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Inflammatory bowel disease ( IBD) is a group of chronic non-specific inflammatory bow-el diseases that requires lifelong treatment and long-term follow-up. In recent years,the incidence of IBD in children is increasing year by year, which seriously affects children's quality of life, growth and mental health. The diagnosis of IBD requires a comprehensive analysis of patients'history,lab biochemistry,radiolo-gy,endoscopy and histopathology examinations and so on. There are no reliable non-invasive tests and bio-markers for follow-up. Trefoil factor family 3 ( TFF3 ) , identified essencial in the repairment of intestinal inflammation and promoting mucosal regeneration, playsan important rolein the pathogenesis of IBD. We review the relationship between intestinal trefoil factor and IBD,and further to discuss the possibility whether intestinal trefoil factor can act as a serum marker to assess the activity of IBD.
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Objective To explore the clinical application of DKK-1,TFF3 and CA72-4 detection in the diagnosis and treatment of gastric cancer.Methods Seventy-five cases(gastric cancer group) of gastric cancer admitted to our hospital from January 2013 to May 2015 were selected.Seventy cases of benign gastric disease(benign gastric disease group) and 70 persons undergoing the physical examination(healthy control group) were selected as the research subjects.The concentration of CA72-4 in each group was detected by the electrochemiluminescence analyzer.The serum DKK-1 and TFF3 levels in each group were detected by enzyme linked immunosorbent assay(ELISA).The receiver operating characteristic(ROC) curve was drawn for evaluating the diagnostic efficiency of each index in each group.The sensitivity,specificity,positive predictive rate and negative predictive rate of 3 indicators for diagnosing gastric cancer before operation were compared.The concentration change of various indexes after gastric cancer radical resection were compared..Results The concentrations of DKK-1,TFF3 and CA72-4 in the gastric cancer group were significantly higher than those in the benign gastric disease group and healthy control group,the difference was statistically significant(P<0.05).The area under ROC curve of DKK-1,TFF3 and CA72-4 were 0.876(95%CI 0.803-0.950),0.944 4(95%CI 0.894-0.975) and 0.818(95%CI 0.726-0.884) respectively.The sensitivity of CA72-4 was 78.6% and the specificity was 84.3%,the sensitivity of DKK-1 was 93.6% and the specificity was 87.1%,the sensitivity and specificity of TFF3 was 92.4% and 90.1% respectively.The concentrations of DKK-1,TFF3 and CA72-4 after radical resection in the gastric cancer group were significantly reduced,the difference was statistically significant compared with before treatment(P<0.05).Conclusion The detection of DKK-1,TFF3 and CA72-4 has a certain clinical value for the diagnosis of gastric cancer.The combined detection of these 3 indicators is conducive to improve the specificity and sensitivity of gastric cancer diagnosis.
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Objective To investigate whether 17β-estradiol (E2) can stimulate the proliferation,migration,and secretion of trefoil factor family 1 (TFF1) in papillary thyroid cancer K-1 cells and explore the molecular mechanisms.Methods ELISA was used to detect the content of TFF1 in the supernatant of K-1 cells after the treatment of E2,propylpyrazoletriol (PPT,ERα agonist) or diarylpropionitrile (DPN,ERβ agonist).The expression of ERα and ERβ in the untreated cells was measured by Western blotting.ERα siRNA and ERβ siRNA by RNA interference were designed and synthesized,and the change of TFF1 was measured by ELISA again after the transfection.The interaction between TFF1 promoter and ER was evaluated by chromatin immunoprecipitation analysis (CHiP).The proliferation and migration were detected in the K-1 cells after E2 treatment by MTT assay and Transwell chamber test respectively.Festults After E2 treatment,the TFF1 content in the supernatant of K-1 cells was increased gradually,reached peak at 24 h,and then declined slowly.PPT treatment enhanced the secretion of TFF1 but DPN decreased it in the K-1 cells.Transfection of ERα siRNA obliterated the inductive effect of E2 on the secretion of TFF1,but that of ERβ siRNA increased the inductive effect in the K-1 cells.Western blotting showed that the expression level of ERα was higher than that of ERβ in the K-1 cells.ChIP results confirmed that ERα protein was bound to the promoter of TFF1 gene in K-1 cells.E2 treatment promoted cell proliferation and improved cell migration in the K-1 cells.Conclusion E2 induces the expression and secretion of TFF1 in K-1 cells through ERα-dependent manner,and thus promotes the proliferation and migration of the cells.
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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 and further deteriorated in the course of sepsis.
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Objective To assemble fusion gene of c-myc tagged human trefoil factor family 2(hTFF2)(in vitro) and construct a cloning vector of this fusion gene.Methods Based on amino acid sequence of hTFF2 and codon of lactococcus lactis,cDNA of htff2 sequence was designed and extended at their 5' ends with a sequence encoding the c-myc tag;and the sequence of fusion gene c-myc-htff2 was designed.According to restriction enzyme sites of pBluescript Ⅱ sk(+),the SalⅠ and BamHⅠ were arranged at 5′ and 3′ ends of the fusion gene respectively.Instructed by DNAWORKS program,the fusion gene sequence of c-myc-htff2 was designed as 14 oligonucleotides that overlapped each other.The target gene fragment of cmyc-htff2 fusion gene was obtained by the means of polymerase chain reaction(PCR) based gene assembly.Then,the c-myc-htff2 was subcloned into vector of pBluescript II sk(+) for identification of the fusion gene by restricting enzyme excision and DNA sequencing.Results Assembly of c-myc-TFF2 fusion gene(in vitro) and construction of pBS-TFF2 had been completed successfully;and DNA sequencing showed that the sequence of synthetic gene accorded with the expectation.Conclusion With the help of DNAWORKS program,the design and assembly of oligonucleotides (in vitro) is effective to synthesize a target gene,and the cloning vector of c-myc-htff2 fusion gene has been successfully constructed.