目的 探讨RNF167对病毒感染的小鼠腹腔巨噬细胞产生IFN-β的调控作用.方法 RNA病毒VSV和DNA病毒HSV-1感染小鼠腹腔巨噬细胞后,Western blot检测RNF167的表达水平.利用RNA干扰减少小鼠原代腹腔巨噬细胞中RNF167的表达后,病毒感染小鼠腹腔巨噬细胞,实时荧光定量PCR法检测IFN-β的mRNA水平,ELIAS法检测细胞上清中IFN-β的浓度.Western blot法检测IFN-β的转录因子IRF3的磷酸化(p-IRF3)水平.结果 VSV感染巨噬细胞4和8h后,RNF167表达水平显著下降(P＜0.01),而HSV-1感染后RNF167的表达没有显著变化.si-RNF167降低小鼠腹腔巨噬细胞RNF167表达水平后,与对照细胞相比,感染RNA病毒后细胞中IFN-β的mRNA水平及上清中IFN-β水平显著下降(P＜0.01),p-IRF3水平也显著下降.而感染HSV-1病毒后上述指标均无差异.结论 RNF167能够特异性地调控RNA病毒感染的巨噬细胞中IFN-β的表达.

Objective To investigate the role of miR-350 in inflammatory responses.Methods Lipopolysaccharide(LPS) was used to generate inflammatory responses model in mouse peritoneal macrophages.We confirmed that the target region of miR-350 by software prediction and dual luciferase reporter system.We detected the expression of the gene targeted by miR-350 via real-time quantitive PCR.Results MiR-350 was down-regulated by LPS stimulation in mouse peritoneal macrophages.MiR-350 targeted to the 3' UTR region of IL-6.Overexpression or down-regulation of miR-350 decreased or increased the mRNA expression of IL-6 in LPS-stimulated mouse peritoneal macrophages.Conclusion With LPS stimulation,the level of miR-350 expression was decreased, which inhibited pro-inflammatory cytokine IL-6 responses stimulated in mouse peritoneal macrophages.

目的:观察消旋卡多曲联合甘草锌治疗婴幼儿急性水样腹泻的临床疗效。方法:选择急性水样腹泻婴幼儿96例,随机分为观察组49例和对照组47例。对照组在退热、补液等常规治疗基础上,给予十六角蒙脱石加金双歧治疗,观察组加用消旋卡多曲及甘草锌治疗,对比两组临床疗效。结果:(1)两组治疗后第2天、第3天便次及平均止泻时间比较,差异显著(P<0.05)。(2)观察组显效40例,有效7例,无效2例,总有效率95.9%;对照组显效29例,有效10例,无效8例,总有效率83.0%。两组总有效率比较,差异显著(P<0.05)。(3)观察组治疗期间仅出现恶心2例、便秘1例,未发现皮疹、腹痛、白细胞减少等不良反应。结论:消旋卡多曲及甘草锌是婴幼儿急性水样腹泻有效且安全的治疗药物。

我国小儿腹泻病原构成比中,轮状病毒感染约占40%(欧美国家50%左右)[1-2].2004年11月～2006年2月,我们应用免疫球蛋白口服液治疗小儿轮状病毒肠炎43例,疗效满意.现报告如下.