孟鲁司特对哮喘患者肺功能及炎症因子IL-25、IL-33的影响

目的 观察白三烯受体拮抗剂孟鲁司特对哮喘患者外周血白细胞介素25（IL-25）、白细胞介素33（IL-33）及肺功能的影响.方法 将78例哮喘患者分为2组：哮喘对照组和哮喘观察组,哮喘对照组给予常规吸入糖皮质激素及β受体激动剂加安慰剂治疗,哮喘观察组在哮喘对照组治疗的基础上给予孟鲁司特片口服,用药前均行肺功能检测及哮喘控制评分,并应用ELISA检测血清中IL-25、IL-33的水平,治疗3个月后再次测量肺功能、哮喘控制评分及血清中IL-25、IL-33的含量.结果 两组治疗后肺功能及ACT评分均较前好转,但哮喘观察组改善更明显（P＜0.05）,治疗后血清中IL-25、IL-33的水平均降低,但以哮喘观察组降低更明显（P＜0.05）.结论 应用白三烯受体拮抗剂可显著改善哮喘患者的炎症指标,并显著改善患者肺功能.     

正交设计试验多目标同步优化氨利口腔膜剂处方

目的：对氨利口腔膜剂进行处方优化.方法：以聚乙烯醇（PVA17-88）、羧甲基纤维素纳（CMC-Na）、甘油为成膜材料,以膜的柔软性、成膜性、光滑性、均匀性、溶出度作为考察指标,采用正交设计优化处方.结果：最佳成膜材料处方为PVA17-88 3.0 g,CMC-Na 2.0 g,甘油2.5 ml.按照最优处方制备的膜剂符合《中国药典》的有关规定,膜剂体外释药曲线符合Higuchi方程.结论：该膜剂处方和制备工艺可行.     

细辛脑对成人哮喘患者血清IL-25、ECP、IL-27的影响

目的：观察细辛脑治疗成人哮喘患者血清白细胞介素-25（IL-25）、嗜酸性粒细胞阳离子蛋白（ECP）、白细胞介素-27（IL-27）的影响。方法：100例支气管哮喘患者随机分为观察组（55例）和对照组（45例）,对照组给予常规对症治疗（吸氧、解痉平喘、抗感染等）,观察组在常规治疗基础上加用细辛脑注射液24mg加入0．9％氯化钠注射液250ml,ivd,qd,疗程14d。比较两组临床疗效,检测两组患者血清IL-25、ECP、IL-27治疗前后水平的变化。结果：观察组总有效率为92．7％,高于对照组（P〈0．05）。细辛脑可以降低支气管哮喘患者血清IL-25、ECP、IL-27浓度的浓度,差异有统计学意义（P〈0．05或0．01）。结论：细辛脑注射液可降低哮喘患者血清中IL-25、ECP、IL-27浓度,抑制炎症细胞生成,可以减轻哮喘患者的气道炎症反应。     

Emodin inhibits ATP-induced IL-1β secretion,ROS production and phagocytosis attenuation in rat peritoneal macrophages via antagonizing P2X7 receptor

Context: Previous in vitro studies have demonstrated that emodin (1,3,8-trihydroxy-6-methyl-anthraquinone), an anthraquinone derivative from the rhizome of Rheum palmatum L., can inhibit the activation of P2X₇ receptors (P2X₇R) as a potential antagonist. However, the effects of emodin on P2X₇R-related inflammatory processes remain unclear.

Objective: This study aimed to investigate the effects of emodin on different inflammation responses of macrophages induced by ATP, the natural ligand of P2X₇R.

Materials and methods: Rat peritoneal macrophages were treated with millimolar ATP and emodin (0.1, 0.3,?1,?3,?10?µM) or brilliant blue G (BBG, 0.1,?1,?10?µM). Cytosolic Ca²⁺ concentration ([Ca²⁺]_c) was detected by fluorescent Ca²⁺ imaging. Interleukin-1β (IL-1β) release was measured by rat IL-1β ELISA kits. Reactive oxygen species (ROS) generation was examined by dihydroethidium (DHE) fluorescent staining. Phagocytic activity was tested by neutral red uptake assay.

Results: We found that the [Ca²⁺]_c increase evoked by ATP (5?mM) was inhibited by emodin, in a dose-dependent manner with IC₅₀ of 0.5?μM. Furthermore, emodin reduced the IL-1β release induced by ATP (2?mM) in lipopolysaccharide (LPS)-activated macrophages, with an IC₅₀ of 1.6?μM. Emodin also strongly suppressed the ROS production and phagocytosis attenuation triggered by ATP (1?mM), with IC₅₀ values of 1?μM and 0.7?μM, respectively. Besides, BBG, a specific antagonist of P2X₇R, exhibited similar suppressive effects on these inflammation responses.

Conclusion: These results showed the inhibitory effects of emodin on ATP-induced [Ca²⁺]_c increase, IL-1β release, ROS production and phagocytosis attenuation in rat peritoneal macrophages, by inhibiting the activation of P2X₇R.     

Fungal transformation of androsta-1,4-diene-3,17-dione by Aspergillus brasiliensis

Background

The biotransformation of steroids by fungal biocatalysts has been recognized for many years. There are numerous fungi of the genus Aspergillus which have been shown to transform different steroid substances. The possibility of using filamentous fungi Aspergillus brasiliensis cells in the biotransformation of androsta-1,4-diene-3,17-dione, was evaluated.

Methods

The fungal strain was inoculated into the transformation medium which supplemented with androstadienedione as a substrate and fermentation continued for 5 days. The metabolites were extracted and isolated by thin layer chromatography. The structures of these metabolites were elucidated using ¹H-NMR, broadband decoupled ¹³C-NMR, EI Mass and IR spectroscopies.

Results

The fermentation yielded one reduced product: 17β-hydroxyandrost-1,4-dien-3-one and two hydroxylated metabolites: 11α-hydroxyandrost-1,4-diene-3,17-dione and 12β-hydroxyandrost-1,4-diene-3,17-dione.

Conclusions

The results obtained in this study show that A. brasiliendsis could be considered as a biocatalyst for producing important derivatives from androstadienedione.     

Silymarin improved 6-OHDA-induced motor impairment in hemi-parkisonian rats: behavioral and molecular study

Background

Neuroinflammation and oxidative stress has been shown to be associated with the development of Parkinson disease (PD). In the present study, we investigated the effect of intraperitoneal (i.p.) administration of silymarin, on 6-OHDA-induced motor-impairment, brain lipid per-oxidation and cerebrospinal fluid (CSF) levels of inflammatory cytokine in the rats.

Results

The results showed that silymarin is able to improve motor coordination significantly (p < 0.001) in a dose dependent manner. There was a significant (p < 0.001) increase in MDA levels of 6-OHDA-lesioned rats whereas; in silymarin (100, 200 and 300 mg/kg, i.p. for 5 days) pre-treated hemi-parkinsonian rats MDA levels was decreased markedly (p < 0.001). Furthermore the CSF levels of IL-1β was decreased (p < 0.001) in silymarin (100, 200 and 300 mg/kg) pre-treated rats up to the range of normal non-parkinsonian animals.

Conclusion

We found that pre-treatment with silymarin could improve 6-OHDA-induced motor imbalance by attenuating brain lipid per-oxidation as well as CSF level of IL-1β as a pro-inflammatory cytokine. We suggest a potential prophylactic effect for silymarin in PD. However, further clinical trial studies should be carried out to prove this hypothesis.