BACKGROUND Ulcerative colitis(UC)is a main form of inflammatory bowel disease.Due to complicated etiology and a high rate of recurrence,it is quite essential to elucidate the underlying mechanism of and search for eff...BACKGROUND Ulcerative colitis(UC)is a main form of inflammatory bowel disease.Due to complicated etiology and a high rate of recurrence,it is quite essential to elucidate the underlying mechanism of and search for effective therapeutic methods for UC.AIM To investigate the effects of astragalus polysaccharides(APS)combined with matrine on UC and associated lung injury.METHODS UC was induced in rats by colon mucosal tissue sensitization combined with trinitro-benzene-sulfonic acid-ethanol.Then,the effects of the treatments of salazopyrine,APS,matrine,and APS combined with matrine on histopathological changes of lung and colon tissues,disease activity index(DAI),colon mucosal damage index(CMDI),serum endotoxin(ET)level,serum diamine oxidase(DAO)activity,the contents of tumor necrosis factor-αand interleukin-1β,and the activities of myeloperoxidase,superoxide dismutase,and malondialdehyde in lung tissues,as well as the protein expression of zonula occludens(ZO)-1,Occludin,and trefoil factor 3(TFF3)were detected in UC rats.RESULTS The treatments of salazopyrine,APS,matrine,and APS combined with matrine reduced DAI scores and improved histopathological changes of colon and lung tissues,as well as decreased CMDI scores,ET levels,and DAO activities in UC rats.Moreover,in lung tissues,inflammatory response and oxidative stress injury were relieved after the treatments of salazopyrine,APS,matrine,and APS combined with matrine in UC rats.Furthermore,the expression of ZO-1,Occludin,and TFF3 in lung and colon tissues was increased after different treatments in UC rats.Notably,APS combined with matrine exerted a better protective effect against UC and lung injury compared with other treatments.CONCLUSION APS combined with matrine exert a synergistic protective effect against UC and lung injury,which might be associated with regulating TFF3 expression.展开更多
目的:分析三叶因子3(TFF3)在不同胃黏膜病变中的表达及其与间质微血管密度(MVD)值的关系,探讨其在胃癌、癌前病变及胃腺瘤发生、发展中的作用.方法:应用免疫组织化学PV6000法检测20例正常胃黏膜、20例胃腺瘤、20例萎缩性胃炎伴肠化生、2...目的:分析三叶因子3(TFF3)在不同胃黏膜病变中的表达及其与间质微血管密度(MVD)值的关系,探讨其在胃癌、癌前病变及胃腺瘤发生、发展中的作用.方法:应用免疫组织化学PV6000法检测20例正常胃黏膜、20例胃腺瘤、20例萎缩性胃炎伴肠化生、20例不典型增生、40例胃癌组织中TFF3的表达,同时检测MVD值,以抗CD34标记.结果:TFF3在胃腺瘤、萎缩性胃炎伴肠化生、不典型增生和胃癌各组表达均高于正常组(50.0%,65.0%,70.0%,57.5% vs 5.0%,均P<0.01).胃癌MVD值高于正常胃黏膜、胃腺瘤、萎缩性胃炎伴肠化生和不典型增生(30.65±6.04 vs 14.87±3.06,22.33±3.78,23.16±3.20,25.22±4.66,均P<0.01),各组MVD值均高于正常胃黏膜组(均P<0.01).TFF3表达和MVD值与胃癌淋巴结转移和分期有关(均P<0.05),MVD值还与胃癌浸润深度有关(P<0.05).TFF3阳性表达组的MVD值明显高于TFF3阴性组(34.53±4.45 vs 25.39±3.25,P<0.01).结论:TFF3可能是胃黏膜癌变过程中的早期分子事件,在胃黏膜癌变和癌变后的恶性演进过程中起作用,对胃癌早期诊断和预测胃癌发生转移可能具有重要的提示作用.展开更多
目的研究三叶因子3(TFF3)基因在宫颈癌组织和正常组织中的表达情况,同时探讨微小RNA-7-5p(miR-7-5p)调控TFF3对人宫颈癌细胞增殖和迁移能力的影响。方法实时聚合酶链反应检测TFF3在30例宫颈癌及其邻近正常组织中的表达;采用脂质体转染法...目的研究三叶因子3(TFF3)基因在宫颈癌组织和正常组织中的表达情况,同时探讨微小RNA-7-5p(miR-7-5p)调控TFF3对人宫颈癌细胞增殖和迁移能力的影响。方法实时聚合酶链反应检测TFF3在30例宫颈癌及其邻近正常组织中的表达;采用脂质体转染法将TFF3-siRNA、miR-7-5p转染入宫颈癌HeLa及SiHa细胞中。采用CCK-8、Transwell实验和平板克隆实验检测瞬时转染TFF3-siRNA及miR-7-5p mimics对宫颈癌细胞增殖、迁移及克隆形成能力的影响;并利用双荧光素酶报告实验检测miR-7-5p与TFF3的相互关系。结果 TFF3在73.33%(22/30)宫颈癌组织中表达量明显高于其邻近正常组织( P <0.001)。与阴性对照组比较,TFF3 siRNA转染宫颈癌细胞株HeLa和SiHa 3~5 d后,细胞增殖明显受到抑制( P <0.05)。Transwell细胞迁移实验表明: HeLa和SiHa阴性对照组迁移细胞分别为(170±15)个/高倍镜视野和(155±10)个/高倍镜视野,TFF3干扰组迁移细胞分别为(70±20)个/高倍镜视野和(54±8)个/高倍镜视野,迁移能力被显著抑制( P <0.05)。克隆形成实验表明: HeLa和SiHa阴性对照组克隆形成数分别为(160±34)个和(183±17)个,TFF3干扰组细胞克隆数分别为(45±15)个和(33±12)个,形成能力明显减弱( P < 0.05)。荧光素报告系统表明miR-7-5p可抑制含野生型TFF3 3′UTR序列的荧光素酶活性( P <0.01),但对含突变型TFF3 3′UTR的荧光素酶活性影响不显著( P >0.05)。与阴性对照组比较,miR-7-5p mimics转染宫颈癌细胞株HeLa和SiHa 4~5 d后,增殖明显受到抑制( P <0.05)。Transwell细胞迁移实验表明: HeLa和SiHa阴性对照组迁移细胞为(364±48)个/高倍镜视野和(411±27)个/高倍镜视野,miR-7-5p mimics转染组迁移细胞为(165±15)个/高倍镜视野和(100±208)个/高倍镜视野,迁移能力被显著抑制( P <0.05)。克隆形成实验表明: HeLa和SiHa阴性对照组克隆形成数为(83±11)个和(129±21)个,miR-7-5p mimics转染组细胞克隆数为(25±7)个和(14�展开更多
BACKGROUND： Sepsis has become the greatest threat to in-patients, with a mortality of over 25%.The dysfunction of gut barrier, especially the immunological barrier, plays an important role in the development of sepsi...BACKGROUND： Sepsis has become the greatest threat to in-patients, with a mortality of over 25%.The dysfunction of gut barrier, especially the immunological barrier, plays an important role in the development of sepsis. This dysfunction occurs after surgery, but the magnitude of change does not differentiate patients with sepsis from those without sepsis. Increased intestinal permeability before surgery is of no value in predicating sepsis. The present study aimed to observe the changes of intestinal mucosal immunologic barrier in rat models of sepsis induced by cecal ligation and puncture.METHODS： Sixty Sprague-Dawley rats were randomly divided into a sepsis group （n=45） and a control group （n=15）. The rats in the sepsis group were subjected to cecal ligation and puncture （CLP）, whereas the rats in the control group underwent a sham operation. The ileac mucosa and segments were harvested 3, 6 and 12 hours after CLP, and blood samples were collected. Pathological changes, protein levels of defensin-5 （RD-5） and trefoil factor-3 （TFF3） mRNA, and lymphocytes apoptosis in the intestinal mucosa were determined. In an additional experiment, the gut-origin bacterial DNA in blood was detected.RESULTS： The intestinal mucosa showed marked injury with loss of ileal villi, desquamation of epithelium, detachment of lamina propria, hemorrhage and ulceration in the sepsis group. The expression of TFF3 mRNA and level of RD-5 protein were decreased and the apoptosis of mucosal lymphocyte increased （P〈0.05） in the sepsis group compared with the control group. Significant differences were observed in RD-5 and TFF3 mRNA 3 hours after CLP and they were progressively increased 6 and 12 hours after CLP in the sepsis group compared with the control group （P〈0.05, RD-5 F=11.76, TFF3 F=16.86 and apoptosis F=122.52）. In addition, the gut-origin bacterial DNA detected in plasma was positive in the sepsis group.CONCLUSION： The immunological function of the intestinal mucosa was impaired in septic rats 展开更多
基金Supported by National Natural Science Foundation of China,No.81704059
文摘BACKGROUND Ulcerative colitis(UC)is a main form of inflammatory bowel disease.Due to complicated etiology and a high rate of recurrence,it is quite essential to elucidate the underlying mechanism of and search for effective therapeutic methods for UC.AIM To investigate the effects of astragalus polysaccharides(APS)combined with matrine on UC and associated lung injury.METHODS UC was induced in rats by colon mucosal tissue sensitization combined with trinitro-benzene-sulfonic acid-ethanol.Then,the effects of the treatments of salazopyrine,APS,matrine,and APS combined with matrine on histopathological changes of lung and colon tissues,disease activity index(DAI),colon mucosal damage index(CMDI),serum endotoxin(ET)level,serum diamine oxidase(DAO)activity,the contents of tumor necrosis factor-αand interleukin-1β,and the activities of myeloperoxidase,superoxide dismutase,and malondialdehyde in lung tissues,as well as the protein expression of zonula occludens(ZO)-1,Occludin,and trefoil factor 3(TFF3)were detected in UC rats.RESULTS The treatments of salazopyrine,APS,matrine,and APS combined with matrine reduced DAI scores and improved histopathological changes of colon and lung tissues,as well as decreased CMDI scores,ET levels,and DAO activities in UC rats.Moreover,in lung tissues,inflammatory response and oxidative stress injury were relieved after the treatments of salazopyrine,APS,matrine,and APS combined with matrine in UC rats.Furthermore,the expression of ZO-1,Occludin,and TFF3 in lung and colon tissues was increased after different treatments in UC rats.Notably,APS combined with matrine exerted a better protective effect against UC and lung injury compared with other treatments.CONCLUSION APS combined with matrine exert a synergistic protective effect against UC and lung injury,which might be associated with regulating TFF3 expression.
文摘目的:分析三叶因子3(TFF3)在不同胃黏膜病变中的表达及其与间质微血管密度(MVD)值的关系,探讨其在胃癌、癌前病变及胃腺瘤发生、发展中的作用.方法:应用免疫组织化学PV6000法检测20例正常胃黏膜、20例胃腺瘤、20例萎缩性胃炎伴肠化生、20例不典型增生、40例胃癌组织中TFF3的表达,同时检测MVD值,以抗CD34标记.结果:TFF3在胃腺瘤、萎缩性胃炎伴肠化生、不典型增生和胃癌各组表达均高于正常组(50.0%,65.0%,70.0%,57.5% vs 5.0%,均P<0.01).胃癌MVD值高于正常胃黏膜、胃腺瘤、萎缩性胃炎伴肠化生和不典型增生(30.65±6.04 vs 14.87±3.06,22.33±3.78,23.16±3.20,25.22±4.66,均P<0.01),各组MVD值均高于正常胃黏膜组(均P<0.01).TFF3表达和MVD值与胃癌淋巴结转移和分期有关(均P<0.05),MVD值还与胃癌浸润深度有关(P<0.05).TFF3阳性表达组的MVD值明显高于TFF3阴性组(34.53±4.45 vs 25.39±3.25,P<0.01).结论:TFF3可能是胃黏膜癌变过程中的早期分子事件,在胃黏膜癌变和癌变后的恶性演进过程中起作用,对胃癌早期诊断和预测胃癌发生转移可能具有重要的提示作用.
文摘目的研究三叶因子3(TFF3)基因在宫颈癌组织和正常组织中的表达情况,同时探讨微小RNA-7-5p(miR-7-5p)调控TFF3对人宫颈癌细胞增殖和迁移能力的影响。方法实时聚合酶链反应检测TFF3在30例宫颈癌及其邻近正常组织中的表达;采用脂质体转染法将TFF3-siRNA、miR-7-5p转染入宫颈癌HeLa及SiHa细胞中。采用CCK-8、Transwell实验和平板克隆实验检测瞬时转染TFF3-siRNA及miR-7-5p mimics对宫颈癌细胞增殖、迁移及克隆形成能力的影响;并利用双荧光素酶报告实验检测miR-7-5p与TFF3的相互关系。结果 TFF3在73.33%(22/30)宫颈癌组织中表达量明显高于其邻近正常组织( P <0.001)。与阴性对照组比较,TFF3 siRNA转染宫颈癌细胞株HeLa和SiHa 3~5 d后,细胞增殖明显受到抑制( P <0.05)。Transwell细胞迁移实验表明: HeLa和SiHa阴性对照组迁移细胞分别为(170±15)个/高倍镜视野和(155±10)个/高倍镜视野,TFF3干扰组迁移细胞分别为(70±20)个/高倍镜视野和(54±8)个/高倍镜视野,迁移能力被显著抑制( P <0.05)。克隆形成实验表明: HeLa和SiHa阴性对照组克隆形成数分别为(160±34)个和(183±17)个,TFF3干扰组细胞克隆数分别为(45±15)个和(33±12)个,形成能力明显减弱( P < 0.05)。荧光素报告系统表明miR-7-5p可抑制含野生型TFF3 3′UTR序列的荧光素酶活性( P <0.01),但对含突变型TFF3 3′UTR的荧光素酶活性影响不显著( P >0.05)。与阴性对照组比较,miR-7-5p mimics转染宫颈癌细胞株HeLa和SiHa 4~5 d后,增殖明显受到抑制( P <0.05)。Transwell细胞迁移实验表明: HeLa和SiHa阴性对照组迁移细胞为(364±48)个/高倍镜视野和(411±27)个/高倍镜视野,miR-7-5p mimics转染组迁移细胞为(165±15)个/高倍镜视野和(100±208)个/高倍镜视野,迁移能力被显著抑制( P <0.05)。克隆形成实验表明: HeLa和SiHa阴性对照组克隆形成数为(83±11)个和(129±21)个,miR-7-5p mimics转染组细胞克隆数为(25±7)个和(14�
基金This study was supported by the National Natural Science Foundation of Guangdong Province （06021323）.
文摘BACKGROUND： Sepsis has become the greatest threat to in-patients, with a mortality of over 25%.The dysfunction of gut barrier, especially the immunological barrier, plays an important role in the development of sepsis. This dysfunction occurs after surgery, but the magnitude of change does not differentiate patients with sepsis from those without sepsis. Increased intestinal permeability before surgery is of no value in predicating sepsis. The present study aimed to observe the changes of intestinal mucosal immunologic barrier in rat models of sepsis induced by cecal ligation and puncture.METHODS： Sixty Sprague-Dawley rats were randomly divided into a sepsis group （n=45） and a control group （n=15）. The rats in the sepsis group were subjected to cecal ligation and puncture （CLP）, whereas the rats in the control group underwent a sham operation. The ileac mucosa and segments were harvested 3, 6 and 12 hours after CLP, and blood samples were collected. Pathological changes, protein levels of defensin-5 （RD-5） and trefoil factor-3 （TFF3） mRNA, and lymphocytes apoptosis in the intestinal mucosa were determined. In an additional experiment, the gut-origin bacterial DNA in blood was detected.RESULTS： The intestinal mucosa showed marked injury with loss of ileal villi, desquamation of epithelium, detachment of lamina propria, hemorrhage and ulceration in the sepsis group. The expression of TFF3 mRNA and level of RD-5 protein were decreased and the apoptosis of mucosal lymphocyte increased （P〈0.05） in the sepsis group compared with the control group. Significant differences were observed in RD-5 and TFF3 mRNA 3 hours after CLP and they were progressively increased 6 and 12 hours after CLP in the sepsis group compared with the control group （P〈0.05, RD-5 F=11.76, TFF3 F=16.86 and apoptosis F=122.52）. In addition, the gut-origin bacterial DNA detected in plasma was positive in the sepsis group.CONCLUSION： The immunological function of the intestinal mucosa was impaired in septic rats
