ABSTRACT
Objective To study the glutamine combined with early enteral nutrition’s effects on severe acute pancreatitis’systemic inlfammation. Methods 150 Cases with severe acute pancreatitis were divided into total parenteral nutrtion group(TPN group), early enteral nutrition group(EEN group) and Glutamine and early enteral nutrition group(G+EEN group) according to their therapeutic methods. The curative effects, APACHEⅡscore and liver and kidney function were compared after treatment. Inlfammatory cytokines of hs-CRP, TNF-α, IL-1β, IL-6, IL-8 and IL-10 before and after treatment were detected and compared. Results The efifciency rate in G+EEN group was signiifcantly better than that in TPN and EEN group(P<0.05), with lower APACHEⅡscore and better liver and kidney function. The level of hs-CRP, TNF-α, IL-1β, II-6 and IL-8 after treatment in G+EEN group were signiifcantly lower than that in TPN and EEN group(P<0.05), except IL-10, which was signiifcantly higher than that in TPN and EEN group (P<0.05). Conclusion Glutamine combined with early enteral nutrition could signiifcantly ameliorate severe acute pancreatitis’systemic inlfammation, its curative effects is better than early enteral nutrition and total parenteral nutrition.
ABSTRACT
We studied the regulatory effects of the estragen receptorbeta (ERbeta) gene on the downstream estrogen signal transfection pathway in colon cancer cells and the possible mechanisms involved. A human ERbeta gene recombinant expression plasmid, pEGFP-C1-ERbeta, was constructed and transfected into the Caco-2 colon cancer cell line, a line with low ERbeta gene expression. The expression of ERbeta mRNA and protein was detected 72 h after transfection. RT-PCR was used to examine the expression levels of the progesterone recepror (PR) gene containing the classic estrogen response element (ERE), the C-fos oncogene containing the AP-1 site (a non-classical ER binding site), the epigenetic modifying genes, such as Dnmt1, Dnmt3a, Dnmt3b, and histone methyltransferase (HMT), and the human mismatch repair gene hMLH1. Methylation-specific PCR was used to detect the changes in the methylated sites of the CpG islands in the promoters of the ERbeta, PR, and C-fos genes. The results indicated that the human ERbeta gene recombinant expression plasmid pEGFP-C1-ERbeta was successfully constructed and transfected into Caco-2 cells. As compared with the control group, the mRNA and protein expression of ERbeta gene was increased significantly 72 h after the transfection of pEGFP-C1-ERbeta into the Caco-2 cells. As compared with the control group, the mRNA expression of the PR, C-fos, Dnmt3a and Dnmt3b genes was increased significantly 72 h after the transfection of pEGFP-C1-ERbeta into the Caco-2 cells, but the mRNA expression of the Dnmt1, HMT, and hMLH1 genes decreased significantly (P<0.05). As compared with the control group, different degrees of demethylation occurred in the promoters of the ERbeta, progesterone receptor (PR), and C-fos oncogene 72 h after the transfection of pEGFP-C1-ERbeta into the Caco-2 cells. The methylation index of the estrogen signal transfection pathway in Caco-2 cells was decreased significantly following the expression restoration of ERbeta gene (P<0.05). It is concluded that the restoration or up-regulation of the ERbeta gene in Caco-2 cells may significantly activate the expression of the related target genes in the downstream estrogen signal transfection pathway and may result in the demethylation changes of the pathway. During the process, the expression level and activity of the epigenetic modifying genes and the human mismatch repair gene have changed simultaneously. The regulatory effect of the ERbeta gene on the estrogen signal transfection pathway to a certain extent partly involves demethylation.