丙戊酸钠通过EGFR下调CD44表达抑制胶质瘤细胞生长

目的:探讨丙戊酸钠通过抑制A172胶质瘤细胞表皮生长因子受体（epidermal growth factor receptor，EGFR）的活化，下调CD44表达，进而调节细胞生长的机制。方法:实时荧光定量PCR和Western blot检测A172胶质瘤细胞中CD44以及siRNA下调CD44表达的情况，MTT检测CD44和丙戊酸钠对细胞生长的影响，Western blot检测丙戊酸钠对细胞中p-EGFR、EGFR和CD44表达影响。结果:丙戊酸钠抑制A172胶质瘤细胞生长，并具有浓度依赖性。A172胶质瘤细胞表达CD44，siRNA下调CD44表达后，细胞生长较正常组显著减缓。活化EGFR促进A172胶质瘤CD44蛋白表达，而EGFR的抑制剂Lapatinib可显著抑制上述效应。丙戊酸钠抑制EGFR磷酸化，下调CD44蛋白表达。结论:丙戊酸钠抑制A172胶质瘤细胞的生长。抑制A172胶质瘤细胞中EGFR的活化，下调CD44的表达，是丙戊酸钠抑制胶质瘤细胞生长的其中一个机制。     

艳山姜挥发油通过调控巨噬细胞CD36和ABCA1表达抑制泡沫细胞的形成

目的:观察艳山姜挥发油对氧化低密度脂蛋白(ox-LDL)诱导巨噬细胞转化为泡沫细胞的抑制作用,并探索其机制。方法:使用佛波酯(PMA,100μg·L^-1)诱导人白血病单核细胞(THP-1)24 h后形成巨噬细胞,实验分为4组,分别为空白组(无血清RPMI 1640),模型组(80 mg·L^-1ox-LDL),艳山姜挥发油低剂量组(80 mg·L^-1ox-LDL+4μg·L^-1艳山姜挥发油),艳山姜挥发油高剂量组(80 g·L^-1ox-LDL+20μg·L^-1艳山姜挥发油)。噻唑蓝(MTT)比色法检测艳山姜挥发油对巨噬细胞的活性的影响,蛋白免疫印迹法(Western blot)检测巨噬细胞中白细胞分化抗原36(CD36)和三磷酸腺苷结合盒转运体A1(ABCA1)的表达,酶联免疫吸附测定(ELISA)检测巨噬细胞内胆固醇酯含量,油红O染色法检测巨噬细胞中脂质小滴的含量。结果:艳山姜挥发油对巨噬细胞无毒性。与空白组比较,模型组的巨噬细胞内脂滴和胆固醇酯的含量显著增加(P<0.01),CD36蛋白表达显著上升(P<0.01),ABCA1蛋白表达无显著变化;与模型组比较,艳山姜挥发油显著抑制巨噬细胞中脂滴和胆固醇酯的含量(P<0.01),下调CD36的蛋白表达(P<0.01),上调ABCA1蛋白的表达(P<0.01),艳山姜挥发油可抑制巨噬细胞向泡沫细胞的转化。结论:艳山姜挥发油对ox-LDL诱导的巨噬细胞向泡沫细胞的形成具有抑制作用,该药理作用与艳山姜挥发油下调巨噬细胞CD36和上调ABCA1蛋白的表达有关。     

A Positive Feedback Loop Between Th17 Cells and Dendritic Cells in Patients with Endplate Inflammation

Background: Endplate inflammation remains a difficult disease to treat, in part due to its unclear pathology. Previous experiments showed that patients with idiopathic inflammation presented a systemic upregulation of Th17 cells. Here, we investigated how this change might affect the inflammatory environment in endplate inflammation.

Methods: Peripheral blood was obtained from patients and healthy controls, and Th17 cells were examined.Results: Th17 cells significantly increased the differentiation of CD11c+ and DC-SIGN+ dendritic cells (DCs) from circulating monocytes in the absence of exogenous stimulation as well as in the presence of LPS stimulation. Th17 cells also increased CD80 and CD86 expression by DCs. Importantly, although Th17 cells from both healthy controls and patients with endplate inflammation could induce CD11c, DC-SIGN, CD80, and CD86 expression, Th17 cells from patients with endplate inflammation showed significantly more potent capacity. Both contact-dependent and IL-17-dependent mechanisms were employed by Th17 cells, since blocking cell-to-cell contact significantly inhibited Th17-mediated differentiation of CD11c+ DCs, and neutralization of IL-17 reduced the expression of CD80 and CD86. Strikingly, DCs following incubation with Th17 cells, but not the DCs derived directly from monocytes without Th17 cells, could significantly promote the expression of IL-17 from naive CD4+ T cells.

Conclusions: These results demonstrated that Th17 cells from patients with endplate inflammation could potently induce the differentiation and activation of DCs that preferentially promoted IL-17 response in a positive feedback loop.     

细胞黏附分子CD99在人髓母细胞瘤中的表达及意义

目的 探讨细胞黏附分子CD99在人髓母细胞瘤组织中的表达特点及其临床意义。方法 采用免疫组化法检测107例髓母细胞瘤及15例瘤旁正常脑组织标本中CD99的表达。所有病人均随访至死亡或截止至2013年12月，随访时间为12~80个月，利用Kaplan-Meier生存曲线进行生存分析。结果 髓母细胞瘤CD99阳性表达率（57.94%，62/107）明显高于瘤周正常脑组织（0%，0/15；P<0.05）。CD99的表达水平与病人性别、年龄、肿瘤的病理组织学分型和分子亚型均无明显相关性（P>0.05）。CD99的高表达与髓母细胞瘤病人的预后呈显著负相关（P<0.05）。结论 CD99高表达与髓母细胞瘤预后显著相关，可作为预后判断的指标及治疗髓母细胞瘤潜在的新靶点。     

Pannexin 1 channels facilitate communication between T cells to restrict the severity of airway inflammation

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