Objective. To investigate the expression of glutathione peroxidase 2 (GPX2) in human lung adenocarcinoma tissues and its effect on the biological function of lung adenocarcinoma A549 cells. Methods. The expression of GPX2 in lung adenocarcinoma and its effect on survival were analyzed by the TCGA database and the GEPIA 2 database. A total of 45 cases of primary lung adenocarcinoma tissue specimens and 45 cases of their paracancerous tissue specimens were collected, and the expression of GPX2 in the two types of tissues was detected by immunohistochemistry. Lung adenocarcinoma A549 cells were divided into the GPX2 overexpression group (GPX2), the GPX2 knockdown group (si-GPX2), the empty vector group (Vector), the siRNA negative control group (si-NC), and the WT group; the mRNA level and protein expression of GPX2 in each group of A549 cells were detected by real-time fluorescence quantitative PCR and Western blotting; the proliferation activity of each group of cells was detected by the CCK-8 assay; the effect of GPX2 on cell migration and invasion ability was detected by the scratch assay and the Transwell invasion assay; the apoptosis of each group of cells was detected by flow cytometry; Western blotting was performed to detect the expression levels of Bax, Bcl-2, E-cadherin, vimentin, and MMP2 and MMP9 proteins in each group of cells. Results. Bioinformatics analysis showed that the expression of GPX2 was strongly correlated with the prognosis of lung adenocarcinoma patients ( P < 0.01 ). The positive expression rates of GPX2 in lung adenocarcinoma and its paracancerous tissues were 66.0% and 15.7%, respectively ( P < 0.05 ). The results of RT-qPCR and Western blotting showed that the expression level of GPX2 mRNA and protein in A549 cells in the GPX2 group increased, which was significantly higher than that in the WT group ( P < 0.05 ); the expression levels of GPX2 mRNA and protein in A549 cells in the si-GPX2 group were the same, that is, significantly lower than the WT group ( P < 0.05 ). GPX2 overexpression promoted the proliferation, migration, and invasion of A549 cells and inhibited their apoptosis; the results in the si-GPX2 group were opposite to those in the GPX2 group. Compared with the WT group, the expression of Bcl-2, vimentin, and MMP2 and MMP9 protein in the GPX2 group increased ( P < 0.05 ), while the expression of Bax and E-cadherin protein decreased in the GPX2 group ( P < 0.05 ); the results in the si-GPX2 group were opposite to those in the GPX2 group. Conclusion. The expression of GPX2 in lung adenocarcinoma is related to the prognosis of patients. It is proved that GPX2 can promote the migration and invasion of lung adenocarcinoma cells and is related to the EMT/β-catenin pathway. Thus, GPX2 is expected to be an important target for the diagnosis and treatment of lung adenocarcinoma.

Background. Peroxiredoxin 6 (PRDX6) is an important antioxidant enzyme, with a potential application value in the treatment of diseases caused by oxidative damage. Methods. PRDX6 and a mutant (mPRDX6) were heterologously expressed by using an E.coli expression system and purified by Ni-affinity chromatography. Isoproterenol (ISO) was used to induce a myocardial cell injury model and an animal myocardial injury model. After the treatment with PRDX6 and mPRDX6, the proliferation activity of H9C2 cells was detected by Cell Counting Kit-8 (CCK8) method; the apoptosis was evaluated by flow cytometry, and the histological changes of myocardial cells were observed by hematoxylin and eosin (H&E) staining, the levels of catalase (CAT), glutathione peroxidase (GPX), malondialdehyde (MDA), and superoxide dismutase (SOD) in ISO-treated H9C2 cells as well as in the heart tissue and serum of rats treated with ISO were detected, and the expression levels of Bax, Bcl-2 and peroxisome proliferators-activated receptors-γ (PPAR-γ) proteins were detected by Western blot. Results. PRDX6 and mPRDX6 were successfully expressed and purified. The results of efficacy study showed that the mutant mPRDX6, in which the phospholipaseA2 (PLA2) activity of PRDX6 was deleted by site directed mutation, had a better protective effect against the myocardial injury than PRDX6. CCK8 results showed that compared with that in ISO group, the proliferation activity of H9C2 cells was significantly enhanced ( P < 0.01 ), the apoptosis rate was significantly decreased ( P < 0.01 ), and the fluorescence intensity of reactive oxygen species (ROS) was significantly decreased ( P < 0.01 ) in mPRDX6 group. The results of H&E staining showed that the myocardial injury was alleviated to a certain extent in mPRDX6 group. Compared with those in ISO group, the activities of CAT, GPX, and SOD in H9C2 cells and the heart tissue and serum of rats were significantly increased ( P < 0.05 ), while the contents of MDA were significantly decreased ( P < 0.05 ). Western blot analysis showed that the expression level of Bcl-2 in H9C2 cells was significantly decreased ( P < 0.01 ), and that of Bax and PPAR-γ was significantly increased ( P < 0.05 ). Conclusion. mPRDX6 has a protective effect against the myocardial injury induced by ISO, and the mechanism may be related to its antioxidation. This study may provide a theoretical basis for the research and development of drugs used for the treatment of myocardial injury.

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Objective This study aimed to investigate the effects of epidural analgesia administered as early as cervical dilatation of 1 cm on labor interventions and maternal and neonatal outcomes. Methods This retrospective research recruited 1007 full‐term primigravidas, who were distributed to two separate cohorts for eligibility: epidural analgesia 1 (cervical dilatation = 1 cm) and epidural analgesia 2 (cervical dilatation >1 cm). Labor interventions (artificial rupture of membranes and oxytocin administration) and duration of labor were the primary outcomes. Results The effect of initiation timing of epidural analgesia on artificial membrane rupture was not statistically significant (adjusted odds ratio [OR]: 0.85 [0.58–1.24], p > 0.05). Less oxytocin was used in the epidural analgesia 2 group compared with the epidural analgesia 1 group (the adjusted OR: 0.68 [0.49–0.95], p < 0.05). There were no significant differences in the median time to latent phase of labor, active phase of labor, second, and third stages of labor (p > 0.05). There were no significant differences in maternal and neonatal outcomes between the epidural analgesia 1 group and the epidural analgesia 2 group. Conclusion Epidural analgesia could be administered at cervical dilatation = 1 cm.