To explore the changes of leukotrienes (LT) in cerebral cortex and lung tissues in ovalbumin-induced rat asthma model and effects of different anti-asthma drugs on the changes. METHODS: Aerosol antigen-induced changes of inflammation in bronchoalveolar lavage fluids (BALF), pulmonary and brain histologic section in sensitized rats were investigated. Changes of LTB4 and LTC4 in lung and cerebral cortex homogenates were analyzed by reverse-phase high performance liquid chromatography (RP-HPLC). RESULTS: The number of inflammatory cells in BALF and the score of lung and brain histological examination from antigen- challenged rats were significantly higher than that from control group (P<0.05). Dexamethason (DXM, 0.5mg/kg, ip) and ketotifen fumarate (KF, 5mg/kg, ig) markedly reduced total leukocyte number in BALF, and inhibited eosinophil accumulation, reduced the infiltration of eosinophils, and improved mucous edema and epithelial lesion of bronchi and bronchioles. In addition, RP-HPLC results shown LTB4 in lung and cerebral cortex homogenates were increased in antigenchallenged rats [(4.1

目的：探讨致敏大鼠抗原攻击后脑皮层和肺气道中干扰素-γ（-IFN-γ）和白介素-4（IL-4）出现的相关性变化。方法：观察致敏大鼠吸入抗原诱导的支气管肺灌洗液（BAIF）和肺组织切片炎症变化，用ELISA法测定BALF和脑皮层-IFN-γ和JL-4水下变化。结果：抗原攻击组BAIF中的炎症细胞数目明显高于对照未攻击组（p<0.05）。地塞米松（DXM，0.5mg/kg，ip）明显减少BAIF中的白细胞总数，几乎完全抑制嗜酸性粒细胞（EOS）和淋巴细胞的聚集，但增加中性粒细胞数目。抗原攻击组的组织学检查积分（EOS浸润、粘膜水肿和上皮损伤）也明显高于对照未攻击组（P<O.05）。 DXM （0.5mg/kg，ip）减少支气管和细支气管的：EOS数目，改善粘膜水肿和上皮损伤。致敏人鼠抗原攻击后。BAIJF中的IFN，7水平降低伴随IL-4升高导致了IFN-γ/IL-4比例下降与此同时，脑皮层匀浆中也出现相似的改变。DXM（0.5mg/kg，Ip）能反转BALF和脑皮层匀浆中的IFN-γ/IL-4比例下降。结论：致敏大鼠抗原攻击后脑皮层和肺气道中的IFN-γ/IL-4出现相关性变化。

The aim of this study was to investigate whether transforming growth factor-h1 (TGF-h1) could induce alveolar epithelial to mesenchymal transition (EMT) in vitro. Alveolar epithelial cells (AECs) from SD rats were isolated by elastase cell dispersion and IgG panning. Expression of a-smooth muscle actin (a-SMA) was assayed using Western blotting and immunostaining analysis. Morphological changes, the markers of epithelial cell (E-cadherin), and stress fiber by actin reorganization were detected by an indirect immunostaining. The contents of collagen I were determined by spectrophotometry. The levels of endogenous TGF-h1 were measured with ELISA. Incubation of AECs with TGF-h1 (0.1～10ng/mL) induced abundant expression of a-SMA protein, and a-SMA expression in AECs reached a plateau when TGF-h1 was N 3ng/mL. Furthermore, we found that TGF-h1 (3ng/mL) exposure of AECs induced an authentic EMT characterized by abundant expression of a-smooth muscle actin, transformation of myofibroblastic morphology, increased formation of stress fiber by actin reorganization, and loss of epithelial marker E-cadherin. Meanwhile, significant increase in the levels of collagen I from 32.0 F 6.6mg/g in control to 98 F 10.8mg/g in TGF-h1-treated group was found over a 72h incubation period. Moreover, following stimulated by TGF-h1 (3ng/mL), a marked and time-dependent increase in endogenous TGF-h1 released from AECs was observed. At time points 72h, TGFh1 release mounted to 3451pg/ml, which was much enough to induce EMT in vitro. These results demonstrated that AECs, under stimulation of TGF-h1, underwent a conversion process into myofibroblasts in vitro.

探讨隐孔菌发酵物（Cryp top orus volvatus ferment substance, CVFS）对中性粒细胞释放白三烯的影响。方法：给大鼠腹腔注射糖原诱导中性粒细胞聚集，16h后收集腹腔灌洗液，分离中性粒细胞，以calcium ionopho re A 23187刺激离体中性粒细胞释放白三烯，再用HPLC法测定中性粒细胞中白三烯（LT）B4、L TC4和LTD4的含量。结果：CVFS 0.25、1、4mg•L-1呈浓度依赖抑制中性粒细胞释放LTB4、LTC4和LTD4，对LTB4抑制率分别为27.4%、54.2%和78.8%；对LTC4抑制率分别为65.1%、74.3 和79.0%；对LTD4抑制率分别为5516%、60.9%和72.8%。与生理盐水对照组比较有显著性差异（P<0.05）。结论：CVFS抑制中性粒细胞释放LTB4、LTC4和LTD4可能是其抗炎平喘作用机制之一。

To study the inductive expression of human phosphodiesterase 4A (hPDE4A) in yeast cell GL62 and investigate the inhibitory effects of theophylline, rolipram, and acetamide-45 on PDE4A activity of the expressed product in yeast cell GL62. METHODS: Yeast cell GL62 were transfected with human PDE4A gene cloned in the expression plasmid p138NB. Expression was induced by adding CuSO4 to a final concentration of 150μmol/L, and the expressed product was extracted. The activity of PDE4A was detected by HPLC. RESULTS: Yeast cell GL62 expressed a certain protein at CuSO4 150μmol/L, the size of the expressed product was between 62 kDa and 83 kDa, the activity of PDE4A of the expressed product at 3 h was in maximum (188±23)μmol×g-1×min-1, and the Km was (17.7±2.6) mmol/L. Theophylline, rolipram, and acetamide-45 could inhibit the activity of PDE4A extracted from yeast cell GL62. The IC50 (95% confidence limits) of theophylline, rolipram, and acetamide-45 were 1642 (989-2727), 4.58 (3.45-6.08), and 275 (170-444) mmol/L respectively. CONCLUSION: PDE4A expressed in yeast cell GL62 is biologically active. Theophylline, rolipram, and acetamide-45 can inhibit the PDE4A activity. The expressed product in yeast cell GL62 may be used in the research work of PDE4 and its inhibitors.