA from fresh lung tissue of 38 NSCLC patients was amplified by RT-PCR and half-quantified.Immunohistochemical technique was performed to find out the expression of MIP-1β in paraffin-embedded lung tissue from 66 patients with NSCLC.The area and degree of stain were evaluated to determine the positive rate，which was compared between with or without metastasis of lymph nodes，different pathological types and TNM clinical stages.Results MIP-1β protein was found in cytoplasm of malignant cells of squama cell cancer and adenocarcinoma without significant difference between them，while not found in bronchus-alveolus cell cancer.The MIP-1β mRNA expression in squama cell cancer and adenocarcinoma were significant higher than which in bronchus-alveolus cell cancer without significant difference between each other.The positive rates of MIP-1β in lung cancer of Ⅰ，Ⅱ and Ⅲ stages were 74.2%，29.4% and 85.7% respectively，which of Ⅰ and Ⅲ stages cancer were significant higher than Ⅱ stage without significant difference between each other.The positive rates of MIP-1β in lung cancer with or without metastasis of lymph nodes were 45.8% and 76.3% respectively with significant difference between them.Conclusion MIP-1β is expressed in lung cancer cells and relates to the pathological type，TNM stage and the metastasis of lymph nodes.
Objective To establish a beta 2 adrenergic receptor ( β2 R) down-regulative asthmatic model, to explore the mechanism of β2 R down-regulation and effectiveness of corticosteroids. Methods Thirty-two BALB/c mice were divided into four groups, ie. a control group, an asthmatic group, a β2R downregulative group, and a dexamethasone group. The asthmatic group, the β2 R down-regulative group and the dexamethasone group were sensitized on 0th, 14th and 21th day by intraperitoneal injection of ovalbumin ( OVA) together with aluminumhydroxide in a total volume of 200 μL. Fromthe 28th day on, the mice were challenged with an aerosol of 1% OVA( W/V) in saline using an ultrasonic nebulizer 30 min/d for a week.The β2 R down-regulative group and the dexamethasone group underwent the same procedure as the asthmatic group besides daily intraperitoneal injection of 60 μg salbutamol and inhaling an aerosol of 0. 01%salbutamol 30 min/d for a week half an hour before challenged with OVA. The dexamethasone group was injected dexamethasone 5 mg·kg- 1·d - 1 for a week by intraperitoneal injection on the basis of OVA challenge and salbutamol intervention. The control group was sensitized and challenged with PBS. Airway resistance was measured by plethysmography. IL-4 and IFN-γlevels in BALF, and total IgE concentration in serum were measured by ELISA. Total and differential cell counts in bronchial alveolar lavage fluid ( BALF)were measured. Total amount and number of β2 R in lung tissue were evaluated by immune blotting analysis and radioligand receptor binding assay, respectively. Results Compared to the control group and the dexamethasone group, airway resistance of the asthmatic group and the β2 R down-regulative group increasedobviously provocated by a high dose of acetylcholine ( P lt;0. 01) . Eosinophil, neutrophil, lymphocyte counts in BALF, IL-4 level in BALF, and total IgE in serumincreased significantly also ( P lt;0. 01) , while IFN-γin BALF decreased significantly. Compared to the control group, the asthmatic group and the dexamethasonegroup, the total amount and number of β2 R significantly decreased in the β2 R down-regulative group ( P lt;0. 01) , while no significant difference was found among the control group, the asthmatic group and the dexamethasone group. Conclusions β2 R down-regulative asthmatic model can be successfully establishedby peritoneal injection and inhalation of salbutamol on the basis of OVA sensitization and challenge.Dexamethasone can prevent the down-regulation of β2 R.