Remodeling of motor cortex function in acute cerebral infarction patients following human urinary kallidinogenase A functional magnetic resonance imaging evaluation after 6 months

A total of 29 patients were treated within 48 hours after acute subcortical cerebral infarction with Xuesaitong or Xuesaitong plus human urinary kallidinogenase for 14 days. Neurological deficits, activity of daily living, and evaluations of distal upper limb motor functions at the 6-month follow-up showed that patients treated with Xuesaitong plus human urinary kallidinogenase recovered better than with Xuesaitong alone. In addition, functional MRI revealed that activation sites were primarily at the ipsilesional side of injury in all patients. Human urinary kallidinogenase induced hyperactivation of the ipsilesional primary sensorimotor cortex, premotor cortex, supplementary motor area, and contralesional posterior parietal cortex. Results showed that human urinary kallidinogenase improved symptoms of neurological deficiency by enhancing remodeling of long-term cortical motor function in patients with acute cerebral infarction.

Effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction

Objective: To study the effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction. Methods:The patients with massive cerebral infarction who received treatment in our hospital between January 2016 and December 2017 were selected and randomly divided into the group A receiving Butylphthalide treatment, the group B receiving Urinary Kallidinogenase treatment and the group C receiving Butylphthalide combined with Urinary Kallidinogenase treatment on the basis of conventional treatment. 14 d after treatment, serum levels of nerve markers, coagulation indexes, growth factors and oxidative stress indexes were determined. Results:After treatment, visinin-like protein-1 (VILIP-1), neuron-specific enolase (NSE), S100B protein (S100B), thromboxane A2 (TXA2), lysophosphatidic acid (LPA), D-dimer (D-D), 8-isoprostanes F2α (8-iso-PGF2α) and malondialdehyde (MDA) levels of 3 groups significantly decreased whereas nitric oxide (NO), nitric oxide synthase (NOS), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) levels significantly increased, and VILIP-1, NSE, S100B, TXA2, LPA, D-D, 8-iso-PGF2α and MDA levels of the group C after treatment were significantly lower than those of the group A and group B whereas NO, NOS, VEGF, BDNF, IGF-I, SOD and T-AOC levels were significantly higher than those of the group A and group B. Conclusion: Butylphthalide combined with Urinary Kallidinogenase is better than monotherapy in improving the pathological course of nerve damage in patients with massive cerebral infarction.

Meta-analysis of the clinical efficacy and safety of Urinary Kallidinogenase in the treatment of acute cerebral infarction

Objective:To evaluate the clinical efficacy and safety of Urinary Kallidinogenase for Injection in the treatment of acute cerebral infarction.Methods:PubMed,The Cochrane Library,Embase,CNKI,VIP,Wan Fang and bibliographic database of Chinese medicine were searched by computer to collect randomized controlled trials of Urinary Kallidinogenase's treatment of acute cerebral infarction.The time limit was set up until September 2019.At the same time,the references and grey literature in the literature were manually screened.Two independent researchers were screened,evaluated and extracted according to inclusion and exclusion criteria.Meta-analysis was carried out by RevMan 5.3 software.Results:A total of 17 randomized controlled trials involving 2,066 patients,including 1,033 in the experimental group,and 1,033 in the control group.meta-analysis results showed that compared with the conventional treatment,Urinary Kallidinogenase had better effect in the treatment of acute cerebral infarction[OR=3.26,95%CI(2.56,4.16),P<0.00001];the national institule of Health Stroke Scale of the Urinary Kallidinogenase group was significantly better than that of the control group.Urinary Kallidinogenase group activity of daily living scale was better than the control group[OR=21.33,95%CI(6.64,36.01),P=0.004];a total of 7 articles reported adverse reactions,including 19 cases in the trial group and 21 cases in the control group,the main adverse reactions were blood pressure drop,other symptoms were chest tightness,facial redness,dizziness fever,nausea and vomiting,arrhythmia,and no other serious adverse reactions.It can recover itself.Conclusion:the available evidence shows that Urinary Kallidinogenase can effectively improve the symptoms of neurological deficits and improve the ability of daily living in patients with acute cerebral infarction,and is safe.However,the quality of the study is limited.

Effects of Urinary Kallidinogenase combined with mNGF on neurotrophic status, apoptosis and oxidative stress in patients with ischemic stroke

Objective:To study the effects of Urinary Kallidinogenase combined with mouse nerve growth factor (mNGF) on neurotrophic status, apoptosis and oxidative stress in patients with ischemic stroke.Methods: Patients with acute ischemic stroke who were treated in Jiangmen Central Hospital between March 2015 and October 2017 were selected and divided into two groups according to random number table method, the control group received conventional therapy, and the observation group received Urinary Kallidinogenase combined with mNGF therapy on the basis of routine therapy. The contents of neurotrophic cytokines, soluble apoptosis molecules and oxidative stress markers in serum were measured before treatment and 14d after treatment.Results:Serum BDNF, NTF, VEGF, HGF and IGF-1 levels of observation group after treatment were higher than those before treatment whereas serum BDNF, NTF, VEGF, HGF and IGF-1 levels of control group after treatment were not significantly different from those before treatment;serum sFas, sFasL, sTRAIL, 8-OHdG, Hcy and MDA levels of both groups after treatment were lower than those before treatment whereas Livin, Bcl-2, SOD and GSH-Px levels were higher than those before treatment;serum sFas, sFasL, sTRAIL, 8-OHdG, Hcy and MDA levels of observation group after treatment were lower than those of control group whereas BDNF, NTF, VEGF, HGF, IGF-1, Livin, Bcl-2, SOD and GSH-Px levels were higher than those of control group.Conclusion: Urinary Kallidinogenase combined with mNGF can improve the neurotrophic state and inhibit the apoptosis and oxidative stress response in patients with ischemic stroke.

Mechanism of edaravone combined with urinary kallidinogenase for acute cerebral infarction patients

Objective:To observe the effects of edaravone combined with urinary kallidinogenase on serum ox-LDL, PCT, hs-CRP, TNF-α and T cell subsets in patients with acute cerebral infarction, so as to explore the mechanisms of combination therapy on patients with acute cerebral infarction. Methods:86 cases of patients with acute cerebral infarction in our hospital from March 2014 to May 2016 were randomly divided into two groups:control group and observation group, 43 cases in each group. All patients were given general treatment according to their own specific conditions, including hypoglycemic, pressure adjustment, prevention and treatment of complications, symptomatic support therapy, etc. The control group were given 30 mg Edaravone Injection on this basis with once per day for 14 d;The observation group was treated with 0. 15 PNA urinary kallidinogenase intravenous drip with once per day for 14 d on the basis of the control group. The levels of serum x-LDL, PCT, hs-CRP, TNF-αand CD3+, CD4+, CD8+, CD4+/CD8+were detected and compared between the two groups. Results:(1) Before treatment, there was no significant difference between the two groups on the levels of serum ox-LDL, PCT, hs-CRP, and TNF-α;after treatment, the serum levels of ox-LDL, PCT, hs-CRP and TNF-αin the two groups were significantly lower than that before treatment, and the difference was significant (P<0.05);(2) Before treatment, there was no significant difference between the two groups on the levels of serum CD3+, CD4+, CD8+, CD4+/CD8+;after treatment, the serum levels of CD3+, CD4+and CD4+/CD8+were significantly increased in the two groups, and the level of CD8+was significantly decreased compared with the same group before treatment, and the difference was significant (P<0.05);and the levels of serum CD3+, CD4+, CD8+and CD4+/CD8+in the observation group were significantly better than those in the control group, and the difference was significant (P<0.05). Conclusions:The treatment of combined application of urinary kallidinogenase and edaravone in patients with acute cerebral infarction, can significantly improve the serum levels of ox-LDL, PCT, hs-CRP, TNF-αand T cell subsets, further illustrates the synergistic effect of the combination, also shows that the two drugs for acute cerebral infarction can inhibit thrombosis to expand, reduce inflammation, relieve cerebral tissue damage, and improve neurological function.

乌贼墨对H_(22)癌细胞TPK、PKC及PKA活性的影响

利用γ- 32 P- ATP作为反应启动剂掺入外源性底物的方法测定 TPK、PKC及 PKA活性 ,研究了乌贼墨对 H2 2 癌细胞 TPK、PKC及 PKA活性的影响。结果发现 :癌细胞质膜、胞浆及线粒体 TPK活性均显著升高而以质膜 TPK活性升高最为显著 ;胞浆、线粒体及胞核 PKC活性均显著升高而以胞核 PKC升高最为明显 ;胞浆内 PKA活性升高。给予乌贼墨作用后 ,癌细胞质膜、胞浆及线粒体 TPK活性均显著下降 ;线粒体及胞核PKC活性均显著下降 ;胞浆 PKA活性却继续明显升高。结果提示 :乌贼墨能明显的逆转癌细胞异常改变的TPK、PKC和 PKA活性 ,引起 Ras- MAPK信号传导系统的正调节作用减弱和负调节作用增强 ,结果抑制或阻断了 Ras- MAPK信号传导系统的信号级联传导 ,使癌细胞由去分化性增殖向分化性增殖转变 。

半边旗有效化合物对肺癌细胞DNA拓扑异构酶、TPK及c-myc基因的影响

研究半边旗有效化合物6F和A对肺癌细胞DNA拓扑异构酶(TOPO)Ⅰ和Ⅱ活性的影响;化合物A对细胞胞浆和胞膜酪氨酸蛋白激酶(TPK)活性及癌基因c -myc蛋白表达的影响。方法 :通过电泳法测定化合物6F和A对肺癌细胞DNA拓扑异构酶(TOPO)Ⅰ、Ⅱ活性的影响;用液体闪烁计数法测定化合物A对酪氨酸蛋白激酶(TPK)活性的影响;流式细胞仪间接荧光检测法测定化合物A对c -myc基因蛋白表达的影响。结果 :化合物6F和A可抑制细胞DNA拓扑异构酶Ⅰ、Ⅱ的活性,1 0mg/L的6F和A即开始抑制TOPOⅠ的活性,随浓度升高抑制作用增强 ;0 01mg/L的6F和10 0mg/L的A对TOPOⅡ的活性有强烈的抑制作用;化合物A对细胞中胞膜TPK活性有一定的抑制作用,但对胞浆TPK的活性几乎没有影响;化合物A对c -myc基因的蛋白表达有抑制作用。结论 :DNA拓扑异构酶是化合物6F和A抑制细胞生长的靶点之一,化合物A对TPK活性有一定的抑制作用,对c

人新基因hbrp的染色体定位及其对TPK活性的抑制作用(简报)

hbrp(Human BSP-Related Protein)是我们实验室最近在睾丸组织中克隆的一个人与BSP(bovine seminal plasma)蛋白相关的新基因.为了将有关该新基因信息与现有人类基因组转录图相整合,我们应用荧光原位杂交(fluorescent in situ hybridization-FISH)法进行了该基因的人染色体基因定位,结果成功地将hbrp基因定位在人19号染色体长臂1区3带上.hbrp基因是在对BSP蛋白功能的研究过程中发现并克隆的,其同源性分析发现,与其序列最相近的是BSP蛋白家族.hbrp基因编码的蛋白质氨基酸序列中含有四个纤连蛋白Ⅱ型结构域,而BSP蛋白结构中含有两个前后排列的纤连蛋白Ⅱ型结构域,表明该蛋白可能是一种与BSP蛋白相关的结合蛋白.以前的研究中,我们发现BSP不仅能抑制PKC的活性,还能抑制酪氨酸蛋白激酶(TPK)的活性,根据BSP的这一功能,对HBRP蛋白与TPK的关系进行了研究,结果证明HBRP蛋白对TPK活性有明显的抑制作用.现将实验方法及所观察结果报道如下:

VB_1对育雏和育成鹅生长性能、消化酶活力、肝脏TPK1基因表达量的影响及相关性研究

本试验以鹅为试验对象,研究饲粮中不同VB1水平对鹅生长性能、消化道消化酶活力和TPK1基因表达量的影响及其相关性,以确定鹅育雏和育成期VB1的需要量。试验选用1日龄肝用型青农灰鹅360只,随机分为6个处理,每个处理6个重复,每个重复10只。试验各组VB1的水平分别为:0～4周龄为1.0、2.8、4.6、6.4、8.2、10.0mg·kg-1;5～15周龄为0.8、2.6、4.4、6.2、8.0、9.8mg·kg-1。试验期共15周。结果表明:1)日增重在2个生长阶段与需要量成二次曲线变化,0～4周龄以5.60mg·kg-1为最佳,5～15周龄以4.98mg·kg-1为最佳;胃蛋白酶活力在2个生长阶段与需要量成二次曲线变化,0～4周龄以5.48mg·kg-1为最佳,5～15周龄以6.03mg·kg-1为最佳;胰脏胰蛋白酶活力在0～4周龄时与需要量成二次曲线变化,最适需要量为5.46mg·kg-1;十二指肠内容物胰蛋白酶活力0～4和5～15周龄时均与需要量成二次曲线变化,最适需要量分别为5.36和5.41mg·kg-1。2)15周龄鹅生长速度与消化道胃蛋白酶、胰脏胰蛋白酶、胰脏淀粉酶、肠胰蛋白酶、肠淀粉酶活力均呈极显著正相关(P<0.01),与胰脏脂肪酶活力呈显著正相关(P<0.05);3)15周龄时6.2mg·kg-1 VB1显著提高鹅肝脏中硫胺焦磷酸激酶(TPK1)基因的表达量(P<0.05),且TPK1基因的表达量与胃蛋白酶、胰脏脂肪酶、肠淀粉酶活力呈极显著正相关(P<0.01)。试验结果表明:从生长性能分析,VB1的需要量随日龄的增加而出现下降趋势,0～4和5～15周龄饲粮VB1适宜需要量分别为5.60和4.98mg·kg-1;VB1影响鹅肝脏中TPK1基因的表达,而TPK1基因又调控了胃蛋白酶、胰脏脂肪酶、肠淀粉酶的活力,从而调节了生长性能。

烟草TPK2基因的克隆与生物信息学分析

根据烟草的EST片段,采用3’RACE与5’RACE相结合的方法,克隆到了一个烟草推测钾转运基因TPK2。该基因所编码的蛋白包含563个氨基酸,分子量为62.6 kDa,等电点7.94。在结构上,TPK2具有植物行使钾转运功能的c15781保守域;同源性分析表明,TPK2与模式植物拟南芥、水稻等高亲和钾转运蛋白同源性较高。

优质肉鸡硫胺素含量以及TPK1基因的多态性分析

为研究大恒优质肉鸡硫胺素沉积规律及大恒肉鸡不同家系间硫胺素的差异,选取大恒优质肉鸡的4个品系(S08、S07×S01、D2、D1)为试验材料,采用高效液相色谱法对硫胺素含量进行测定,并对其相关基因TPK1进行多态性分析。结果显示:10周龄时,S08品系胸肌中硫胺素含量极显著高于品系D1、D2(P<0.01),4个品系中公鸡胸肌中的硫胺素含量均高于母鸡,差异不明显;10周龄时,公鸡、母鸡中腿肌的硫胺素含量极显著高于胸肌(P<0.01),公鸡中的腿肌、胸肌硫胺素含量均分别高于母鸡的腿肌、胸肌,但都差异不明显。对大恒肉鸡5个品系(S07×S05、S07、S08、S07×01、S08×01)TPK1基因的所有外显子及部分3'非编码区进行了多态性位点的检测,在3'非编码区发现了1个G878A单碱基突变,该SNP位点对腹脂质量具有显著影响(P<0.05),该基因座上的基因型NN个体的腹脂质量显著高于基因型MN个体的腹脂质量,但与大恒优质肉鸡2个品系鸡肉中硫胺素含量差异不显著。

DHA复合物对小鼠H_(22)肝癌细胞TPK活性影响

目的研究二十二碳六烯酸(DHA)复合物抗癌作用机制。方法以移植H22肝癌细胞的小鼠为模型,利用[γ-32P]三磷酸腺苷(ATP)作为反应启动剂掺入外源性底物的方法测定酪氨酸蛋白激酶(TPK)活性,观察DHA复合物对H22癌细胞内TPK活性的影响。结果DHA复合物的体内抑瘤率可高达70%以上;癌细胞细胞核、细胞质、细胞膜、内质网、线粒体中TPK的活性普遍升高(P<0.01)。给予DHA复合物作用后,癌细胞上述各组分中TPK的活性均显著下降(P<0.01)。结论DHA复合物具有抑制TPK活性,降低细胞内的信号传递,抑制癌细胞增殖的作用。

bFGF及TPK抑制剂对听神经瘤细胞增殖的影响

目的 研究碱性成纤维细胞生长因子(bFGF)和酪氨酸蛋白激酶(TPK)抑制剂对培养的听神经瘤细胞增殖和DNA合成的影响作用,初步探讨其作用机制。方法 选取10例手术切除的新鲜听神经瘤组织若干,常规细胞培养,细胞种植于含10％胎牛血清的培养基中,早期传代细胞用于下一步试验。通过细胞计数和3H-TdR摄取率测定观察bFGF及TPK抑制剂genestein对听神经瘤细胞增殖及DNA合成的影响。结果 在无血清培养条件下,所测10例标本中应用bFGF有9例(9/10)测得的活细胞数和3H-TdR摄取率较对照组显著增加(P<0.05)。genistein在4例标本中对瘤细胞增殖和DNA合成均产生明显抑制效应(P<0.01),亦可阻抑bFGF的促增殖作用(P<0.01)。结论bFGF可能以自或旁分泌形式参与听神经瘤细胞增殖的调节。TPK抑制剂在体外能有效抑制听神经瘤细胞增殖,至少部分是通过抑制bFGF受体功能来实现的。

aFGF对人脐静脉内皮细胞TPK、PKC活性及Ca^(2+)浓度的影响

为了观察酸性成纤维细胞生长因子 ( acidic fibroblast growth factor,a FGF)与人脐静脉内皮细胞 ( human umbilical vein endothelial cell,HUVEC)膜上特异受体结合后引起的细胞内信号转导途径 ,探讨 a FGF导致细胞增殖的机理 ,经 Scatchard曲线分析人脐静脉内皮细胞膜受体性质 .以不同浓度的 a FGF处理人脐静脉内皮细胞 ,利用 [γ- 3 2 P]ATP参入外源性底物的方法测定受体的酪氨酸蛋白激酶 ( tyrosine protein kinase,TPK)及蛋白激酶 C( protein kinase C,PKC)的活性 ;用 Fura-2 /AM为荧光指示剂测定 [Ca2 + ]i.结果显示 :Scatchard曲线证明 a FGF与 HUVEC膜受体特异结合呈一条曲线 ,即受体为一种结合位点 ,Kd 为 3.6× 1 0 -10～ 9.6× 1 0 -10 mol/L,每个细胞受体数为2 70 90 .随着 a FGF浓度增加 ,TPK及 PKC活性随之升高 .当 a FGF浓度为 1 .1 2 mg/L时 ,a FGF处理组的 TPK活性是对照组的 3倍 ;膜 PKC活性是对照组 3.4倍 ,胞浆 PKC活性是对照组的 1 .87倍 .胞浆 [Ca2 + ]是对照组的 3倍 .结果指出 :该细胞中 a FGF受体具有 TPK活性 .TPK激活后进一步促进蛋白质和酶磷酸化级联反应 ,而使 PKC活性及 [Ca2 + ]i 升高 ,即 PKC和 Ca2 + 为 TPK的下游信号分子 ,进一步促进基因表达增加 ,导致细胞增殖 .

缺氧复合梭曼中毒对PC_(12)细胞中IL-4、IL-8和TPK活性的影响

目的研究缺氧复合梭曼中毒PC12细胞中白介素-4、白介素-8(IL-4、IL-8)和酪氨酸蛋白激酶(TPK)活性的变化。方法采用ELISA法和放射免疫技术检测缺氧复合梭曼中毒PC12细胞的IL-4、IL-8和TPK活性。结果单纯梭曼中毒PC12细胞胞浆、胞核的TPK以及IL-4、IL-8活性在中毒2 h升高,12 h活性水平最高,24 h活性降低。缺氧复合梭曼中毒组PC12细胞胞浆、胞核的TPK以及IL-4、IL-8活性在缺氧中毒2 h升高,6 h最高,12 h活性降低,各时相点均明显高于正常对照组。结论提示酪氨酸蛋白激酶、IL-4、IL-8参与缺氧复合梭曼中毒所致脑损伤的发病机制。

HL－60细胞诱导分化过程中TPK和PTPP活力的时空改变

对ＲＡ、ＨＨＴ和ＷＰ_（８５２）诱导ＨＬ－６０细胞分化过程中胞浆和膜溶脱部分中的ＴＰＫ和ＰＴＰＰ活力变化进行了研究．结果表明，在诱导早期，ＴＰＫ的活力就有明显的波动变化；随着诱导时间的延长，胞浆部分ＴＰＫ活力下降，膜溶脱部分的ＴＰＫ活力则升高．诱导后，胞浆部分和膜溶脱部分的ＰＴＰＰ活力均明显升高。与ＴＰＫ活力变化相比较，ＰＴＰＰ变化幅度比ＴＰＫ的大。

体外循环和非体外循环病人胰岛素受体TPK活性及血浆TNF-α变化及意义

目的 观察体外循环和非体外循环手术中骨骼肌胰岛素受体TPK活性及血浆TNF α改变 ,探讨胰岛素抵抗产生的机制。方法 随机选择 8例动脉导管患者及 1 5例房缺或室缺患者 ,于麻醉前、麻醉后、开胸后 2 0min、术毕、术后 6h采取血样 ,测定血糖、胰岛素、TNF α的浓度 ,并于手术开始即刻、术毕关胸即刻取骨骼肌标本 ,测定胰岛素受体酪氨酸蛋白激酶 (TPK)活性的变化。结果 体外循环组血糖、胰岛素、TNF α均明显升高 ,手术结束时骨骼肌胰岛素受体TPK活性明显低于手术开始时。动脉导管组血糖明显升高 ,胰岛素及TNF α有所升高 ,但不显著 ,手术前后骨骼肌胰岛素受体TPK活性无明显改变。结论 体外循环手术机体胰岛素抵抗程度明显强于非体外循环手术 ,体外循环可作为一个独立损伤因素影响胰岛素受体TPK活性从而干扰了胰岛素的正常信号传导 ,产生明显的胰岛素抵抗 ,TNF

aFGF、bFGF和genistein对大肠癌细胞CCL229TPK、PKC及ERK活性的影响

目的观察aFGF、bFGF及TPK抑制剂genistein对大肠癌细胞CCL229细胞内TPK,PKC及ERK活性的影响,探讨其信号传导途径。方法以不同浓度的aFGF(0.15μg/ml,0.3μg/ml,0.6μg/ml,1.2μg/ml)、bFGF(25ng/ml,50ng/ml,75ng/ml,100ng/ml)和genistein(6μg/ml,12μg/ml,24μg/ml,48μg/ml)诱导CCL229细胞,利用[γ-32P]ATP掺入外源性底物的方法,液体闪烁测定TPK,PKC及ERK活性。结果随着aFGF/bFGF浓度的增加,TPK、PKC及ERK活性随之升高,与aFGF/bFGF浓度呈显著正相关(P<0.05)。对比之下,胞膜PKC活性比胞质PKC活性升高更为明显。Genistein抑制细胞内TPK、PKC及ERK活性,且与genistein浓度呈剂量依赖效应(P<0.05)。Genistein对bFGF诱导的TPK、PKC及ERK活性抑制更显著。结论aFGF和bFGF诱导大肠癌细胞CCL229后,TPK、PKC及ERK活性均增高,且与aFGF及bFGF呈剂量依赖效应。PKC激活时发生膜转移现象。Genistein诱导CCL229细胞后,TPK、PKC及ERK活性均低于对照组;随着genistein浓度的升高,活性降低的趋势越明显,提示大肠癌中PKC及ERK位于TPK下游。

奈特液对H22荷瘤鼠TPK、PKC活性影响

奈特液对Ｈ２２荷瘤鼠ＴＰＫ、ＰＫＣ活性影响贾光，白新生，孙克任（北京医科大学公共卫生学院劳动卫生教研室北京１０００８３山东新华制药厂淄博２５５００５山东医科大学卫生系毒理教研室济南２５００１２）本研究选择体重１８─２２ｇ健康昆明种小鼠３０只，随机分为...

两株鼻咽癌细胞中TPK、PKC的活性研究

目的：研究ＣＮＥ－１和ＣＮＥ－２Ｚ细胞浆中ＰＫＣ、ＴＰＫ及胞膜ＴＰＫ活性，及槲皮素对它们的影响；方法：常规培养ＣＮＥ－１、ＣＮＥ－２Ｚ和淋巴细胞，用特异底物法、特异激活剂法分别测定其ＴＰＫ、ＰＫＣ活性，两两比较用ｔ检验；结果：ＣＮＥ－１细胞胞浆ＰＫＣ、ＴＰＫ均明显高于脐带血淋巴细胞（Ｐ＜０．０１），而胞膜ＴＰＫ无明显变化；ＣＮＥ－２Ｚ细胞胞浆ＰＫＣ却明显低于淋巴细胞（Ｐ＜０．０１），胞浆、胞膜ＴＰＫ活性均明显增高（Ｐ＜０．０１）。槲皮素（１００μｍｏｌ／Ｌ）使ＣＮＥ－２Ｚ细胞中胞膜ＴＰＫ明显的增高（Ｐ＜０．０１），而对其胞浆ＰＫＣ、ＴＰＫ均无明显影响；该浓度下的槲皮素也能使ＣＮＥ－１细胞中胞膜ＴＰＫ活性明显升高（Ｐ＜０．０１），但强烈抑制其胞浆ＴＰＫ活性（Ｐ＜０．０１），而对其胞浆ＰＫＣ也没有明显影响；结论：胞浆。