This study was aimed to investigate the clinical effect of tetramethylpyrazine in combination with ipratropium bromide in the treatment of bronchial asthma and its effects on inflammatory factors and leptin. According to inclusion criteria, a total of 124 bronchial asthma cases were included and randomly divided into two groups, which were the control group (n = 62) and the observation group (n = 62) with the random number table. Besides conventional treatments, the control group was given ipratropium bromide; while the observation group was given tetramethylpyrazine in combination with ipratropium bromide. Then, comparisons were made between two groups on the therapeutic efficacy rate, pulmonary function, inflammatory factor, leptin, and incidence of adverse reactions. The results showed that the total therapeutic efficacy rate was 96.8% in the observation group, which was obviously higher than that of 87.1% in the control group (P < 0.05). In comparison with the control group, the posttreatment pulmonary function indexes PEF and FEV1/FVC increased, inflammatory factors IL-6 and IL-4 decreased, and IL-12 increased in the observation group with statistical significance (P < 0.05). One week, 2 weeks and 4 weeks after the treatment, the level of leptin in the observation group was significantly lower than that in the control group (P < 0.05). During the treatment, there were no severe adverse reactions. The incidence of adverse reactions in the observation group was 11.3%, which was statistically the same with that of 14.5% in the control group (P > 0.05). It was concluded that tetramethylpyrazine in combination with ipratropium bromide was effective for bronchial asthma treatment, which can significantly increase curative efficacy, improve pulmonary function, alleviate inflammatory reaction and reduce leptin level with minor adverse reactions. It required further studies in the clinical practice.

ObjectiveTo investigate the mechanism of anti-inflammatory effect of diallyl sulfide (DAS) in protection against acute lung injury (ALI) in rats with paraquat poisoning.Methods Eighty male Wistar rats were randomly divided into four groups, namely: control group, model group, dexamethasone (DXM) treatment group, and DAS treatment group, with 20 rats in each group. The model of paraquat poisoning was reproduced by single does of 70 mg/kg given by gavage, while the same volume of normal saline (NS) was given in same manner in control group. 100 mg/kg of DAS, the same volume of NS, or 1 mg/kg DXM injection were given respectively in DAS treatment group, model group, or DXM treatment group intraperitoneally after exposure to paraquat, once a day for 14 days. Five rats in each group were sacrificed at 1, 3, 7, 14 days, respectively. The inferior lobe of right lung was harvested, and the degree of lung injury was observed with hematoxylin and eosin (HE) staining under optical microscope; the upper lobe of right lung was used to determine the lung wet/dry weight (W/D) ratio and for evaluation of the degree of pulmonary edema. The expression of nuclear factor -κB (NF-κB) in the middle lobe of right lung was assessed with immunohistochemistry. The expression of tumor necrosis factor -α (TNF-α) mRNA in the left lung was determined with the reverse transcription-polymerase chain reaction (RT-PCR).Results① The pulmonary structure in control group was found to be intact. However, in the model group there were progressive pathological changes in lung, including marked edema and thickening of alveolar walls, collapse of alveoli, infiltration of inflammatory cells, alveolar wall, and obvious bleeding in the local lung tissue, and formation of transparent membrane in alveolar space. Less infiltration of inflammatory cells and no obvious destruction were found in alveolar structure in the DAS and DXM treatment groups.② Lung W/D ratio: lung W/D ratio of model group was apparently higher than that in control group at every time point, and peaking on the 3rd day (6.15±0.54 vs. 4.15±2.10,P< 0.05), and the ratio of lung W/D of DAS and DXM treatment groups was obviously lower than that in model group at every time point, especially on the 3rd day (3.99±1.26, 4.30±0.70 vs. 6.15±0.54, bothP< 0.05), but there was no significant difference between DAS and DXM treatment groups in this regard.③ The immunocytochemistry analysis revealed minimal NF-κBp65 expression in the cell nuclei of the control group, while extensive NF-κBp65 expression was found in model group. Minimal NF-κBp65 positive expression in the cytoplasm and even less positive expression in the nucleus was found in the DAS and DXM treatment groups, and integralA value was significantly lower in the DAS and DXM treatment groups than that of the model group, especially on the 3rd day [(17.98±0.06)×107, (18.53±0.04)×107 vs. (28.85±0.61)×107, bothP< 0.01], but there was no significant difference between DAS and DXM treatment groups.④ It was shown by RT-PCR that the expression of TNF-α mRNA in lung tissue of the model group was significantly higher than that in the control group on the 3rd day (gray value: 3.63±0.62 vs. 0.51±0.13, P< 0.05). The expression of TNF-α mRNA in lung tissue was significantly decreased in DAS and DXM treatment groups compared with model group (gray value: 2.49±0.57, 2.02±0.26 vs. 3.63±0.62, bothP< 0.05), but there was no significant difference between DAS and DXM treated groups.ConclusionTreatment with an intraperitoneally injection of DAS is capable of attenuate the extent of PQ-induced ALI in rats by alleviating pulmonary edema, inhibiting the expression of NF-κB and TNF-α in lung tissue, and ameliorating pathological changes in lung tissue.

[摘 要] 目的：探讨过表达miR-497靶向细胞周期蛋白E1（cyclin E1，CCNE1）对肺癌A549细胞上皮间质转化（epithelial-mesenchymal transition，EMT）的影响。方法：常规培养人肺癌A549细胞，细胞实验分为正常组（不加干预）、对照组（转染miR-497 mimics-NC）、实验组（转染miR-497 mimics）。采用Transwell小室实验、免疫荧光染色、qPCR、Western blotting法分别检测各组细胞迁移和侵袭能力、蛋白间质标志物α-SMA和上皮标志物E-cadherin的表达、miR-497和CCNE1的表达水平，荧光素酶基因基因报告实验验证miR-497和CCNE1的靶向关系。结果：与对照组和正常组相比，实验组A549细胞迁移和侵袭的数量明显减少（均P<0.05），细胞的间质标志物α-SMA的绿色荧光强度明显减弱[（36.95±5.81） vs （98.69±2.36）、（97.94±2.63），均P<0.05]，上皮标志物E-cadherin的绿色荧光强度明显增强[（388.41±10.93） vs （100.95±6.37）、（102.55±3.18），均P<0.05]，miR-497的表达明显升高（均P<0.05），CCNE1的表达均明显下降（均P<0.05）。miR-497能够靶向调控CCNE1的表达。结论：在肺癌A549细胞中miR-497能够靶向调控CCNE1的表达，上调miR-497的表达后能明显抑制A549细胞迁移和侵袭能力，影响EMT相关蛋白的表达。

As a type of
Humans ; Legionella/genetics* ; Legionella longbeachae/genetics* ; Legionellosis/drug therapy* ; Pneumonia/diagnosis* ; Retrospective Studies