LncRNA CDKN2B­AS1 sponges miR­28­5p to regulate proliferation and inhibit apoptosis in colorectal cancer.

Long noncoding RNA (lncRNA) CDKN2B­antisense RNA 1 (AS1) functions as a tumor oncogene in numerous cancers. However, the roles and mechanism of CDKN2B­AS1 in colorectal cancer (CRC) have not been explored. The present study aimed to investigate whether and how CDKN2B­AS1 contributes to CRC progression. The data revealed that CDKN2B­AS1 expression was upregulated in CRC tissues. Loss­of­function assays demonstrated that CDKN2B­AS1 in CRC modulated cell proliferation and apoptosis, which was mediated by cyclin D1, cyclin­dependent kinase (CDK) 4, p­Rb, caspase­9 and caspase­3. Bioinformatics analysis and luciferase reporter assays indicated direct binding of microRNA (miR)­28­5p to CDKN2B­AS1. Moreover, the results herein revealed that the expression of miR­28­5p was negatively correlated with that of CDKN2B­AS1 in CRC tissue. Moreover, CDKN2B­AS1 acted as a miR­28­5p competing endogenous RNA (ceRNA) to target and regulate the expression of URGCP. These findings indicated that CDKN2B­AS1 plays roles in CRC progression, providing a potential therapeutic target or novel diagnostic biomarker for CRC.

Pathological changes at early stage of multiple organ injury in a rat model of severe acute pancreatitis.

BACKGROUND: Severe acute pancreatitis (SAP) is a commonly seen acute abdominal syndrome characterized by sudden onset, rapid progression and high mortality rate. The damage in peripheral organs may be more severe than that in the pancreas, and can even lead to multiple organ dysfunction. It is critical to recognize early pathological changes in multiple organs. This study aimed to assess the early pathological features of damaged organs in a rat model of SAP. METHODS: Thirty clean grade healthy male Sprague-Dawley rats weighing 250-300 g were randomly divided into a model control group (n=15) and a sham-operated group (n=15). The SAP rat model was induced by sodium taurocholate. Samples of blood and from multiple organs were collected 3 hours after operation. We assessed the levels of IL-6, TNF-alpha, PLA2, NO, ET-1, MDA, amylases and endotoxin in blood and observed the early pathological changes in multiple damaged organs. RESULTS: Levels of IL-6, TNF-alpha, PLA2, NO, ET-1 and MDA in serum and of amylase and endotoxin in plasma of the model control group rats were significantly higher than those of the sham-operated group (P<0.01). Different degrees of pathological change were observed in multiple damaged organs. CONCLUSION: Multiple organ injury may occur at the early stage of SAP in rats.

Preparation method of an ideal model of multiple organ injury of rat with severe acute pancreatitis.

AIM: To establish an ideal model of multiple organ injury of rats with severe acute pancreatitis (SAP). METHODS: SAP models were induced by retrograde injection of 0.1 mL/100 g 3.5% sodium taurocholate into the biliopancreatic duct of Sprague-Dawley rats. The plasma and samples of multiple organ tissues of rats were collected at 3, 6 and 12 h after modeling. The ascites volume, ascites/body weight ratio, and contents of amylase, endotoxin, endothelin-1 (ET-1), nitrogen monoxidum (NO), phospholipase A(2) (PLA(2)), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) in plasma were determined. The histological changes of multiple organs were observed under light microscope. RESULTS: The ascites volume, ascites/body weight ratio, and contents of various inflammatory mediators in blood were higher in the model group than in the sham operation group at all time points [2.38 (1.10), 2.58 (0.70), 2.54 (0.71) vs 0.20 (0.04), 0.30 (0.30), 0.22 (0.10) at 3, 6 and 12 h in ascites/body weight ratio; 1582 (284), 1769 (362), 1618 (302) (U/L) vs 5303 (1373), 6276 (1029), 7538 (2934) (U/L) at 3, 6 and 12 h in Amylase; 0.016 (0.005), 0.016 (0.010), 0.014 (0.015) (EU/mL) vs 0.053 (0.029), 0.059 (0.037), 0.060 (0.022) (EU/mL) at 3, 6 and 12 h in Endotoxin; 3.900 (3.200), 4.000 (1.700), 5.300 (3.000) (ng/L) vs 41.438 (37.721), 92.151 (23.119), 65.016 (26.806) (ng/L) at 3, 6 and 12 h in TNF-alpha, all P < 0.01]. Visible congestion, edema and lamellar necrosis and massive leukocytic infiltration were found in the pancreas of rats of model group. There were also pathological changes of lung, liver, kidney, spleen, ileum, lymphonode, thymus, myocardium and brain. CONCLUSION: This rat model features reliability, convenience and a high achievement ratio. Complicated with multiple organ injury, it is an ideal animal model of SAP.