We investigated the effect of different concentrations of morphine and tramadol on the differentiation of human adult helper T cells in vitro. Twenty outpatients without any immune diseases were selected and their peripheral blood was collected. Whole blood or peripheral blood mononuclear cells (PBMCs) were pretreated with different concentrations of morphine or tramadol for 48 h, while the control group received neither. The ratio of CD4+IFN-g+IL-2+=CD4+IL-4+IL-10+ was analysed by three-color flow cytometry.1 The intracellular cytokines, after stimulation with PMA and Ionomycin (Ion), were detected by trace whole blood technology. The CD4+CCR5+ and CD4+ CCR3+ cells in PBMCs were counted in order to observe the imbalance of Th1=Th2. After treatment with morphine or tramadol, the number of Th2 increased significantly and the ratio of Th1=Th2 decreased dramatically in both groups. At the same time the number of CD4+IFN-g+ IL-2+ cells decreased and CD4+IL-4+IL-10+ cells increased sharply as compared with the control group. Both morphine and tramadol can direct Th0 cells toward Th2, especially morphine. The Th2 redirection, as well as the changes in cytokines, showed a dose dependent fashion in both drugs

Treatment of rat pheochromocytoma cells(PC12)cells with β-amyloid peptide-(1-42)for 24h induced a concentration-dependent decrease in cellular redox activity in the dose range of 1 to 20μM. These effects were markedly attenuated by pretreatment with 2 mM LiCl for 7 days, whereas 1-day pretreatment was ineffective. Measurements of live and dead cells by double-staining with fluorescein diacetate and propidium iodide, respectively revealed that protracted lithium pretreatment attenuated PC 12 cell death induced by β-amyloid-(1-42) and cerebellar granule cell death induced by β-amyloid-(25-35). Preceding PC 12 cell death, β-amyloid peptide elicited a slight decrease in protein levels of Bcl-2. Conversely, 7-day pretreatment with lithium resulted in an approximate doubling of Bcl-2 protein levels in cells treated with or without β-amyloid peptide-(1-42). Lithium-induced Bcl-2 upregulation was temporally associated with the cytoprotective effects of this drug. Thus, lithium protection against β-amyloid peptide neurotoxicity might involve Bcl-2 overexpression, and lithium treatment for Alzheimer’s disease should be reexamined.

目的 观察不同浓度曲马多和吗啡预先给药对成人静脉血辅助性T淋巴细胞（Th细胞）分化的影响。方法 采集无免疫性疾病的15例门诊小手术病人外周静脉血20ml，进行全血和外周血单个核细胞（PBMCs）培养。随机分为空白对照组（C组）、不同浓度吗啡组[10ng•ml-l（M1组）、100ng•ml-l（M2组）、1000ng•ml-1（M3组）]及不同浓度曲马多组[50ng•ml-l（Q1组）、500ng•ml-l（Q2组）、5000ng•ml-1（Q3组）]。培养的全血和PBMCs在体外均用相应浓度药物预先作用24h，随后用刺激剂刺激。24h后采用三色流式细胞术检测各组全血及PBMCs中20000个淋巴细胞中Thl细胞及Th2细胞百分率，并计算Thl细胞与Th2细胞的比值（Thl/Th2）。结果 Thl细胞百分率及Thl/Th2：与C组比较，M1、M2、M3、Q1、Q2、Q3组均降低（P<0.05）；与M1组比较，M2、M3组降低，Q1组升高（P<0.05）；与M2组比较，M3组降低，Q2组升高（P<0.05>；与Q．组比较，Q2、Q3组降低（P<0.05）。与Q2组比较，Q3组降低（P<0.05）0Th2细胞百分率：与C组比较，M1、M2、M3、Q1、Q2、Q3组均升高；与M1组比较，M2.M3组升高，Q1组降低（P<0.05）；与M2组比较，M3组升高，Q1组降低；与Q1组比较，Q2、Q3组升高。与Q2组比较，Q3组升高（P<0.05）。结论 在体外曲马多和吗啡均可抑制细胞免疫功能，并呈浓度依赖性，曲马多的抑制作用弱于吗啡。

目的 评价不同镇痛方法对子宫切除术后患者血清细胞因子IL6、ILIO和热休克蛋白70（HSP70）水平的影响。方法 择期行子宫切除术患者48例，随机分为4组（n=12）；术后分别采用罗哌卡因混合芬太尼硬膜外镇痛（1组）；芬太尼静脉镇痛（Ⅱ组）；罗哌卡因混合曲马多硬膜外镇痛（III组）；曲马多静脉镇痛（Ⅳ组）。所有患者均行硬膜外麻醉，手术关腹时开始病人自控镇痛（PCA），均以LCP模式给药：负荷剂量5ml+背景剂量1ml/h+PCA剂量lInJ，锁定时间IOmin。检测麻醉前、术后2、24、48和72h时患者血清IL6、ILlO和HSP70水平。结果 四组术后VAS评分均在4分以下，术后患者血清IL-6、IIrl0和HSP70水平均升高。术后24h，I、Ⅲ组血清IL6和HSP70水平低于Ⅱ、Ⅳ组（JP<0.01）；术后2、24h，Ⅳ组血清IIrl0水平高于其它各组，且Ⅳ组IL-6/IL-10小于Ⅱ组（P<0.05）。结论 硬膜外镇痛较静脉镇痛更能有效地降低子宫切除术后患者血清IL-6和HSP70水平升高程庋。硬膜外罗哌卡因复合曲马多更适合用于术后镇痛。