β—淀粉样蛋白31—35和载脂蛋白E4对大鼠海马神经元存活和生长的影响

目的 :研究 β 淀粉样蛋白 (Betaamyloidpritein ,Aβ)与载脂蛋白E4(ApolipoproteinE ,ApoE4)对神经元的共同作用 ,探讨老年性痴呆发病的细胞分子机制。材料与方法 :体外培养神经细胞 ,采用MTT比色法和免疫组化标记 ,结合图像分析技术 ,研究Aβ3 1 3 5和ApoE4对海马神经元存活和生长的作用。结果 :(1 )Aβ3 1 3 5(1 0 0 μmol/L) +ApoE4(1 0 μg/ml)和Aβ3 1 3 5(2 0 μmol/L) +ApoE4(1 0 μg/ml)的OD值 ,分别为 0 .1 97± 0 .0 2 1和 0 .1 91± 0 .0 2 4,明显低于对照组 0 .2 2 9± 0 .0 0 3 μm(P <0 .0 5 )。 (2 )这两组神经元胞体的最长径分别为 1 0 .0 7± 1 .98μm和 1 0 .0 1± 1 .68μm ;最短径分别为 6.40± 0 .77μm ,6.2 8± 0 .89μm ,明显低于对照组 1 2 .73± 3 .0 0 μm、7.0 5± 1 .0 4μm ,Aβ3 1 3 5组 1 2 .0 9± 2 .45 μm、7.0 1± 1 .0 2 μm ,最长径和最短径 (P <0 .0 5 ) ;(3 )两组神经元突起平均长度分别为 2 6.3 6± 7.73 μm和2 3 .86± 7.2 9μm ,明显低于对照组 3 0 .88± 9.79μm、2 8.3 4± 4.40 μm ,P <0 .0 5。 (4 )Aβ3 1 3 5(2 0 μmol/L)组的平均突起长度 (2 6.81± 5 .42 μm) ,明显低于对照组和ApoE4组 3 0 .60± 7.3 0 μm(P <0 .0 5 )。ApoE4对海马神经元的存     

中药脊髓Ⅰ号对脊髓厚片Ca~(2+)荧光强度的影响

目的　探讨中药脊髓Ⅰ号对脊髓厚片Ca2 + 荧光强度的影响。方法　将 33只Wistar大鼠随机分为 3组 :下胸段脊髓半横断组 (损伤组 )、对照组和中药脊髓Ⅰ号治疗组。快速处死大鼠 ,取下胸段脊髓 ,切脊髓厚片 ,用Fluo 3荧光染料孵育 ,激光共聚焦显微镜观察。结果　损伤组、对照组和中药治疗组左侧Ca2 + 荧光强度分别为 12 6 3± 3 2 7、13 34± 3 5 1和 12 89±3 31,右侧分别为 2 1 6 8± 3 6 9、14 72± 2 12和 12 97± 3 6 0 ,损伤组脊髓厚片损伤侧Ca2 + 荧光强度显著升高 ,治疗组两侧灰质Ca2 + 荧光强度无显著差异。结论　 (1)损伤侧Ca2 + 荧光强度显著升高 ;(2 )中药脊髓Ⅰ号对Ca2 + 荧光强度的升高有一定抑制作用。     

Aβ_((31-35))和ApoE_4对培养大鼠海马神经元的存活和生长的影响

为探讨β-淀粉样蛋白 ( Aβ)和载脂蛋白 E4( Apo E4)对培养大鼠海马神经元的作用 ,本文采用了神经细胞培养、MTT比色法、免疫组化及图象分析等技术进行了研究。结果显示 :( 1) MTT法测得 Aβ( 3 1 - 3 5) ( 10 μmol/ L) +Apo E4( 10 μg/ ml)和 Aβ( 3 1 - 3 5)( 2 0μmol/ L ) +Apo E4( 10μg/ ml)的 OD值 ,分别为 0 .197± 0 .0 2 1和 0 .191± 0 .0 2 4,明显低于对照组 ( 0 .2 2 9± 0 .0 3,P<0 .0 5 )。( 2 )这两组神经元胞体的最长径分别为 ( 10 .0 7± 1.98)μm和 ( 10 .0 1± 1.6 8)μm;最短径分别为 ( 6 .40± 0 .77)μm和 ( 6 .2 8± 0 .89) μm,明显低于对照组、Apo E4组、Aβ( 3 1 - 3 5) 组的最长径和最短径 ( P<0 .0 5 ) ;其突起平均长度分别为 ( 2 6 .36± 7.73) μm和 ( 2 3.86± 7.2 9)μm,明显低于对照组 ( 30 .88± 9.79)μm、Apo E4组 ( 30 .6 0± 7.30 )μm以及 Aβ( 3 1 - 3 5) ( 10μmol/ L )组 ( 2 8.34± 4.40 )μm( P<0 .0 5 )。 ( 3) Aβ( 3 1 - 3 5) ( 2 0 μmol/ L)组的突起平均长度为 ( 2 6 .81± 5 .42 ) μm,也明显低于对照组 ( 30 .88± 9.79) μm和Apo E4组 ( 30 .6 0± 7.30 )μm ( P<0 .0 5 )。本研究结果提示 ,Aβ( 3 1 - 3 5) +Apo E4对神经元的抑制作用较 Aβ(     

IL-2的真核表达载体对乙肝病毒基因疫苗的免疫佐剂效应

单以乙肝病毒S区基因疫苗 (pCR3 1 S)或联合IL 2真核表达载体 (pDOR IL 2 )注射BALB/c小鼠 (H 2 d)股四头肌 ,ELISA法检测小鼠血清抗HBs,4h51Cr释放法检测小鼠脾细胞CTL活性。免疫 8周后 ,单注射pCR3 1 S及共注射IL 2真核表达载体的小鼠血清 45 0nmA值分别为 1 2 4± 0 1及 1 98± 0 17。CTL细胞杀伤活性分别为 (5 0 5± 6 4) %、 (6 1 9± 7 1) % ,两组均有明显差异 (P <0 0 1)。脾细胞悬液经抗CD4+ 单克隆抗体处理后CTL细胞杀伤活性分别为 (4 8 3± 5 9) %、 (5 6 2±6 1) % ,抗CD8+ 单克隆抗体处理后分别为 (10 6± 1 4) %、 (13 6± 1 3) %。结果表明 ,IL 2的真核表达载体能够提高小鼠对DNA疫苗的免疫应答 ,CTL细胞杀伤活性主要由CD8+ 执行。基因疫苗可能用于预防及治疗HBV感染。     

永久性心房颤动患者血清TXB2、6-K-PGF1α和PGE2改变的探讨

目的:探讨永久性心房颤动(PAF)患者血清血栓素B2(TXB2)、6-酮-前列腺素F1α(6-K-PGF1α)和前列腺素E2(PGE2)水平的变化及其临床意义.方法:采用放射免疫分析158例PAF患者和40例健康对照组的血清TXB2、6-K-PGF1α和PGE2水平,进行对照统计分析.结果:PAF组血清TXB2水平[(80.89±18.86)ng/L vs (51.38±7.66)ng/L]和 PGE2水平[(11.48±4.20)ng/L vs (7.15±1.26)ng/L]显著高于健康对照组( P<0.01;P<0.01),6-K-PGF1α水平[(49.81±7.53_ng/L vs (81.12±9.02)ng/L]显著低于健康对照组(P<0.01),三者之间均无显著相关性(P均＞0.05).NYHA心功能Ⅰ、Ⅱ、Ⅲ和Ⅳ级组PAF患者血清TXB2和PGE2水平依次升高,具有统计学意义(P均<0.01),6-K-PGF1α水平变化无统计学差异(P>0.05)(方差检验F TXB2=52.75,P<0.01;F 6-K-PGF1α=0.949,P>0.05;F PGE2=62.04;P<0.01).合并脑梗死组血清TXB2水平显著高于无合并组(P<0.01),但6-K-PGF1α和PGE2无统计学差异(P均>0.05).结论:PAF组血清TXB2和PGE2水平显著高于健康对照组,6-K-PGF1α水平显著低于健康对照组;心功能Ⅰ、Ⅱ、Ⅲ和Ⅳ级组PAF患者血清TXB2和PGE2水平依次升高,合并脑梗死组血清TXB2水平显著升高.     

川芎嗪对实验性肾炎肾皮质内血小板活化因子、血栓素B_2的影响

目的 :探讨川芎嗪对实验性肾炎肾皮质内血小板活化因子 (PAF)、血栓素B2 (TXB2 )水平的影响。方法 :复制大鼠加速型抗肾小球基膜 (GBM)肾炎模型。分为肾炎组、肾炎 川芎嗪组 (治疗组 )。结果 :治疗组各期尿蛋白量较肾炎组减少 (P <0 .0 5 ,P <0 .0 1) ,第 2 1d时血清肌酐含量低于肾炎组 (P <0 .0 5 ) ,光镜和电镜下肾脏病理改变较肾炎组为轻 ,同时肾皮质内PAF、TXB2 含量少于肾炎组 (P <0 .0 1)。结论 :川芎嗪治疗实验性肾炎有效 ,其机理可能与减少肾皮质内PAF、TXB2 等有关。     

隐孢子虫病患者与机体细胞免疫功能相关性的研究

目的　探讨隐孢子虫病患者与机体细胞免疫功能的关系。方法　采用生物素 链霉亲和素 (Biotin Streptavidin,BSA)法对卵囊阳性患者分别进行外周血T细胞亚群、膜白介素 2受体 (mIL 2R)检测。结果　隐孢子虫卵囊阳性者的CD3+ 、CD4 + 、CD8+ 和CD4 + /CD8+ 阳性百分率分别为 (5 5 .87± 7.2 3) %、(39.2 6± 6 .4 3) %、(30 .0 4± 5 .6 7) %和 (1 .36± 0 .4 1 ) % ,诱导期mIL 2R表达水平为 (33.4 5± 2 .31 ) % ,两者分别与卵囊阴性者及静息期mIL 2R相比 ,差异有显著性 (P <0 .0 5～ 0 .0 1 )。结论　隐孢子虫病引起细胞免疫功能的变化 ,T细胞亚群、mIL 2R在抗隐孢子虫感染中起重要作用     

妊高征患者外周血红细胞内钙含量的变化及其临床价值

目的　探讨不同程度妊高征患者血红细胞内钙含量 (IECa2 + )、病理机制、危害 ,并与正常妊娠对照。方法　应用Fluo - 3/AM导入红细胞与细胞内游离钙离子结合 ,经流式细胞术检测IECa2 + 的方法 ,对 4 2例不同程度的妊高征患者IECa2 + 进行定量测定 ,并研究与疾病程度和胎儿宫内窘迫发生的关系。结果　轻度妊高征产前 (10 93.5± 90 .4 )及产时IECa2 + 含量 (12 0 3.5± 87.9)与正常妊娠产前 (110 1.7± 89.2 )及产时 (1173.5± 86 .2 )无显著性差异 (P >0 .0 5 ) ,中、重度妊高征者 (产前 :中度 1195 .3± 72 .4、重度 12 0 6 .1± 95 .7;产时 :中度 12 5 6 .1± 81.2、重度 130 7.9± 83.8)明显增加。具体表现为 :妊高征患者IECa2 + 含量显著高于正常妊娠 ,且产时较产前显著性增多 (P <0 .0 5 ,P <0 .0 1) ;IECa2 + 含量与妊高征患者平均动脉压 (MAP)呈正相关系 (P <0 .0 5和 0 .0 1)。结论　采取有效的降压措施能够使IECa2 + 含量趋于正常水平 ,减低其危害。     

2.120 西沙必利对消化间期MMC前列腺素E释放及胃粘膜细胞保护作用

目的我们曾报导(1999)西沙必利可作用于肌间神经丛胃动素神经元释放胃动素增强消化间期移行性复合运动(MMC)和电活动.根据我们最近关于前列腺素E2(prosta glandin E2,PGE2)与胃动素释放相关的工作表明,西沙必利很可能是启动PGE2释放 , 由PGE2激发胃动素释放进而促进MMC运动.已知PGE2是强力细胞保护物质,西沙必利还可能通过PGE2介导降低胃粘膜炎症作用.本文观察西沙必利对PGE2释放作用及其与胃动素释放关系,并探讨西沙必利对胃粘膜的消炎作用.方法用清醒Wister大鼠进行慢性实验,埋植高灵敏度应力传感器于胃窦, 用多导生理记录仪记录胃MMC.在颈外静脉放一硅胶管,通过皮肤穿出体外,供给药及取血样品用.用放射免疫分析法测定血中PGE2和胃动素含量.用肌注消炎痛(15mg/kg)诱发胃粘膜损伤,按Guth方法计算损伤指数.结果 1.正常大鼠胃窦MMC活动及血中PGE2和胃动素含量大鼠消化间期周期性出现MMC活动,Ⅲ相活动期收缩力为34 .6 7±8.45g(n=8).Ⅲ相高峰期血中PGE2含量125.42±18.31pg/mL(n=8),胃动素含量104 .56±9.64(n=8).MMC转入恢复期Ⅳ相时胃动素水平下降(78.24±9.64pg/mL),而PGE 2水平仍保持Ⅲ相的水平(118.25±13.67pg/mL).2.西沙必利对PGE2及胃动素的释放作用在大鼠胃窦MMC Ⅰ相时,静脉注射西沙必利2mg/kg可激发MMC Ⅲ相活动,其收缩力比对照组增加(235.41±80.23)%(P＜0.001).同时也使血中PGE2和胃动素浓度升高 ,分别比对照组升高(147.24±20.62)%和(190.27±13.24)%(均P＜0.01,均n=8) .PGE2高峰出现在胃动素高峰之前,表明胃动素释放可能由PGE2激发.3.胃粘膜损伤对胃窦MMC活动及血中PGE2和胃动素的影响消炎痛致胃粘膜损伤,其损伤指数为19.35± 6.85时,胃运动显示MMC Ⅰ相和Ⅱ相时程延长,Ⅲ相时程缩短,并出现阵发性不规则收缩波,胃窦收缩力比正常对照组下降(54.27±12.41)%(n=8,P＜0.05).血中PGE2和胃动素含量比正常对照组分别下降(81.17±15.24)%和(79.24±13.79)%(均n=8,均P ＜0.05).4.西沙必利对胃粘膜损伤抑制胃运动及PGE2、胃动素释放以及预防胃粘膜损伤作用的影响给大鼠口服西沙必利5mg/kg/d ,15天后肌注消炎痛(15mg/kg).结果表明, 西沙必利能有效地预防消炎痛造成的胃粘膜损伤,损伤指数只有2.12±0.54(n=8),与单独消炎痛组比较,损伤指数下降(89.18±6.24)%(P＜0.001).同时显著增加胃窦收缩力以及增加血中PGE2及胃动素含量,分别比单独消炎痛组增加(81.45±24.25)%、(78 .23±19.37)%和(85.14±27.63)(均P＜0.01).在另一组实验中,先给消炎痛6h后 ,在胃粘膜出现损伤时,给静脉灌流西沙必利2mg/kg/h.结果发现,西沙必利可使损伤指数下降,细胞修复.血中PGE2和胃动素浓度回升至接近正常水平.结论西沙必利可促进PGE2和胃动素释放进而促进MMC收缩活动.西沙必利可抑制胃粘膜损伤是通PGE2介导,实现对胃粘膜的细胞保护作用.     

文拉法新与马普替林及丁螺环酮治疗抑郁症的对照研究

目的　比较文拉法新与马普替林及丁螺环酮治疗抑郁症的效果。方法　随机将抑郁症病人分为 3组。A组为文拉法新治疗组 ( 3 1例 ) ,B组为马普替林治疗组 ( 3 2例 ) ,C组为丁螺环酮治疗组 ( 3 0例 )。 3组均采用中等药物剂量及增量法。以CGI-I、HAMD、HAMA3种量表观察 6周的疗效 ,并以 TESS观察其副反应。结果　 6周后 3组 HAMD减分率分别为 0 .68± 0 .1 5 ,0 .5 7± 0 .2 6,0 .5 1± 1 .1 ,无显著差异 ( P>0 .0 5 ) ,但 A组与 C组在治疗第 2周末减分率分别为 0 .3 1± 0 .2 5 ,0 .0 5±2 .1 ( t=2 .82 ,P<0 .0 5 )有显著差异。3组 HAMA减分率分别为 0 .77± 0 .1 2 ,0 .48± 0 .1 5 ,0 .8± 1 .2 ,故 A组与 C组无显著差异 ( P>0 .0 5 ) ,但 A组与 C组显著优于 B组 ( P<0 .0 5 )。TESS测 6周末加分率 ,3组分别为 3 7.2 1 % ,73 .61 % ,3 4.3 2 %。即 A组与 C组无显著差异 ( t=0 .42 ,P>0 .0 5 ) ,但 B组显著高于 A组 ( t=2 .2 8,P<0 .0 5 )及 C组 ( t=3 .2 1 ,P<0 .0 5 )。结论　文拉法新优于马普替林、丁螺环酮抗抑郁、抗焦虑疗效 ,且副反应较小     

Human Peritoneal Eosinophils and Formation of Arachidonate Cyclooxygenase Products

Human peritoneal eosinophils were obtained from the waste dialysis bags of patients undergoing continuous ambulatory peritoneal dialysis. The number of eosinophils obtained from each bag varied from 3 X 10(7) to 288 X 10(7). The cells were incubated for 1 h in tissue culture medium and prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 (6-keto-PGF1), and thromboxane B2 (TXB2) were determined by radioimmunoassay of the supernatant. The basal release as well as the stimulated release from the purified eosinophils of TXB2 were five times greater than the release of PGE2 and thirty times greater than the release of 6-keto-PGF1. A dose-response curve was achieved for all three cyclooxygenase products with the calcium ionophore A23187. The release of TXB2 was inhibited in a dose-dependent manner by the specific thromboxane A2 (TXA2) synthase inhibitor OKY-1581 and a corresponding increase in PGE2 and 6-keto-PGF1 was obtained. Indomethacin (5.6 X 10(-6) M) inhibited the cyclooxygenase products to almost undetectable levels.     

表达在爪蟾卵母细胞上的大鼠P2X_4受体介导的ATP-激活电流特征

本研究应用显微注射和双电极电压钳技术对P2X4受体介导的三磷酸腺苷(ATP)-激活电流(IATP)的特征进行了研究。结果显示:(1)大鼠P2X4受体可高效表达于非洲爪蟾卵母细胞;(2)外加1μmol/L、10μmol/L和100μmol/LATP,IATP激活相的时间常数τon分别是3.58s±0.20s、2.30s±0.21s和1.3s±0.14s。IATP快失敏相的时间常数τdes分别是11.74s±0.11s、7.52s±0.24s和4.11s±0.18s。IATP慢失敏相的时间常数τoff分别为14.25s±2.30s、25.42s±4.45s和35.71s±5.92s;(3)ATP作用的量-效关系:EC50为(16.03±1.81)μmol/L,Hill系数为1.02±0.09;(4)100μmol/L的PPADS和suramin不改变IATP的幅值;(5)IATP呈电压依赖性和内向整流特性;(6)加药时间分别为20s、30s、45s和60s的情况下,IATP幅值并无显著性差异。以上结果说明了P2X4受体介导的ATP-激活电流的特征,为进一步研究P2X4受体的功能和调控机制奠定了基础。     

当归对人红细胞变形性和聚集性的影响

目的 :研究当归对红细胞变形性和聚集性影响。方法 :健康献血者红细胞 ,自身血浆稀释至红细胞压积为 40 %。用红细胞聚集仪和激光衍射光学旋转细胞分析仪分别测定红细胞聚集性和变形性。结果 :当归组加入当归注射液 2 0mg/ml孵育后与正常对照组比较 ,可显著降低红细胞聚集速度 (Ta :2 .5 9± 0 .35 ,Tf:33.5 4± 2 .6 3vsTa :1.80±0 .16 ,Tf:2 7.11± 1.78,P <0 .0 5 ) ,但不影响红细胞解聚能力。加入Ca2 + 螯合剂可使红细胞变形性降低。当归可以显著逆转A2 3187导致的红细胞变形性降低 (EI:0 .2 9±0 .0 47vs 0 .17± 0 .0 2 4,P <0 .0 1)。结论 :当归可以降低正常红细胞聚集速度 ,减轻Ca2 + 螯合剂导致的红细胞变形性降低。     

Rickettsial effects on leukotriene and prostaglandin secretion by mouse polymorphonuclear leukocytes.

Typhus rickettsiae were incubated with mouse exudative polymorphonuclear leukocytes (PMN), and supernatants were examined for leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) secretion by radioimmunoassay. PMN incubated with native rickettsiae secreted significantly more LTB4 and PGE2 than did those incubated with buffer alone. Autacoid secretion was dependent on both the time of PMN incubation with rickettsiae and the number of rickettsiae present in the incubation suspension. Rickettsial stimulation of LTB4 secretion was associated with rickettsial hemolytic activity; treatments which inactivated the rickettsial hemolysin abolished the ability of rickettsiae to stimulate PMN LTB4 secretion. Trifluoperazine, which did not alter the rate of phagocytosis of rickettsiae by PMN, stimulated rickettsial effects on secretion of both LTB4 and PGE2 but inhibited the PMN LTB4 response to A23187. This suggested that the PMN response to rickettsiae and to the calcium ionophore involved differing mechanisms of activation. Finally, rabbit antirickettsial antiserum, which inhibited rickettsial hemolysis and was opsonic, did not block the effects of rickettsiae on PMN LTB4 secretion.     

Histamine secretion from human skin slices induced by anti-IgE and artificial secretagogues and the effects of sodium cromoglycate and salbutamol

Human cutaneous mast cells show functional differences from their counterparts in other tissues. Following passive sensitization with 1% atopic serum for 30 min at 37° C human skin slices released histamine after challenge with anti-human IgE in a concentration dependent manner. Maximum release of 14 ± 2%, was achieved with a 1/10 dilution of anti-IgE. Passive sensitization with 10% atopic serum increased the secretory response to anti-IgE but histamine release was only concentration related over the entire 1/1000 to 1/10 dilution range in half of the specimens studied, the remainder showing high dose tolerance to anti-IgE, Negligible histamine release occurred with anti-IgE challenge of slices which had not been passively sensitized. The histamine releasing ability of A23187 in human skin slices was similar to that observed in lung and adenoidal mast cells being concentration dependent over the range 0-1 3 μM with a maximum release of 25 ±3%. In contrast to human lung and adenoidal mast cells, poly-L-lysine and compound 48/80 induced histamine release from skin slices. Poly-L-lysine induced a concentration-dependent release of histamine over the range 0-01-10 mUM with a maximum of 27 ± 3%. The response to compound 48/80 was variable, releasing in some but not all specimens. Histamine release caused by anti-IgE. A23187 and poly-L-lysine was shown to be dependent upon extracellular calcium while release stimulated by compound 48/80 was calcium independent. The chemotactic peptide, formyl-methionyl-leucyl-phenylalanine, over the range 0.01 10 μM failed to release histamine from skin slices. Sodium cromoglycate (100 1000 μM) failed to inhibit histamine release and the β-adrenoceptor stimulant salbutamol (1-10 μM) showed only weak activity at the lowest of three different concentrations of anti-IgE used for challenge.     

心肌营养素-1在心肌成纤维细胞增殖中的作用

目的：探讨心肌营养素-1（CT-1）在高血压心室重塑中的作用。方法：3-4代心肌成纤维细胞用于实验，分为对照组、助溶剂（二甲亚砜，DMSO）组、CT-1反义寡核苷酸组（ASODN）、正义寡核苷酸对照组（SODN）、PD98059组、AG490组、LY294002组。利用自制压力培养装置，将各组细胞置于160 mmHg压力下培养8 h。 STAT3、ERK1/2和PI3-K的活性通过Western blotting分析测定；MTT测定心肌成纤维细胞增殖。结果：高静水压明显促进心肌成纤维增殖，CT-1表达上调，CT-1ASODN干预后，CT-1ASODN能抑制高静水压所致的细胞增殖（0.132±0.013 vs 0.154±0.011，P<0.05），STAT3、ERK1/2和 PI3-K蛋白表达水平明显低于对照组（2.09±0.25 vs 2.47±0.28,P<0.05)、(1.13±0.19 vs 1.61±0.22,P<0.05)、（1.25±0.23 vs1.71±0.25,P<0.05)。AG490组明显减弱高静水压的促增殖作用（0.118±0.018 vs 0.155±0.010，P<0.05）并且增加ERK1蛋白磷酸化（1.85±0.18 vs 1.45±0.23，P<0.05）;PD98059增强高静水压的促增殖（0.185±0.011 vs 0.155±0.010，P<0.05）并且增加STAT3蛋白磷酸化（1.83±0.23 vs 1.58±0.22，P<0.05）, PI3/K阻断剂LY294002干预后对高静水压的促增殖作用无影响（0.157±0.015 vs 0.155±0.010，P>0.05）；SOND (0.151±0.010 vs 0.154±0.011, P>0.05) 和DMSO组(0.141±0.017 vs 0.155±0.010, P>0.05)与对照组相比对心肌成纤维细胞增殖无明显差别。结论：高静水压下，心肌成纤维细胞增殖主要通过STAT3通路；ERK1/2通路通过抑制STAT3的活性起负向调节作用，可能在防止心肌成纤维细胞过度增殖起重要的作用；PI3-K没有参与这一作用。上述STAT3通路与ERK1/2通路之间的相互作用可能有助于防止诱导成纤维细胞过度增殖。     

Genistein下调肝癌细胞survivin基因表达和诱导细胞凋亡的实验研究

目的： 探讨三磷酸肌醇(IP3)和survivin蛋白表达变化在genistein诱导肝癌细胞凋亡中的作用。 方法： 以肝癌HepG2细胞培养72 h为对照组，实验各组以60 μmol/L的genistein作用于HepG2细胞不同时间后，应用同位素试剂盒检测细胞IP3含量，Western blotting分析细胞survivin蛋白表达，流式细胞仪检测细胞凋亡率。 结果： 对照组IP3含量为(29.2±0.6) pmol/106cells， survivin蛋白与内参β-actin蛋白灰度和面积之积的比值V-survivin/ V-β-actin为0.63±0.06；细胞凋亡率为（2.6±0.1）%。Genistein作用于肝癌HepG2细胞12 h、24 h、48 h、72 h后IP3分别为（12.0±1.4）pmol/106cells、（7.5±0.8）pmol/106cells、（5.6±0.5）pmol/106cells、（3.3±0.6）pmol/106cells，与对照组(29.2±0.6)pmol/106cells比，P＜0.01。V-survivin/ V-β-actin分别为0.36±0.13、0.33±0.03、0.23±0.04、0.18±0.04，与对照组(0.63±0.06)比，P＜0.01。细胞凋亡率分别为（2.7±0.2）%、（7.4±0.5）%、（20.5±2.0）%、（30.7±1.6）%，与对照组(2.6±0.1)%比，P＜0.01。 结论： Genistein能减少IP3生成，下调survivin基因表达，诱导肝癌细胞凋亡。     

Selective inhibition of polymorphonuclear leukocytes by immunosuppressive concentration of prostaglandin E2.

Prostaglandin E2(PGE2) has been implicated as an immunosuppressive agent and plasma levels of PGE2 are elevated in patients sustaining thermal injury. We examined the effect of 10(-7) M prostaglandin E2(PGE2) on human polymorphonuclear leukocytes (PMN) to determine whether it directly inhibits stimulated responses of these cells. At this concentration, PGE2 alone was incapable of stimulating PMN intracellular hydrogen peroxide production (indirectly assayed by fluorescence of 2'',7''-dichlorofluorescin) or expression of the PMN CD11b/CD16 surface glycoproteins. PMN incubated in the presence of the soluble stimuli phorbol myristate acetate(PMA, 100 ng/ml) or recombinant human C5a(rHC5a, 10(-8) M) generated significant amounts of hydrogen peroxide, increased their CD11b expression and decreased their CD16 expression. Pre-incubation of cells with PGE2 caused significant inhibition of all the observed changes stimulated by rHC5a. In contrast, events stimulated by PMA were not affected by preincubation of cells with PGE2. We conclude that PGE2, in concentrations identical to those found in the plasma of patients with burn injuries, is capable of selectively inhibiting some stimulated events and phenotypic expression of PMN in vitro study.     

Release of leukotriene B4 from human neutrophils and its relationship to degranulation induced by N-formyl-methionyl-leucyl-phenylalanine,serum-treated zymosan and the ionophore A23187.

The release of leukotriene B4 (LTB4) from human neutrophils and its relationship to degranulation induced by the divalent cation ionophore A23187, serum-treated zymosan (STZ), N-formyl-methionyl-leucyl-phenylalanine (FMLP) and arachidonic acid (AA) have been studied. Greatest release of LTB4, measured by specific radioimmunoassay, occurred in response to A23187 (5-10 ng/10(6) cells); lower concentrations were obtained after incubation with STZ (0.2-0.8 ng/10(6) cells) and AA (0.3-2.6 ng/10(6) cells) and low (0.02 ng/10(6) cells) or not detectable amounts from cells incubated with FMLP. Release of LTB4 induced by STZ, FMLP and submaximal concentrations of A23187 was potentiated by simultaneous addition of AA. Lower amounts (0.06-0.3 ng/10(6) cells) of thromboxane B2 (TXB2) were also released by these stimuli, however this release of TXB2 was not potentiated by exogenous AA. The secretion of beta-glucuronidase induced by A23187, STZ and FMLP was not quantitatively related to release of LTB4 or TXB2 and was not potentiated by exogenous AA. Furthermore, FMLP induced degranulation was cytochalasin B (Cyt B)-dependent, whereas LTB4 release in response to this stimulus was only marginally increased by pretreatment of the cells with Cyt B. These data indicate that LTB4 does not mediate degranulation induced by these stimuli.     

Down-regulation of cyclooxygenase product generation by human peritoneal macrophages.

Isolated human peritoneal macrophages under resting conditions synthesize and release significant quantities of the cyclooxygenase products prostaglandin E2 (PGE2) and thromboxane B2 (TXB2). These increased linearly with time and were dependent on de novo protein synthesis. Following the addition of calcium ionophore A23187 there was a marked decrease in total generation of immunoreactive cyclooxygenase products. In contrast, there was a concomitant increase in the release of 5-lipoxygenase products. The down-regulation of both PGE2 and TXB2 was not due to diversion of substrate from the cyclooxygenase pathway to the 5-lipoxygenase pathway nor was it due to inhibitory effects of products of the 5-lipoxygenase pathway on the generation of cyclooxygenase products. Instead, the inhibitory effects of A23187 were thought to be due to a down-regulation of cyclooxygenase itself, a hypothesis supported by the finding that TXA2 synthase proved to be unaltered and Western analysis of crude peritoneal macrophage (PM phi) membranes demonstrated lesser quantities of cyclooxygenase in membranes from A23187-treated PM phi than in those prepared from control cells.