目的:探究γ-干扰素释放试验联合血清高迁移率族蛋白B1(high mobility group box 1,HMGB1)及Fe测定对活动性结核病患者的诊断效能。方法:选取2018年1-12月于本院就诊的活动性肺结核患者作为活动组(n=154),潜伏性结核分枝杆菌感染者作为...目的:探究γ-干扰素释放试验联合血清高迁移率族蛋白B1(high mobility group box 1,HMGB1)及Fe测定对活动性结核病患者的诊断效能。方法:选取2018年1-12月于本院就诊的活动性肺结核患者作为活动组(n=154),潜伏性结核分枝杆菌感染者作为潜伏组(n=158)。比较两组γ-干扰素、HMGB1及Fe水平。比较血清γ-干扰素释放试验、HMGB1及Fe单独及联合检测对活动性结核的诊断效能。结果:活动组γ-干扰素水平明显高于潜伏组(P<0.05)。活动组HMGB1水平高于潜伏组,Fe水平低于潜伏组(P<0.05)。γ-干扰素释放试验的最佳截断值为2.72 IU/mL;血清HMGB1检测的最佳截断值为4.48μg/L;血清Fe检测的最佳截断值为10.3μmol/L。联合诊断的曲线下面积明显高于各项单独检测,且联合诊断的准确度明显高于各项单独检测(P<0.05)。结论:血清γ-干扰素释放试验联合HMGB1及Fe测定可提高活动性结核的诊断准确度,同时保持较好的敏感度,对活动性结核诊断有重要的临床价值。展开更多
OBJECTIVE: To investigate the efficacy of dihydromyricetin(DMY) on nasopharyngeal carcinoma(NPC) cell proliferation, apoptosis and to reveal the underlying mechanism in vitro experiments.METHODS: The CNE-2 cell line w...OBJECTIVE: To investigate the efficacy of dihydromyricetin(DMY) on nasopharyngeal carcinoma(NPC) cell proliferation, apoptosis and to reveal the underlying mechanism in vitro experiments.METHODS: The CNE-2 cell line was treated with different concentrations of DMY and the effects of DMY on cell viability and proliferation were evaluated using cell counting kit-8(CCK-8) assay and plate colony formation assay. Cellular apoptosis was detected by flow cytometry following Annexin V fluorescein isothiocyanate/propidine iodide staining.Nuclei morphology was observed under a fluorescence microscope following Hoechst 333258 staining. The expression of phosphorylated inhibitor of nuclear factor kappa-B kinase subunit beta(p-IKKβ), phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha(p-IKKα), inhibitor of nuclear factor kappa-B alpha(IκB-α), nuclear factor kappa-B(NF-κB)/p65 was examined by Western blot analysis and the nuclear translocation of NF-κB/p65 was observed using a confocal laser scanning microscopy.RESULTS: DMY inhibited the proliferative capability and colony formation of NPC CNE-2 cells. Meanwhile, DMY induced apoptosis of CNE-2 cells in a dose and time-dependent manner via upregulating B-cell lymphoma-2 associated X, but downregulating B-cell lymphoma-2 and pro-caspase-3. Importantly, we found that DMY suppressed tumor necrosis factor alpha(TNF-α)-mediated NF-κB activation via inhibiting p-IKKβ, p-IKKα and blocking NF-κB subunit p65.CONCLUSION: Our experiments demonstrated that DMY had significant antiproliferative and apoptosisinducing effects on CNE-2 cells. Additionally, DMY promoted inactivation of p-IKKβ, p-IKKα,and blocked the nuclear translocation of NF-κB subunit p65. These results suggest that DMY may be an important therapeutic approach for NPC.展开更多
基金Supported by the National Natural Science Foundation of China (Regulation and Mechanism of Bone Marrow Mesenchymal Stem Cells on the Characteristics of Nasopharyngeal Carcinoma Stem Cells, No.81272434)the Medical Research Fund of Guangdong Province (Effect of Berberine on Growth of Transplanted Tumor of Nasopharyngeal Carcinoma in Mice Based on JAK/STAT3 Signaling Pathway, No.A2016431)。
文摘OBJECTIVE: To investigate the efficacy of dihydromyricetin(DMY) on nasopharyngeal carcinoma(NPC) cell proliferation, apoptosis and to reveal the underlying mechanism in vitro experiments.METHODS: The CNE-2 cell line was treated with different concentrations of DMY and the effects of DMY on cell viability and proliferation were evaluated using cell counting kit-8(CCK-8) assay and plate colony formation assay. Cellular apoptosis was detected by flow cytometry following Annexin V fluorescein isothiocyanate/propidine iodide staining.Nuclei morphology was observed under a fluorescence microscope following Hoechst 333258 staining. The expression of phosphorylated inhibitor of nuclear factor kappa-B kinase subunit beta(p-IKKβ), phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha(p-IKKα), inhibitor of nuclear factor kappa-B alpha(IκB-α), nuclear factor kappa-B(NF-κB)/p65 was examined by Western blot analysis and the nuclear translocation of NF-κB/p65 was observed using a confocal laser scanning microscopy.RESULTS: DMY inhibited the proliferative capability and colony formation of NPC CNE-2 cells. Meanwhile, DMY induced apoptosis of CNE-2 cells in a dose and time-dependent manner via upregulating B-cell lymphoma-2 associated X, but downregulating B-cell lymphoma-2 and pro-caspase-3. Importantly, we found that DMY suppressed tumor necrosis factor alpha(TNF-α)-mediated NF-κB activation via inhibiting p-IKKβ, p-IKKα and blocking NF-κB subunit p65.CONCLUSION: Our experiments demonstrated that DMY had significant antiproliferative and apoptosisinducing effects on CNE-2 cells. Additionally, DMY promoted inactivation of p-IKKβ, p-IKKα,and blocked the nuclear translocation of NF-κB subunit p65. These results suggest that DMY may be an important therapeutic approach for NPC.
