不同氢溴酸右美沙芬口服固体制剂的溶出度考察

目的：对6个厂家不同氢溴酸右美沙芬口服固体制剂进行体外溶出度考察，比较体外溶出情况，为临床用药提供参考。方法：采用转篮法，转速100 r·min^-1，用高效液相色谱法测定氢溴酸右美沙芬口服固体制剂在0.1 mol·L^-1盐酸溶液中的溶出曲线；以威布尔方程拟合溶出参数T₅₀、T_d、m，并对参数进行方差分析。结果：氢溴酸右美沙普通片、分散片、胶囊以及软胶囊的平均累积溶出度分别为94.3%、101.3%、105.2%、93.4%。溶出参数T₅₀、T_d差异较大，其中T₅₀最大的是最小的13.4倍。结论：氢溴酸右美沙片、分散片、胶囊以及软胶囊体外溶出行为差别大，产品质量存在较大差异。     

反相高效液相色谱法测定血浆中氢溴酸右美沙芬浓度

本文报道采用反相高效液相色谱法测定人血浆中氢溴酸右美沙芬的浓度。采用ＹＷＧ－Ｃ１８Ｈ３７分析柱，以乙腈－水－乙酸（５０：４９：１，三乙胺调节ｐＨ至４．３）为流动相，利多卡因作内标，在２７８ｎｍ波长处监测洗提液。本法简便，灵敏，专属性好，适用于氢溴酸右美沙芬血药浓度测定及药代动力学研究 。     

高效液相色谱法测定氢溴酸樟柳碱含量

目的：建立了高效液相色谱法测定氢溴酸樟柳碱的含量。方法：采用ＯＤＳ柱,以０．２％十二烷基硫酸钠的甲醇－０．０１ｍｏｌ．Ｌ^-1磷酸二拚钾（用磷酸调节ｐＨ为３．５（ ６０：４０）为流动相,对羟基苯甲酸丁酯为内标物,用紫外检测器于２１０ｎｍ波长处检测。结果：氢溴酸樟柳碱进样量在０．５～３μｇ范围内有良好线笥关系（ｒ＝０．９９９９）。平均回收率为９９．５％,ＲＳＤ为２．６％（ｎ＝３）。最低检出量为０．００６     

氢溴酸右美沙芬片健康人体生物等效性

目的 :研究氢溴酸右美沙芬片在健康人体的药动学及相对生物利用度。方法 :8名健康受试者单剂量随机交叉口服氢溴酸右美沙芬片参比制剂和被试制剂 6 0mg ,采用HPLC法测定用药后不同时间的血药浓度。结果 :2种制剂的体内过程均符合一房室开放模型 ,参比制剂和被试制剂的tmax分别为 (2 72± 0 2 1)h和 (2 74± 0 19)h ,cmax分别为 (5 5 1± 0 4 4) μg·L-1和(5 5 8± 0 2 7) μg·L-1,AUC分别为 (4 5 3± 2 9) μg·h·L-1和 (4 5 7± 3 0 ) μg·h·L-1,被试制剂的相对生物利用度为 (10 1±5 9) %。结论 :2种制剂具有生物等效性。     

HPLC法测定氢溴酸加兰他敏分散片的含量

目的 :建立氢溴酸加兰他敏及其分散片的HPLC分析方法。方法 :采用ODS色谱柱 (15 0mm× 4 .6mm ,5 μm) ,以甲醇 水 冰醋酸 (75∶92 5∶10 )为流动相 ;流速 :1.0ml·min-1,检测波长 :2 89nm ;采用外标法测定氢溴酸加兰他敏分散片的含量。结果 :氢溴酸加兰他敏在 10～ 10 0 μg·ml-1范围内 ,线性关系良好 (r =0 .9998) ;平均回收率为 10 0 .2 % ;日内精密度(RSD =0 .6 % ,n =5 )良好。结论 :本法适用于氢溴酸加兰他敏及其分散片的含量测定 ,方法简便、准确、快速。     

复方制剂珮夫人小儿咳露中主药成分的含量测定

目的 :建立一种采用高效液相色谱检测复方制剂中氢溴酸美沙芬、愈创木酚甘油醚和马来酸氯苯那敏含量的方法。方法 :采用C1 8色谱柱 ,以 0 .0 0 2 5mol·L- 1 IPR -B6 甲醇溶液∶水 (含 2 %三乙胺 )∶磷酸 (12 0∶10 0∶1)为流动相 ,检测波长为 2 5 7nm。结果 :氢溴酸美沙芬、愈创木酚甘油醚和马来酸氯苯那敏 3种成分的回收率分别为10 0 .5 % ,99.5 % ,10 0 .6% ;RSD分别为 2 .2 % ,1.6% ,1.9% (n =7)。结论 :本方法简便 ,结果准确可靠     

Interacting with α7 nAChR is a new mechanism for AChE to enhance the inflammatory response in macrophages

Acetylcholine (ACh) regulates inflammation via α7 nicotinic acetylcholine receptor (α7 nAChR). Acetylcholinesterase (AChE), an enzyme hydrolyzing ACh, is expressed in immune cells suggesting non-classical function in inflammatory responses. Here, the expression of PRiMA-linked G4 AChE was identified on the surface of macrophages. In lipopolysaccharide-induced inflammatory processes, AChE was upregulated by the binding of NF-κB onto the ACHE promotor. Conversely, the overexpression of G4 AChE inhibited ACh-suppressed cytokine release and cell migration, which was in contrast to that of applied AChE inhibitors. AChEmt, a DNA construct without enzymatic activity, was adopted to identify the protein role of AChE in immune system. Overexpression of G4 AChEmt induced cell migration and inhibited ACh-suppressed cell migration. The co-localization of α7 nAChR and AChE was found in macrophages, suggesting the potential interaction of α7 nAChR and AChE. Besides, immunoprecipitation showed a close association of α7 nAChR and AChE protein in cell membrane. Hence, the novel function of AChE in macrophage by interacting with α7 nAChR was determined. Together with hydrolysis of ACh, AChE plays a direct role in the regulation of inflammatory response. As such, AChE could serve as a novel target to treat age-related diseases by anti-inflammatory responses.     

Safety and efficacy of teneligliptin in Japanese patients with type 2 diabetes mellitus: a pooled analysis of two Phase III clinical studies

Objective: To assess the safety and efficacy of long-term administration of teneligliptin alone and in combination with oral antidiabetic drugs in Japanese type 2 diabetes mellitus (T2DM) patients with insufficient glycemic control.

Methods: This post-hoc pooled analysis used data from two Phase III clinical studies involving 702 Japanese patients. We evaluated teneligliptin as monotherapy and combined with a sulfonylurea, glinide, biguanide, or α-glucosidase inhibitor. Safety measures included adverse events (AEs), adverse reactions and hypoglycemia. The main efficacy measure was the change in glycated hemoglobin (HbA_1c) from baseline.

Results: Incidences of AEs and adverse reactions were similar among the teneligliptin monotherapy group and all combination therapy groups except the combination with sulfonylurea. Hypoglycemia was more frequent in the sulfonylurea combination therapy group than in other groups. Teneligliptin administered once daily as monotherapy or combination therapy resulted in a decrease in HbA_1c, which was maintained for 52 weeks. Bodyweight showed no change or a slight increase at the end of 52 weeks in all groups.

Conclusions: This pooled analysis provides evidence for the safety and efficacy of long-term use of teneligliptin as monotherapy or combination therapy in Japanese T2DM patients.     

复方樟柳碱对早期糖尿病视网膜病变多焦视网膜电图的影响

目的：观察复方樟柳碱穴位注射对早期DR的多焦视网膜电图(mfERG)一阶Kernel反应的改变。

方法：连续选取Ⅰ～Ⅱ期糖尿病视网膜病变患者48例48眼,分为对照组和注射组,其中对照组采用控制血糖药物治疗,注射组除采用药物控制血糖外接受复方樟柳碱穴位注射。治疗后行多焦电生理检查,分析参数为mfERG产生的4个象限、6环以及总和反应的波形,对总和反应平均密度、P1和N1的潜伏期与振幅结果进行统计学分析。

结果：注药组和对照组P1波的总和反应平均密度为39.42±6.46、28.50±3.73nV/deg²,N1波为11.12±1.34、6.33±1.14nV/deg²。注药组P1波和N1波总和反应平均密度均高于对照组(P1：t=6.230,P<0.01; N1：t=3.526,P<0.01)。注药组SN、IN、IT和ST象限P1反应波平均密度分别为32.61±9.62、32.31±7.94、29.24±7.84、28.09±5.38nV/deg²,均高于对照组(P<0.05),各象限两组N1反应波平均密度比较均无明显差异。注药组R1～R6 P1、R1～R3 N1反应波平均密度分别为98.11±17.53、73.95±17.20、64.09±14.13、49.43±10.08、40.24±11.55、36.86±6.43、25.27±12.81、21.31±6.76、14.86±5.06nV/deg²,均高于对照组(P<0.05),两组R4～R6 N1反应波平均密度比较无明显差异。注药组IT和ST中P1和N1波幅值1.37±0.35、1.28±0.29、0.31±0.05和0.30±0.10μV,明显高于对照组(P<0.05),两组SN和IN中P1和N1波幅值差异无统计学意义。

结论：复方樟柳碱穴位注射可以改善早期DR部分视网膜功能损伤。