Stem cells for pancreatitis 425 Gastric injury and bacterial overgrowth 433 The effect of visceral fat on SMA configuration 451 Antiplatelet agents in ulcerative colitis 459 Differentiation of BMSCs into intestinal ce 466 GERDOFF ® efficacy in patients with GERD
Objectives
In this study, we focused on the function of nuclear factor E2–related factor 2 (Nrf2) in acute pancreatitis (AP), which has been shown to have protective effects in gliomas, hepatocytes, and astrocytes.
Methods
Acute pancreatitis cell line and animal model were induced by administration of lipopolysaccharide and cerulein into the cell supernatant or intraperitoneal injection. Oxidative stress status was evaluated by measuring the level of amylase, C-reactive protein, malondialdehyde, superoxide dismutase, and myeloperoxidase. Morphological alterations in the pancreas were evaluated by hematoxylin-eosin staining, the wet-to-dry weight ratio, and the pathology injury scores. Western blot, reverse transcription-polymerase chain reaction, and immunofluorescence staining were performed to analyze the expression of Nrf2, Heme oxygenase 1, and NAD(P)H: quinone oxidoreductase 1.
Results
Overexpression of Nrf2 inhibits oxidative stress and inflammatory responses by inducting the expression of superoxide dismutase as well as reducing the level of amylase, malondialdehyde, and myeloperoxidase in the AR42J rat pancreatic acinar cells in AP. Importantly, overexpression of Nrf2 displayed the same protective effect in vivo. Data from an AP rat model showed that Nrf2 could relieve pancreatic damage.
Conclusions
These results indicated that Nrf2 has a protective role in lipopolysaccharide and cerulein-induced cytotoxicity, providing potential therapeutic strategies for the treatment of AP.
Ulcerative colitis (UC) is a persistent and diffuse inflammatory disease of the intestine. It is widely prevalent in developed countries. Approximately 30% of patients with UC suffer from widespread and aggressive colitis and are at increased risk of colon cancer. In this study, the genetic features and potential molecular mechanisms shared between UC and colorectal cancer were investigated. The datasets from GEO and TCGA were analyzed to obtain differentially expressed genes, of which there were 116 overlapping genes. A module containing 15 genes was obtained using String and Cytoscape to analyze the module and identify hub genes. Weighted gene co-expression network analysis (WGCNA) was used to identify co-expression modules associated with UC and colon cancer, with 52 overlapping genes. Functional clustering of the two gene cohorts was performed using the Metascape online tool, with three significant functions or pathways associated with both gene cohorts. A total of 19 key genes were included, and CCT2 was identified after expression and survival analyses. CCT2 is highly expressed in colon cancer and lowly expressed in UC, and its low expression is associated with a poor prognostic ratio. This study reveals, for the first time, that CCT2 may be a promoter of UC transformation into colon cancer and identifies new gene candidates that could be used as biomarkers or potential therapeutic targets.
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