目的探讨清金化痰汤调节慢性阻塞性肺疾病(COPD)模型大鼠气道黏液高分泌的作用机制。方法 Wistar大鼠随机分为正常组、模型组、清金化痰汤组与克拉霉素组,每组10只。除正常组外,其余3组均采用气管内注入脂多糖和烟熏复合法建立COPD模型...目的探讨清金化痰汤调节慢性阻塞性肺疾病(COPD)模型大鼠气道黏液高分泌的作用机制。方法 Wistar大鼠随机分为正常组、模型组、清金化痰汤组与克拉霉素组,每组10只。除正常组外,其余3组均采用气管内注入脂多糖和烟熏复合法建立COPD模型,分别给予生理盐水、清金化痰汤、克拉霉素灌胃,连续30 d。实验第31日,处死大鼠提取肺组织,每组随机选取6只,采用实时荧光定量PCR检测肺组织中性粒细胞弹性蛋白酶(NE)、表皮生长因子(EGFR)、黏蛋白5AC(MUC5AC)基因表达。结果模型组大鼠肺组织NE、MUC5AC m RNA表达较正常组升高;与模型组比较,清金化痰汤组、克拉霉素组NE、MUC5AC m RNA表达均显著降低,清金化痰汤组NE、MUC5AC m RNA表达较克拉霉素组显著降低;清金化痰汤组EGFR m RNA表达较模型组显著降低。结论清金化痰汤通过调节NE/EGFR/MUC5AC信号转导通路,抑制气道黏液高分泌。展开更多
目的:探讨柚皮素(Nar)对呼吸道合胞病毒(RSV)感染引起的气道黏液高分泌的作用。方法:通过RSV A2株感染人肺腺癌上皮细胞构建气道黏液高分泌细胞模型,在RSV感染及Nar干预作用下,采用实时荧光定量PCR、ELISA和细胞免疫荧光技术检测各组细...目的:探讨柚皮素(Nar)对呼吸道合胞病毒(RSV)感染引起的气道黏液高分泌的作用。方法:通过RSV A2株感染人肺腺癌上皮细胞构建气道黏液高分泌细胞模型,在RSV感染及Nar干预作用下,采用实时荧光定量PCR、ELISA和细胞免疫荧光技术检测各组细胞黏蛋白(MUC)5AC的表达情况。结果:RSV感染R1组[感染复数(MOI)=0.5]、R2组(MOI=1.0)、R3组(MOI=5.0)和对照组(C组)MUC5AC m RNA相对表达量分别为1.45±0.10、2.67±0.09、4.82±0.27和1,各组MUC5AC蛋白的表达量分别为(38.61±0.41)μg/L、(44.11±0.96)μg/L、(51.01±0.48)μg/L和(34.38±0.95)μg/L,RSV感染组和C组相比差异均有统计学意义(P<0.05)。R2组和不同浓度Nar干预组N1组(Nar 30μmol/L+RSV MOI=1.0)、N2组(Nar 100μmol/L+RSV MOI=1.0)、N3组(Nar 30μmol/L)、N4组(Nar 100μmol/L)及DMSO组(D组)的MUC5AC m RNA水平依次为2.52±0.10、2.31±0.06、1.90±0.01、0.99±0.04、0.85±0.03、1.20±0.03,MUC5AC蛋白水平依次为(46.72±0.87)μg/L、(43.60±0.45)μg/L、(40.55±0.45)μg/L、(38.73±0.55)μg/L、(37.08±1.35)μg/L、(37.12±0.91)μg/L,C组MUC5AC蛋白水平为(37.62±1.18)μg/L,与C组相比,R2组MUC5AC m RNA和蛋白水平显著增加(P<0.05),N1、N2组与R2组相比,MUC5AC m RNA和蛋白水平显著降低,随Nar浓度增加,抑制效果更明显,呈剂量相关性(P<0.05),N3、N4组与C组相比,MUC5AC m RNA和蛋白表达水平下降,但差异无统计学意义(P>0.05),D组与C组差异无统计学意义(P>0.05)。荧光显微镜观察结果显示RSV感染后细胞质内MUC5AC蛋白表达增加,而Nar可下调其表达。结论:RSV A2株感染A549细胞会导致MUC5AC m RNA和蛋白表达增加,Nar通过抑制其表达,抑制RSV感染引起的气道黏液高分泌。展开更多
Mucinous colorectal adenocarcinoma is a distinct subtype of colorectal cancer(CRC)characterized by the pres-ence of abundant extracellular mucin which accounts for at least 50%of the tumor volume.Mucinous colorectal a...Mucinous colorectal adenocarcinoma is a distinct subtype of colorectal cancer(CRC)characterized by the pres-ence of abundant extracellular mucin which accounts for at least 50%of the tumor volume.Mucinous colorectal adenocarcinoma is found in 10%-20%of CRC patients and occurs more commonly in female and younger patients.Moreover,mucinous colorectal adenocarcinoma is more frequently located in the proximal colon and diagnosed at an advanced stage.Based on its molecular context,mucinous colorectal adenocarcinoma is associated with the over-expression of mucin 2(MUC2)and mucin 5AC(MUC5AC)proteins.At the same time,it shows higher mutation rates in the fundamental genes of the RAS/MAPK and PI3K/Akt/mTOR pathways.Mucinous colorectal adenocarcinoma also shows higher rates of microsatellite instability(MSI)than non-mucinous colorectal adenocarcinoma which might correlate it with Lynch syndrome and the CpG island methylator phenotype.The prognosis of mucinous colorectal adenocarcinoma as to non-mucinous colorectal adenocarcinoma is debatable.Further,the impaired responses of mucinous colorectal adenocarcinoma to palliative or adjuvant chemotherapy warrant more studies to be performed for a specialized treatment for these patients.In this review,we discuss the molecular background and histopathol-ogy of mucinous colorectal adenocarcinoma,and provide an update on its prognosis and therapeutics from recent literatures.展开更多
文摘目的探讨清金化痰汤调节慢性阻塞性肺疾病(COPD)模型大鼠气道黏液高分泌的作用机制。方法 Wistar大鼠随机分为正常组、模型组、清金化痰汤组与克拉霉素组,每组10只。除正常组外,其余3组均采用气管内注入脂多糖和烟熏复合法建立COPD模型,分别给予生理盐水、清金化痰汤、克拉霉素灌胃,连续30 d。实验第31日,处死大鼠提取肺组织,每组随机选取6只,采用实时荧光定量PCR检测肺组织中性粒细胞弹性蛋白酶(NE)、表皮生长因子(EGFR)、黏蛋白5AC(MUC5AC)基因表达。结果模型组大鼠肺组织NE、MUC5AC m RNA表达较正常组升高;与模型组比较,清金化痰汤组、克拉霉素组NE、MUC5AC m RNA表达均显著降低,清金化痰汤组NE、MUC5AC m RNA表达较克拉霉素组显著降低;清金化痰汤组EGFR m RNA表达较模型组显著降低。结论清金化痰汤通过调节NE/EGFR/MUC5AC信号转导通路,抑制气道黏液高分泌。
文摘目的:探讨柚皮素(Nar)对呼吸道合胞病毒(RSV)感染引起的气道黏液高分泌的作用。方法:通过RSV A2株感染人肺腺癌上皮细胞构建气道黏液高分泌细胞模型,在RSV感染及Nar干预作用下,采用实时荧光定量PCR、ELISA和细胞免疫荧光技术检测各组细胞黏蛋白(MUC)5AC的表达情况。结果:RSV感染R1组[感染复数(MOI)=0.5]、R2组(MOI=1.0)、R3组(MOI=5.0)和对照组(C组)MUC5AC m RNA相对表达量分别为1.45±0.10、2.67±0.09、4.82±0.27和1,各组MUC5AC蛋白的表达量分别为(38.61±0.41)μg/L、(44.11±0.96)μg/L、(51.01±0.48)μg/L和(34.38±0.95)μg/L,RSV感染组和C组相比差异均有统计学意义(P<0.05)。R2组和不同浓度Nar干预组N1组(Nar 30μmol/L+RSV MOI=1.0)、N2组(Nar 100μmol/L+RSV MOI=1.0)、N3组(Nar 30μmol/L)、N4组(Nar 100μmol/L)及DMSO组(D组)的MUC5AC m RNA水平依次为2.52±0.10、2.31±0.06、1.90±0.01、0.99±0.04、0.85±0.03、1.20±0.03,MUC5AC蛋白水平依次为(46.72±0.87)μg/L、(43.60±0.45)μg/L、(40.55±0.45)μg/L、(38.73±0.55)μg/L、(37.08±1.35)μg/L、(37.12±0.91)μg/L,C组MUC5AC蛋白水平为(37.62±1.18)μg/L,与C组相比,R2组MUC5AC m RNA和蛋白水平显著增加(P<0.05),N1、N2组与R2组相比,MUC5AC m RNA和蛋白水平显著降低,随Nar浓度增加,抑制效果更明显,呈剂量相关性(P<0.05),N3、N4组与C组相比,MUC5AC m RNA和蛋白表达水平下降,但差异无统计学意义(P>0.05),D组与C组差异无统计学意义(P>0.05)。荧光显微镜观察结果显示RSV感染后细胞质内MUC5AC蛋白表达增加,而Nar可下调其表达。结论:RSV A2株感染A549细胞会导致MUC5AC m RNA和蛋白表达增加,Nar通过抑制其表达,抑制RSV感染引起的气道黏液高分泌。
基金This work was supported by the Natural Science Foundation of Zhejiang Province(Grant No.LY15H160003),which supported the research infrastructure.
文摘Mucinous colorectal adenocarcinoma is a distinct subtype of colorectal cancer(CRC)characterized by the pres-ence of abundant extracellular mucin which accounts for at least 50%of the tumor volume.Mucinous colorectal adenocarcinoma is found in 10%-20%of CRC patients and occurs more commonly in female and younger patients.Moreover,mucinous colorectal adenocarcinoma is more frequently located in the proximal colon and diagnosed at an advanced stage.Based on its molecular context,mucinous colorectal adenocarcinoma is associated with the over-expression of mucin 2(MUC2)and mucin 5AC(MUC5AC)proteins.At the same time,it shows higher mutation rates in the fundamental genes of the RAS/MAPK and PI3K/Akt/mTOR pathways.Mucinous colorectal adenocarcinoma also shows higher rates of microsatellite instability(MSI)than non-mucinous colorectal adenocarcinoma which might correlate it with Lynch syndrome and the CpG island methylator phenotype.The prognosis of mucinous colorectal adenocarcinoma as to non-mucinous colorectal adenocarcinoma is debatable.Further,the impaired responses of mucinous colorectal adenocarcinoma to palliative or adjuvant chemotherapy warrant more studies to be performed for a specialized treatment for these patients.In this review,we discuss the molecular background and histopathol-ogy of mucinous colorectal adenocarcinoma,and provide an update on its prognosis and therapeutics from recent literatures.
