Liver injury was assessed by serum ALT and liver histology. The expression and activity of p38 MAPK were measured by Western blot and kinase activity assays. In addition, DNA binding activities of nuclear factor kappa B (NF-κB) were analyzed by electrophoretic mobility shift assay. The effects of SB203580, a specifi c p38 MAPK inhibitor, on liver injuries and expression of proin? ammatory cytokines (interferon-γ, IL-12, IL-1β and TNF-α) were observed. RESULTS: The activity of p38 MAPK and NF-κB was increased and reached its peak 14 or 21 d AG-014699 价格 after the fi rst syngeneic S-100 administration. Inhibition of p38 MAPK activation by SB203580 decreased the activation of NF-κB and the expression of

proin? ammatory cytokines. Moreover, hepatic injuries were improved significantly KRX-0401体内 after SB203580 administration. CONCLUSION: p38 MAPK and NF-κB play an important role in an animal model of autoimmune hepatitis (AIH) induced by autoantigens.
Since its discovery in 1993,the mitogen-activated protein(MAP) kinase p38 has attracted much attention for its role in a wide range of cellular processes,many of which involve the immune system. Although p38 has been heavily implicated in the function of all type immune cells,research has tended

focus on its role in innate immunity. In this review we attempt to highlight some of the major discoveries that have been made regarding p38′s role in adaptive immunity,and also to discuss the possible future implications of these discoveries.
多种信号分子通过丝裂原激活的蛋白激酶(MAPK)信号转导通路(包括ERK、JNK、P38和BMK1),对肝星状细胞(HSC)的活化、增殖、凋亡、细胞周期产生影响,由此在多个环节干预肝纤维化的形成和逆转过程。
目的观察红茶多酚对牛主动脉内皮细胞(BAECs)增殖的影响,并探讨其作用机制。方法用四甲基偶氮噻唑蓝(MTT)检测细胞增殖活性,用蛋白免疫印迹测定p38丝裂原活化蛋白激酶(MAPK)磷酸化表达。结果不同浓度红茶多酚对牛主动脉内皮细胞(BAECs)均有明显抑制作用,呈剂量时间依赖关系;红茶多酚(0.4mg/L)可以降低佛波酯(PMA)或血管紧张素Ⅱ(AngⅡ)刺激的细胞增殖(P<0.05),这种作用可以用还原型辅酶II(NADPH)氧化酶抑制剂apocynin或p38MAPK阻断剂SB203580预培养来实现;红茶多酚可以推迟血管紧张素II刺激的p38MAPK磷酸化。结论红茶多酚具有抑制内皮细胞增殖的作用,抑制PKC-NADPH氧化酶-p38MAPK信号途径可能是其重要机制之一。
支气管哮喘(简称哮喘)作为一种免疫调节异常的疾病已经取得了普遍的共识。有关哮喘免疫调节紊乱的机制,得到最广泛关注的有著名的”卫生学假说”。卫生学假说的核心是

点击此处 Th1/Th2细胞因子的平衡学说,亦即 Th1/Th2细胞所产生的细胞因子有互相制约彼此表型的分化和功能的特性。当 Th1细胞占优势时,就会抑制 Th2细胞的功能。然而,近来免疫学研究进展对这一假说提出了挑战,试图通过上调 Th1纠正 Th2的免疫偏倚以治疗变应性哮喘的思路可能是把问题过于简单化了。与此同时,有的学者也对哮喘气道高反应发生的气道重塑及细胞学基础提出了重要的论点。

We previously reported that ONO-AE-248,a selective EP3 receptor agonist,has been shown to cause neutrophil death without the typical features of apoptosis and necrosis.However,the mechanism of the neutrophil death is unclear.By using Western blotting,flow cytometry(FACS)and confocal laser scanning microscopy(CLSM),we investigated the cellular signal transduction pathways of the neutrophil death.The research results showed that the neutrophil death induced by ONO-AE-248 did not show the morphologic changes of apoptosis and was not associated with the activity of caspase-3,caspase-8,and phosphorylation of p38-MAPK.However,impairment of mitochondria transmembrane potential has been found during the process of cell death.