目的:评估急诊冠状动脉介入治疗术(PCI)后循环microRNA-26b-5p水平和血糖水平变化的趋势及相关性。方法:根据入选标准和排除标准,共入选接受急诊PCI术的急性前壁心肌梗死患者38例。详细记录临床相关资料,分别于术前、术后24h、术后72h...目的:评估急诊冠状动脉介入治疗术(PCI)后循环microRNA-26b-5p水平和血糖水平变化的趋势及相关性。方法:根据入选标准和排除标准,共入选接受急诊PCI术的急性前壁心肌梗死患者38例。详细记录临床相关资料,分别于术前、术后24h、术后72h行循环血microRNA-26b-5p和血糖水平检测。Real Time PCR法检测血液样本中microRNA-26b-5p表达量的变化。结果:对于成功行急诊PCI的急性心肌梗死患者,术后microRNA-26b-5p表达水平较术前明显升高(P<0.01),术后血糖水平逐渐下降(P<0.01),两者之间存在负相关(r=-0.332,P<0.01)。结论:急性心肌梗死患者往往存在应激性高血糖,microRNA-26b-5p可能参与血糖水平的相关。展开更多
目的讨论血清前B细胞克隆增强因子(pre-B cell colony-enhancing factor,PBEF)、Kruppel样转录因子2(kruppel like factor 2,KLF2)、白介素-26(Interleukin-26,IL-26)与重症肺炎(severe pneumonia,SP)患儿病情严重程度及预后转归的关系...目的讨论血清前B细胞克隆增强因子(pre-B cell colony-enhancing factor,PBEF)、Kruppel样转录因子2(kruppel like factor 2,KLF2)、白介素-26(Interleukin-26,IL-26)与重症肺炎(severe pneumonia,SP)患儿病情严重程度及预后转归的关系。方法选择西安市儿童医院2023年3月-2025年3月收治的180例SP患儿作为研究对象,使用ELISA试剂盒分别检测血清中PBEF、KLF2、IL-26的蛋白水平;根据急性生理与慢性健康评分II(acute physiology and chronic health score,APACHEII评分)判定患儿的病情严重程度并分组为非危重症组(n=60)、危重症组(n=75)和极危重症组(n=45);根据SP患儿预后分为预后良好组(n=127)和预后不良组(n=53);血清PBEF、KLF2、IL-26水平与APACHEII评分的相关性采用Pearson法分析;多因素Logistics回归分析影响SP患儿预后转归的因素;ROC曲线分析血清PBEF、KLF2、IL-26水平对SP患儿预后转归的预测价值。结果与非危重症组比较,危重症组、极危重症组APACHEII评分及血清PBEF、IL-26水平升高(P<0.05),血清KLF2水平均低(P<0.05);与危重症组比较,极危重症组APACHEII评分及血清PBEF、IL-26水平升高,血清KLF2水平降低(P<0.05);SP患儿血清PBEF、IL-26水平与APACHEII评分呈正相关,血清KLF2水平与APACHEII评分呈负相关(P<0.05);预后不良组较预后良好组极危重症患者比例、APACHEII评分及血清PBEF、IL-26水平升高,血清KLF2水平降低(P<0.05);血清PBEF、IL-26水平升高,KLF2水平降低是SP患儿发生预后不良的危险因素(P<0.05);血清PBEF、KLF2、IL-26水平单独及联合预测患儿预后不良的AUC分别为0.769、0.820、0.814、0.933,三者联合预测价值更高(Z=4.112、3.893、4.035,P<0.001)。结论伴随SP患儿病情严重程度的增加,血清PBEF、IL-26水平升高,KLF2水平降低,三者可作为预测患儿预后转归的指标。展开更多
Objective Huangqi Decoction(HQD),a classical traditional Chinese medicine formula,has been used as a valid treatment for alleviating liver fibrosis;however,the underlying molecular mechanism is still unknown.Although ...Objective Huangqi Decoction(HQD),a classical traditional Chinese medicine formula,has been used as a valid treatment for alleviating liver fibrosis;however,the underlying molecular mechanism is still unknown.Although our previous studies showed that microRNA-663a(miR-663a)suppresses the proliferation and activation of hepatic stellate cells(HSCs)and the transforming growth factor-β/small mothers against decapentaplegic(TGF-β/Smad)pathway,whether long noncoding RNAs(lncRNAs)are involved in HSC activation via the miR-663a/TGF-β/Smad signaling pathway has not yet reported.The present study aimed to investigate the roles of lncRNA lnc-C18orf26-1 in the activation of HSCs and the mechanism by which HQD inhibits hepatic fibrosis.Methods The expression levels of lnc-C18orf26-1,miR-663a and related genes were measured by quantitative reverse transcription-polymerase chain reaction.HSCs were transfected with the miR-663a mimic or inhibitor and lnc-C18orf26-1 small interfering RNAs.The water-soluble tetrazolium salt-1 assay was used to assess the proliferation rate of HSCs.Changes in lncRNA expression were evaluated in miR-663a-overexpressing HSCs by using microarray to identify miR-663a-regulated lncRNAs.RNA hybrid was used to predict the potential miR-663a binding sites on lncRNAs.Luciferase reporter assays further confirmed the interaction between miR-663a and the lncRNA.The expression levels of collagen α-2(I)chain(COL1A2),α-smooth muscle actin(α-SMA)and TGF-β/Smad signaling pathway-related proteins were determined using Western blotting.Results Lnc-C18orf26-1 was upregulated in TGF-β1-activated HSCs and competitively bound to miR-663a.Knockdown of lnc-C18orf26-1 inhibited HSC proliferation and activation,downregulated TGF-β1-stimulatedα-SMA and COL1A2 expression,and inhibited the TGF-β1/Smad signaling pathway.HQD suppressed the proliferation and activation of HSCs.HQD increased miR-663a expression and decreased lnc-C18orf26-1 expression in HSCs.Further studies showed that HQD inhibited the expression of COL1A2,α-SMA,TGF-β1,TGF-βtype I receptor(TGF-βRI)and phosphorylated Smad2(p-Smad2)in HSCs,and these effects were reversed by miR-663a inhibitor treatment.Conclusion Our study identified lnc-C18orf26-1 and miR-663a as promising therapeutic targets for hepatic fibrosis.HQD inhibits HSC proliferation and activation at least partially by regulating the lnc-C18orf26-1/miR-663a/TGF-β1/TGF-βRI/p-Smad2 axis.展开更多
文摘目的:评估急诊冠状动脉介入治疗术(PCI)后循环microRNA-26b-5p水平和血糖水平变化的趋势及相关性。方法:根据入选标准和排除标准,共入选接受急诊PCI术的急性前壁心肌梗死患者38例。详细记录临床相关资料,分别于术前、术后24h、术后72h行循环血microRNA-26b-5p和血糖水平检测。Real Time PCR法检测血液样本中microRNA-26b-5p表达量的变化。结果:对于成功行急诊PCI的急性心肌梗死患者,术后microRNA-26b-5p表达水平较术前明显升高(P<0.01),术后血糖水平逐渐下降(P<0.01),两者之间存在负相关(r=-0.332,P<0.01)。结论:急性心肌梗死患者往往存在应激性高血糖,microRNA-26b-5p可能参与血糖水平的相关。
文摘目的讨论血清前B细胞克隆增强因子(pre-B cell colony-enhancing factor,PBEF)、Kruppel样转录因子2(kruppel like factor 2,KLF2)、白介素-26(Interleukin-26,IL-26)与重症肺炎(severe pneumonia,SP)患儿病情严重程度及预后转归的关系。方法选择西安市儿童医院2023年3月-2025年3月收治的180例SP患儿作为研究对象,使用ELISA试剂盒分别检测血清中PBEF、KLF2、IL-26的蛋白水平;根据急性生理与慢性健康评分II(acute physiology and chronic health score,APACHEII评分)判定患儿的病情严重程度并分组为非危重症组(n=60)、危重症组(n=75)和极危重症组(n=45);根据SP患儿预后分为预后良好组(n=127)和预后不良组(n=53);血清PBEF、KLF2、IL-26水平与APACHEII评分的相关性采用Pearson法分析;多因素Logistics回归分析影响SP患儿预后转归的因素;ROC曲线分析血清PBEF、KLF2、IL-26水平对SP患儿预后转归的预测价值。结果与非危重症组比较,危重症组、极危重症组APACHEII评分及血清PBEF、IL-26水平升高(P<0.05),血清KLF2水平均低(P<0.05);与危重症组比较,极危重症组APACHEII评分及血清PBEF、IL-26水平升高,血清KLF2水平降低(P<0.05);SP患儿血清PBEF、IL-26水平与APACHEII评分呈正相关,血清KLF2水平与APACHEII评分呈负相关(P<0.05);预后不良组较预后良好组极危重症患者比例、APACHEII评分及血清PBEF、IL-26水平升高,血清KLF2水平降低(P<0.05);血清PBEF、IL-26水平升高,KLF2水平降低是SP患儿发生预后不良的危险因素(P<0.05);血清PBEF、KLF2、IL-26水平单独及联合预测患儿预后不良的AUC分别为0.769、0.820、0.814、0.933,三者联合预测价值更高(Z=4.112、3.893、4.035,P<0.001)。结论伴随SP患儿病情严重程度的增加,血清PBEF、IL-26水平升高,KLF2水平降低,三者可作为预测患儿预后转归的指标。
基金supported by grants from the National Natural Science Foundation of China (No.82074101 and No.81773979)Shanghai Municipal Health Commission (No.202040486)
文摘Objective Huangqi Decoction(HQD),a classical traditional Chinese medicine formula,has been used as a valid treatment for alleviating liver fibrosis;however,the underlying molecular mechanism is still unknown.Although our previous studies showed that microRNA-663a(miR-663a)suppresses the proliferation and activation of hepatic stellate cells(HSCs)and the transforming growth factor-β/small mothers against decapentaplegic(TGF-β/Smad)pathway,whether long noncoding RNAs(lncRNAs)are involved in HSC activation via the miR-663a/TGF-β/Smad signaling pathway has not yet reported.The present study aimed to investigate the roles of lncRNA lnc-C18orf26-1 in the activation of HSCs and the mechanism by which HQD inhibits hepatic fibrosis.Methods The expression levels of lnc-C18orf26-1,miR-663a and related genes were measured by quantitative reverse transcription-polymerase chain reaction.HSCs were transfected with the miR-663a mimic or inhibitor and lnc-C18orf26-1 small interfering RNAs.The water-soluble tetrazolium salt-1 assay was used to assess the proliferation rate of HSCs.Changes in lncRNA expression were evaluated in miR-663a-overexpressing HSCs by using microarray to identify miR-663a-regulated lncRNAs.RNA hybrid was used to predict the potential miR-663a binding sites on lncRNAs.Luciferase reporter assays further confirmed the interaction between miR-663a and the lncRNA.The expression levels of collagen α-2(I)chain(COL1A2),α-smooth muscle actin(α-SMA)and TGF-β/Smad signaling pathway-related proteins were determined using Western blotting.Results Lnc-C18orf26-1 was upregulated in TGF-β1-activated HSCs and competitively bound to miR-663a.Knockdown of lnc-C18orf26-1 inhibited HSC proliferation and activation,downregulated TGF-β1-stimulatedα-SMA and COL1A2 expression,and inhibited the TGF-β1/Smad signaling pathway.HQD suppressed the proliferation and activation of HSCs.HQD increased miR-663a expression and decreased lnc-C18orf26-1 expression in HSCs.Further studies showed that HQD inhibited the expression of COL1A2,α-SMA,TGF-β1,TGF-βtype I receptor(TGF-βRI)and phosphorylated Smad2(p-Smad2)in HSCs,and these effects were reversed by miR-663a inhibitor treatment.Conclusion Our study identified lnc-C18orf26-1 and miR-663a as promising therapeutic targets for hepatic fibrosis.HQD inhibits HSC proliferation and activation at least partially by regulating the lnc-C18orf26-1/miR-663a/TGF-β1/TGF-βRI/p-Smad2 axis.
