94(95%CI:0.88~0.96),敏感性为93.0%,特异性为86.0%。结论 ELF试验是有效诊断慢性丙肝患者肝纤维化的无创性检查方法,能够准确的诊断肝纤维化分期和肝硬化。
受体相互作用蛋白2(receptor-interacting protein 2,RIP2)属于RIP家族成员,在多种组织中均有分布。RIP2可与多种蛋白相互作用,参与多个受体的信号转导,发挥生理功能,被认为是固有免疫、适应性免疫、凋亡信号途径的重要衔接分子。基于其特殊的分子结构及生物学功能,RIP2在炎症、肿瘤、自身免疫病等多种疾病中发挥着重要作用。本文就RIP2的结构、生物学功能以及其在相关疾病特别是口腔疾病发生发展中所起作用作一综述。
AIM: 而且 To investigate the role of sorafenib(SFN) in autophagy of hepatocellular carcinoma(HCC). We evaluated how SFN affects autophagy signaling pathway in human HCC

cell lines. METHODS: Two different human HCC cell lines, Hep3 B and Huh7, were subjected to different concentrations of SFN. Cell viability and onset of apoptosis were determined with colorimetric assay and immunoblotting analysis, respectively. The changes in autophagy-related proteins, including LC3, ULK1, AMPK, and LKB, were determined with immunoblotting analysis in the presence or absence of SFN. To assess autophagic dynamics, autophagic flux was measured with chloroquine, a lysosomal inhibitor. 无 The autophagic responsiveness between different HCC cell lines was compared under the autophagy enhancing conditions.RESULTS: Hep3 B cells were significantly more resistant to SFN than Huh7 cells.

Immunoblotting analysis revealed a marked increase in SFN-mediated autophagy flux in Huh7 cells, which was, however, absent in Hep3 B cells. While both starvation and rapamycin enhanced autophagy in Huh7 cells, only rapamycin increased autophagy in Hep3 B cells. Immunoblotting analysis of autophagy initiation proteins showed that SFN substantially increased 查找更多 phosphorylation of AMPK and consequently autophagy in Huh7, but not in Hep3 B cells.CONCLUSION: The autophagic responsiveness to SFN is distinct between Hep3 B and Huh7 cells. Resistance of Hep3 B cells to SFN may be associated with

altered autophagy signaling pathways.
目的探讨姜黄素对脂多糖(lipopolysaccharide,LPS)刺激腹腔巨噬细胞(peritoneal macrophages,PMs)分泌炎症因子的影响。方法分离、培养腹腔巨噬细胞,用不同浓度姜黄素(12.5、25、50 mg/L)预处理细胞12 h,进而使用100ng/ml LPS刺激细胞,12 h后收集培养基上清液,ELISA检测促炎介质肿瘤坏死因子(tumor necrosis factor-α,TNF-α)、白介素6(interleukin-6,IL-6)的含量;30 min后收集细胞裂解物,Western blot检测p38 MAPK激酶活性。结果未经处理的腹腔巨噬细胞经LPS刺激12 h后,上清中TNF-α、IL-6的表达水平显著上升(p0.05);而50、25 mg/L姜黄素可以明显抑制LPS诱导的TNF-α、IL-6的表达(p
神经变性疾病是由于神经元或者髓鞘的损伤、丢失引起的神经系统疾病,其病因复杂,影响因素甚多,发病机制尚不完全明确。蛋白激酶在神经变性疾病的发生发展过程中发挥着重要的作用。然而,蛋白激酶抑制剂能有效保护神经细胞,缓解或减轻神经变性疾病的病情。本文就阿尔茨海默病、帕金森病、亨廷顿病等神经变性疾病中所涉及的蛋白激酶及其抑制剂进行综述,分析各蛋白激酶与主要神经变性疾病疾病之间的相互关系,为针对这些疾病的药物研发提供新的思路和策略,认为新型复方药物可能成为治疗神经变性疾病药物研发的方向。
目的探讨番荔枝内酯Bullatacin诱导肿瘤细胞凋亡的机制。方法采用MTT法检测不同浓度(6.25、12.