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1)  mitogen activated protein kinase (MAPK) p38
有丝分裂原激活蛋白激酶p38
2)  p38 mitogen-activated protein kinase
p38丝裂原激活蛋白激酶
1.
Objective:To identify the role of p38 mitogen-activated protein kinase(p38 MAPK)and its specific inhibitor,SB203580,in airway inflammation and mucus hypersecretion in vivo.
目的探讨小鼠吸入丙烯醛后是否出现气道黏液高分泌及其产生机制,观察p38丝裂原激活蛋白激酶(p38MAPK)信号通路在气道炎症损伤、黏液高分泌中的作用,以及应用p38MAPK特异性抑制剂SB203580干预后对气道炎症、MUC5AC的影响。
2.
Objective: To investigate the effects of pentoxifylline (PTX) on activation of p38 Mitogen-activated protein kinase, and to study the protective mechanism of PTX on endothel cell monolayer permeability.
目的:观察己酮可可碱(PTX)对p38丝裂原激活蛋白激酶(MAPK)激活的影响,探讨PTX保护内皮细胞单层通透性的机制。
3.
Though there was one literature about p38 mitogen-activated protein kinase(MAPK) involed in regulation of LPS-induceed ICAM- 1 protein.
尽管已有文献报道p38丝裂原激活蛋白激酶（MAPK）可能参与LPS诱导内皮细胞ICAM-1蛋白的表达，但仍不清楚p38MAPK作用的位点是在ICAM-1蛋白翻译水平或是在基因转录水平。
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3)  p38MAPK
p38丝裂原激活蛋白激酶
1.
OBJECTIVE To investigate the effect of astilbin on activation of p38 mitogen activated protein kinase(p38MAPK) in activated T cells of mouse heart transplantation model with acute rejection.
目的:用小鼠心脏移植急性排斥反应体外模型,探讨落新妇苷对心脏移植排斥反应中活化T细胞p38丝裂原激活蛋白激酶(p38MAPK)信号传导通路的影响。
2.
This article was presented to study the effects of tetrandrine(Tet) on phenotypic modulation of vascular smooth muscle cells(VSMC) and p38 mitogen-activated protein kinase(p38MAPK) as well as mitogen-activated protein kinase phosphotase-1(MKP1) after vascular intimal injury.
研究粉防己碱(tetrandrine,Tet)抑制内膜损伤后血管平滑肌细胞(VSMC)表型转化和对p38丝裂原激活蛋白激酶(p38MAPK)及丝裂原激活蛋白激酶磷酸酶-1(MKP-1)表达的影响。
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4)  p38 MAPK
p38丝裂原激活蛋白激酶
1.
[Objectives] To clarify the effect of p38 MAPK on airway inflammation and mucus hypersecretion and the possible cross-talk between p38 MAPK and MMP-9 in mucin gene transcription.
[目的]探讨p38丝裂原激活蛋白激酶(p38 MAPK)信号通路及其特异性抑制剂SB203580在气道炎症、黏液高分泌中的作用，阐明p38MAPK、基质金属蛋白酶-9(MMP-9)在黏液高分泌与黏蛋白基因转录中的相互作用机制。
2.
Objective To investigate the expression of phosphorylated p38 mitogen activated protein kinase(p-p38 MAPK) and protein expression levels at different ischemic time point in focal cerebral ischemic core and penumbra of rats.
目的研究大鼠局灶性脑缺血不同缺血时间皮质半暗带和中心区p38丝裂原激活蛋白激酶(p38 MAPK)磷酸化水平和蛋白水平的表达。
3.
Objective To explore the effect of hypoxic preconditioning(HPC) on middle cerebral artery occlusion(MCAO)-induced brain injury of mice and the changes of P38 mitogen activated protein kinase(P38 MAPK) phosphorylation and protein expression levels in the ischemic cortex.
目的探讨P38丝裂原激活蛋白激酶(P38 MAPK)磷酸化和蛋白表达水平在低氧预适应(HPC)降低脑中动脉阻塞(MCAO)所致缺血性脑损伤中的变化。
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5)  p38
丝裂原激活蛋白激酶p38
6)  p38 MAPK
p38分裂原激活蛋白激酶
1.
The effects of vincristine on the activity of p38 MAPK in gastric cancer cell SGC7901 and multidrug resistant cell SGC7901/VCR.;
p38分裂原激活蛋白激酶信号转导途径与胃癌细胞长春新碱耐药相关
补充资料：乙酰化纤溶酶原-链激酶激活剂复合物
药物名称：乙酰化纤溶酶原-链激酶激活剂复合物

英文名：APSAC

该药对血块有选择性高亲和力且半衰期长，清除半衰期为70分钟，故纤维蛋白溶解作用缓慢而持久。用药后5-8小时仍可维持有效溶栓血药浓度，有报告作用维持7-10天，而SK用药后3小时血中即完全清除，因此可视为长效SK。

APSAC用药特点是短RV间内一次给予全部剂量。据报告冠状动脉内溶栓5分钟内注射5-30mg，1-4小时后闭塞动脉再通率为70-83％。静脉给药5分钟内注入5-30mg，再通率为60-100％。该药全身纤溶作用微弱，用药简单，药物作用时间长，然而再闭塞率可达20％，但平均再闭塞率仍较SK、rt-PA为低。


类别：溶栓药
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