Objective To explore the expression of miR-146a and its target gene LIN52 in advanced gastric cancer and their potential impact on clinical prognosis.Methods Total RNAs were extracted from 93gastric cancer tissues and their corresponding adjacent non-tumor tissues to quantify the relative expression of miR-146a by using real-time quantitative PCR (RT-qPCR).Expression of LIN52 was detected in tumors and normal tissues by immunohistochemistry.Correlation analysis was assessed between the expression of miR-146a and LIN52 and clinicopathological parameters,including clinical diagnostic specificity,tumor TNM staging,lymph node metastasis,differentiation grade,curative effect and prognosis of gastric cancer.Results The expression of miR-146a in gastric carcinoma was negatively correlated with lymph node metastasis (P ＜0.05).The expression of miR-146a had a significant correlation with the prognosis of the patients (P ＜ 0.01).The patients with high expression of miR-146a had higher survival rate (P ＜ 0.05),but the patients with high expression of LIN52 had lower survival rate (P ＜ 0.05).The receiver operating characteristic curve regression analysis showed that sensitivity and specificity of miR-146a were 94.1％ and 61.5 ％ to diagnose gastric cancer.Conclusions As a tumor suppressor gene in gastric cancer,miR-146a has significantly negative correlation with LIN52.High expression of miR-146a in the gastric cancer tissue might be associated with improved treatment efficacy of chemotherapy,suggesting that miR-146a may be a molecular marker for the diagnosis and prognosis of gastric cancer.

Objective : To investigate whether NaHS，a hydrogen sulfide donor，can improve myocardial injury in sepsis by inhibiting oxidative stress and activating the Xc －/ GPX4 signaling pathway in ferroptosis． Methods : Lipopolysacc-haride(LPS) induced H9c2 in rat cardiomyocytes to form an in vitro model of myocardial injury in sep- sis，which was divided into Control group，LPS group and LPS + NaHS group．The kits were applied to detect the changes of cardiomyocyte viability，Fe2 + ，LDH and CK-MB，determine the levels of oxidative stress indexes GSH and MDA，detect the changes of cellular ROS and mitochondrial membrane potential levels by fluorescent probes， and detect the expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 by Western blot. Results: Compared with the Control group，H9c2 cell viability decreased，Fe2 + concentration increased ，GSH ，MDA and ROS levels increased，mitochondrial JC-1 monomer increased ，expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 decreased，and cell damage increased after LPS stimulation (P＜0. 05) ．Compared with the LPS group，NaHS attenuated LPS-induced H9c2 cell injury and elevated Fe2 + concentration，decreased the level of LPS-induced oxidative stress in H9c2 cells ，and increased the expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 (P＜0. 05 ) ． Conclusion The mechanism by which NaHS attenuates myocardial injury in sepsis may be related to the inhibition of oxidative stress and activation of the Xc －/ GPX4 signaling pathway in fer- roptosis.