OBJECTIVE: To investigate the effects of prophylactic drugs on allergic rhinitis. METHOD: Thirty patients diagnosed as allergic rhinitis based on mugwort allergen were randomly divided into three groups: budesonide group (n = 10), saline group (n = 10) and control group (n = 10). The patients in budesonide group and saline group respectively received budesonide nasal spray (64 microg per, 256 microg once daily) and saline nasal spray twice daily starting two weeks before the date which the patient onset last year and continuing up to the end of the pollen season. The patients in control group were treated without any processing. The nasal symptom scores and attack times of the three groups was recorded. RESULT: During the pollen season, 2 patients attacked in the budesonide group (20%), and all the patients attacked in saline group and control group (100%). Statistical significance was found among the three groups (P < 0.01), and between budesonide group and the other two groups (P < 0.01). The budesonide group had lower symptom score than the other two groups and a postponed attack time. All the differences had Statistical significance (Value of chi-square statistic = 21. 558, P < 0.01, Fisher exact test P < 0.01). CONCLUSION Prophylactic administration of budesonide, starting two weeks before the date which the patient onset may release symptom and even avoid the attack of the allergic rhinitis based on mugwort allergen.
Adolescent ; Adult ; Aged ; Anti-Inflammatory Agents ; therapeutic use ; Budesonide ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Pollen ; Rhinitis, Allergic, Seasonal ; drug therapy ; immunology ; prevention & control ; Young Adult

Objective To evaluate the effect of sevoflurane on unfolded protein response-related cell apoptosis during acute lung injury in rats undergoing cardiopulmonary bypass ( CPB) . Methods For-ty-eight clean-grade healthy adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 250-300 g, were allocated into 3 groups ( n=16 each) using a random number table method: sham operation group ( Sham group) , CPB group and sevoflurane group ( Sev group) . Left common carotid artery and right internal jugu-lar vein were only cannulated in group Sham. After establishing CPB, the flow rate was gradually adjusted to the maximum (100 ml·kg-1·min-1) and maintained for 60 min in group CPB. Two percent sevoflurane was inhaled for 30 min, and 15 min later the model of CPB was established in Sev group. Rats were sacri-ficed at 1 h after the end of CPB, lungs were removed and lung tissues were obtained. The pathological changes and ultrastructure of lung tissues were examined with a light microscope and with an electron micro-scope, respectively. The wet to dry weight ratio ( W∕D ratio) , apoptosis in lung cells ( by TUNEL assay) , expression of glucose-regulated protein 78 ( GRP78) , CCAAT∕enhancer-binding protein homologous protein (CHOP), c-Jun N-terminal kinase (JNK) and caspase-12 mRNA was determined by real-time polymerase chain reaction. The expression of GRP78, CHOP, phosphorylated JNK (p-JNK) and caspase-12 was de-tected by Western blot. The index of quantitative assessment of histologic lung injury ( IQA) was measured, and apoptotic index ( AI) was calculated. Results Compared with Sham group, the W∕D ratio, IQA and AI were significantly increased, the expression of GRP78, CHOP, JNK and caspase-12 was up-regulated ( P<0. 05) , and the pathological changes of lung tissues were accentuated in CPB group. Compared with CPB group, the W∕D ratio, IQA and AI were significantly decreased, the expression of GRP78, CHOP, JNK and caspase-12 was down-regulated ( P<0. 05) , and the pathological changes of lung tissues were sig-nificantly attenuated in Sev group. Conclusion The mechanism by which sevoflurane mitigates acute lung injury induced by CPB is related to inhibiting unfolded protein response related cell apoptosis in lung tissues of rats.

Objective: To evaluate the effect of dexmedetomidine on pyroptosis during lung ischemia-reperfusion (I/R) in rats. Methods: Adult male Sprague-Dawley rats, weighing 250-320 g, were used in this study.The model of isolated lung perfusion was established using an IL-2 Isolated Perfused Rat or Guinea Pig Lung System after the rats were anesthetized.Thirty lungs in which an ex vivo lung perfusion model was successfully established were divided into 3 groups (n=10 each) by a random number table method: control group (C group), I/R group and dexmedetomidine group (DEX group). The lungs were continuously perfused with K-H solution for 150 min in C group.After 15 min of perfusion, lungs were subjected to 60-min suspension of ventilation and perfusion, followed by 75 min of reperfusion and ventilation to establish the model of lung I/R injury in I/R and DEX groups.In DEX group, dexmedetomidine 10 nmol/L was added to K-H solution at the beginning of reperfusion.Lung tissues were obtained for determination of wet/dry weight ratio (W/D ratio) and for examination of pathological changes (with a light microscope) and ultrastructure (using an electron microscope), and the alveolar damage rate (IAR) was calculated.The expression of pyroptosis-related factors including NOD-like receptor family protein 3 (NLRP3), caspase-1, interleukin-1β (IL-1β), IL-18 and gasdermin D (GSDMD) protein and mRNA was detected by Western blot or by real-time polymerase chain reaction. Results: Compared with C group, the W/D ratio and IAR in lung tissues were significantly increased, and the expression of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD protein and mRNA was up-regulated in I/R and DEX groups (P<0.05). Compared with I/R group, the W/D ratio and IAR in lung tissues were significantly decreased, the expression of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD protein and mRNA was down-regulated (P<0.05), and the pathological changes were significantly attenuated in DEX group. Conclusion The mechanism by which dexmedetomidine reduces isolated rat lung I/R injury may be related to inhibiting pyroptosis.

Objective:To explore the relationship between NOX4 and radiosensitivity of nasopharyngeal carcinoma cells.Methods:Western blot was used to test the expression of NOX4 in nasopharyngeal carcinoma cells (CNE1, CNE2 and HONE1) and normal nasopharyngeal epithelial cells (NP69). The lentiviral vectors for RNA interference and overexpression of NOX4 gene were constructed and nasopharyngeal carcinoma cells were transfected. After treatment with radiation or/and PI3K/AKT inhibitor LY294002, the expressions of related proteins in cells were tested by Western blot, and the cell proliferation was detected by CCK-8 assay and the cell apoptosis was determined by flow cytometry. GraphPad Prism 5 was used for statistical analysis, and P<0.05 was statistically significant. Results:The expressions of NOX4 in nasopharyngeal carcinoma cells were higher than those in normal nasopharyngeal epithelial cells. Compared with the siNC group, the siNOX4 group of nasopharyngeal carcinoma cell had lower proliferation capacity [72 h absorbance ( A) value:1.16 vs. 0.75] and higher apoptosis rate (2.9% vs. 10.0%). In contrast,compared with the vector group, the NOX4 group of nasopharyngeal carcinoma cell had higher proliferation capacity [72 h absorbance ( A) value: 1.01 vs. 1.32] and lower apoptotic rate (1.7% vs. 1.1%).Treatment with LY294002 for nasopharyngeal carcinoma cells of NOX4 overexpression,compared with the NOX4 group, the proliferation ability of nasopharyngeal carcinoma cells in the NOX4+LY294002 group was reduced (72 h absorbance ( A) value: 1.32 vs. 0.77), while the apoptotic rate was increased (1.1% vs. 3.1%).Treatment with radiotherapy, compared with the siNC/Vector group, the proliferation ability of nasopharyngeal carcinoma cells in the siNOX4 group was reduced (72 h absorbance ( A) value: 0.72 vs. 0.33), and the apoptotic rate was increased (7.8% vs. 17.3%). However, in the NOX4 group, the proliferation of nasopharyngeal carcinoma cells was enhanced (72 h absorbance ( A) value:0.65 vs. 0.78), and the apoptotic rate was reduced (8.1% vs. 3.8%). Compared with the NOX4+radiation group, the proliferation ability of nasopharyngeal carcinoma cells in the NOX4+radiation+LY294002 group was reduced (72 h absorbance ( A) value: 0.79 vs. 0.56), while the apoptotic rate was increased (3.8% vs. 8.1%). Conclusion:NOX4 can inhibit radiosensitivity of nasopharyngeal carcinoma cells possibly by activating PI3K/AKT pathway.

Objective To determine the role of Bmi-1 in the submandibular gland (SMG) of mice.Methods SMG of 4-week wild-type(WT) and Bmi-1 null(Bmi-1-/-) mice was analyzed on the weight,salivary flow rate,hematoxylin-eosin staining morphological differences and the changes in proliferation and aging by histology,immunohistochemistry and Western blotting.Results Compared with WT mice,the average static salivary flow rate [WT:(0.21 ±0.02) μg/min,Bmi-1-/-:(0.10 ±0.02) μg/min] (P =0.001) and the submandibular gland weight [WT:(1.89 ± 0.15) μg],Bmi-1-/-:[(1.34 ± 0.07) μg] (P =0.003) of the male Bmi-1-/-mice were significantly decreased,the number of gland duct increased,and the granular convoluted duct showed reduced diameter and branches.More senescence-associated β-galactosidase positive cells existed in SMG of Bmi-1-/-mice (WT:0.00,Bmi-1-/-:0.18 ± 0.02),and Ki-67 immunopositive cells decreased in SMG of Bmi-1-/-mice(WT:0.40 ～ 0.47,Bmi-1-/-:0.18 ～ 0.20) (P =0.000).The expression of p16 (WT:1.00 ± 0.12,Bmi-1-/-:0.00 ±0.00) (P =0.003) and p19(WT:0.97 ±0.09,Bmi-1-/-:5.09 ±0.21) (P =0.004) were up-regulated dramatically in SMG of the Bmi-1-/-mice.Conclusions Bmi-1 gene deficiency causes abnormal function of SMG by inducing senescence phenotype of SMG.