[Effects and mechanism of osthole on intestinal ischemia-reperfusion injury in mice].

OBJECTIVE: To explore the protective role of osthole in intestinal ischemia-reperfusion (I/R) injury in mice and examine its underlying mechanism. METHODS: A murine model of intestinal I/R injury was established with clamping of superior mesenteric artery for 120 min and then clamping was relieved for 60 min. Forty-five SD male mice weighing 27-31 g were randomly divided into 3 groups (n = 15 each): sham group (S), I/R injury group (I/R) and I/R plus osthole treatment group (Ost+). Intestinal wet/dry weight ratio, superoxide dismutase (SOD), malondialdehyde (MDA) in serum were examined by colorimetric assay and diamine oxidase (DAO) was examined by automatic biochemical analyzer, the levels of tumor necrosis factor (TNF) -α, interleukin (IL)-1ß and IL-2 were examined by enzyme-linked immunosorbent assay (ELISA). Intestinal barrier permeability was detected by Evans blue (EB) test. One-way ANOVA was used to analyze all experimental data variance. RESULTS: Intestinal tissues wet/dry weight ratios, Evans blue content and Chiu's score of I/R group mice were significantly higher than those of S and Ost+ groups (0.80% ± 0.03% vs 0.77% ± 0.02% & 0.78% ± 0.02%, (0.11 ± 0.04) vs (0.05 ± 0.02) & (0.06 ± 0.02) µg/mg, 3.42 ± 0.73 vs 0.87 ± 0.35 & 2.63 ± 0.58, P < 0.05 or P < 0.01) . Serum level of DAO, MDA, IL-1ß & TNF-α of I/R group mice were significantly higher than those of S and Ost+ groups ( (18.9 ± 4.0) vs (14.5 ± 2.3) & (16.0 ± 2.6) U/L, (8.4 ± 1.2) vs (6.9 ± 1.7) & (6.1 ± 2.4) µmol/L, (93 ± 6) vs (51 ± 4) & (67 ± 5) ng/L, (467 ± 31) vs (235 ± 21) & (323 ± 30) ng/L, P < 0.01 or P < 0.05) . Serum SOD activity and IL-2 level were significantly lower than those of S and Ost+ groups ( (75 ± 7) vs (93 ± 16) & (89 ± 5) U/ml, (95 ± 16) vs (198 ± 14) & (139 ± 11) ng/L, all P < 0.05) . All parameters showed no significant difference between S and Ost+ groups (all P > 0.05). CONCLUSIONS: Treatment of osthole may protect murine intestinal tissue against intestinal I/R injury. And the mechanisms may be due to its actions of preventing oxygen stress and inflammatory responses.

LINC01436 Promotes the Progression of Gastric Cancer via Regulating miR-513a-5p/APE1 Axis.

BACKGROUND: Gastric cancer (GC) is one of the deadliest cancer worldwide. Multiple long non-coding RNAs (lncRNAs) are recently identified as crucial oncogenic factors or tumor suppressors in GC. In this study, we aimed to probe into the effect of LINC01436 on GC progression. METHODS: LINC01436 and miR-513a-5p expressions in GC tissue samples were measured using quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was used to detect the expression of apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) expression. Human GC cell lines AGS and BGC-823 were employed to investigate the function and mechanism of LINC01436 in GC. Cell counting kit-8 (CCK-8) assay was used to assess the effect of LINC01436 on proliferation. Flow cytometry was utilized to explore the effect of LINC01436 on apoptosis, and Transwell assay was conducted to detect the effect of LINC01436 on the migration and invasion. Colony formation assay was performed to evaluate the effect of LINC01436 on radioresistance of GC cells. Furthermore, luciferase reporter assay and RNA immunoprecipitation assay were conducted to confirm the binding relationship between miR-513a-5p and LINC01436. Additionally, Western blot was used to study the regulatory function of LINC01436 and miR-513a-5p on APE1. RESULTS: LINC01436 expression of GC clinical samples was remarkably increased and LINC01436 was correlated with unfavorable pathological indexes. LINC01436 high expression was associated with shorter overall survival time. Its overexpression observably promoted the proliferation, metastasis and radioresistance of GC cells, and its knockdown suppressed the malignant phenotypes of GC cells. LINC01436 overexpression markedly reduced the miR-513a-5p expression via sponging it and enhanced the APE1 expression. MiR-513a-5p overexpression or APE1 knockdown reversed the effects of LINC01436 on GC cells. CONCLUSION: LINC01436 is a molecular sponge of tumor suppressor miR-513a-5p, which indirectly enhances the APE1 expression and functions as the oncogenic lncRNA in GC.

Anti-NY-ESO-1 autoantibody may be a tumor marker for intrahepatic cholangiocarcinoma.

Anti-NY-ESO-1 antibody is observed in a multitude of malignancies. This study was aimed to evaluate the expression of serum anti-NY-ESO-1 antibodies and its prognostic value in intrahepatic cholangiocarcinoma. A total of 103 patients with intrahepatic cholangiocarcinoma were enrolled in the study. Enzyme-linked immunosorbent assay (ELISA) was performed to detect the serum level of anti-NY-ESO-1 antibody. Western blotting was performed to assess the NY-ESO-1 expression in tumor and adjacent tissues. The serum NY-ESO-1 antibody was detected in 18.4% of patients with intrahepatic cholangiocarcinoma, a value that was significantly higher than that in patients with chronic Hepatitis B. Serum NY-ESO-1 antibody was positively correlated with tumor differentiation, lymphatic metastasis, cTNM stage and abdominal pain. Finally, there was a higher cumulative survival rate in patients with serum NY-ESO-1 positivity than in those with serum NY-ESO-1 negativity among the patients with stage III + IV. Our data uncovered that NY-ESO-1 antibody might be a helpful tumor marker and prognostic predictor in intrahepatic cholangiocarcinoma.