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501.
目的 探讨经纤维支气管镜注入利福平治疗支气管结核的临床疗效.方法 将本院治疗的86例支气管结核患者随机分入对照组与观察组,对照组患者接受单纯口服抗结核药物治疗,观察组患者在口服化疗药物同时接受由纤维支气管镜注入利福平注射液治疗,比较两组临床疗效及痰菌转阴率.结果 观察组治疗总有效率显著高于对照组,差别具有统计学意义(100% vs 75.0%,P〈0.05);观察组治疗后1月,2月,6月及12月痰菌阴转率显著高于对照组(P〈0.05).结论 经纤维支气管镜注入利福平治疗支气管结核可显著提高临床疗效,促进痰菌阴转. 相似文献
502.
Nassr Nassr reas Huennemeyer Rolf Herzog Oliver von Richter Robert Hermann Manuela Koch Kevin Duffy Karl Zech & Gezim Lahu 《British journal of clinical pharmacology》2009,68(4):580-587
AIMS
To evaluate the effect of co-administration of rifampicin, an inducer of cytochrome P450 (CYP)3A4, on the pharmacokinetics of roflumilast and roflumilast N-oxide. Roflumilast is an oral, once-daily phosphodiesterase 4 (PDE4) inhibitor, being developed for the treatment of chronic obstructive pulmonary disease. Roflumilast is metabolized by CYP3A4 and CYP1A2, with further involvement of CYP2C19 and extrahepatic CYP1A1. In vivo, roflumilast N-oxide contributes >90% to the total PDE4 inhibitory activity.METHODS
Sixteen healthy male subjects were enrolled in an open-label, three-period, fixed-sequence study. They received a single oral dose of roflumilast 500 µg on days 1 and 12 and repeated oral doses of rifampicin 600 mg once daily on days 5–15. Plasma concentrations of roflumilast and roflumilast N-oxide were measured for up to 96 h. Test/Reference ratios and 90% confidence intervals (CIs) of geometric means for AUC and Cmax of roflumilast and roflumilast N-oxide and for oral apparent clearance (CL/F) of roflumilast were estimated.RESULTS
During the steady-state of rifampicin, the AUC0–∞ of roflumilast decreased by 80% (point estimate 0.21; 90% CI 0.16, 0.27); Cmax by 68% (0.32; CI 0.26, 0.39); for roflumilast N-oxide, the AUC0–∞ decreased by 56% (0.44; CI 0.36, 0.55); Cmax increased by 30% (1.30; 1.15, 1.48); total PDE4 inhibitory activity decreased by 58% (0.42; 0.38, 0.48).CONCLUSIONS
Co-administration of rifampicin and roflumilast led to a reduction in total PDE4 inhibitory activity of roflumilast by about 58%. The use of potent cytochrome P450 inducers may reduce the therapeutic effect of roflumilast. 相似文献503.
BACKGROUND: Previous studies have shown that rifampicin exhibits neuroprotective effects, but the precise mechanisms remain unclear. Rifampicin is thought to exert the neuroprotective effect as a hydroxyl free radical scavenger. OBJECTIVE: To investigate the protective effects of rifampicin pretreatment on rotenone-induced mitochondrial oxidative stress in differentiated PC12 cells. DESIGN, TIME AND SETTING: A repeated measure, cell-based study was performed at the Department of Neurology, Second Affiliated Hospital, Sun Yat-sen University, China between December 2007 and November 2008. MATERIALS: PC12 cells were a kind gift from the Physiology Laboratory of Zhongshan Medical School, Sun Yat-sen University, China. Rotenone and rifampicin were purchased from Sigma, USA. METHODS: PC12 cells were differentiated by culturing with 100 ng/mL 7S nerve growth factor for 9 days in Dulbecco's modified Eagle's medium/Nutrient Mix F12 (DMEM/F12) supplemented with 10% fetal bovine serum. The cells were assigned to six groups according to various treatment conditions: control, cultured with normal media; rifampicin group, treated with 300 μmol/L rotenone for 26 hours; rotenone group, treated with 2.5 μmol/L rotenone for 24 hours; rifampicin pretreatment groups, pretreated with 100,200, and 300 μmol/L rifampicin for 2 hours, respectively, followed by 2.5 μmol/L rotenone for 24 hours. MAIN OUTCOME MEASURES: Mitochondrial membrane potential was measured by fluorescence microscopy and flow cytometry, respectively, using rhodamine 123 staining. Intracellular reactive oxygen species formation was analyzed by flow cytometry using 2', 7'-dichlorofluorescin-diacetate staining, and intracellular reduced glutathione was measured with a microplate reader. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. Cell apoptosis was detected by Hoechst 33342 staining and flow cytometry. RESULTS: Increased apoptosis in rotenone-induced, differentiated, PC12 cells was accompanied by the loss of mitochondrial transmembrane potential, the formation of reactive oxygen species, and reduced glutathione depletion (P < 0.01). Rotenone-induced mitochondrial dysfunction was blocked in a dose-dependent manner by rifampicin (P< 0.05 or P< 0.01). CONCLUSION: Pretreatment of differentiated PC12 cells with rifampicin blocked rotenone-induced apoptosis by ameliorating mitochondrial dysfunction and oxidative stress. 相似文献