Background To investigate the function of miR‐191‐5p in lung adenocarcinoma and its possible mechanism. Methods QRT‐PCR was adopted for the detection of the expression levels of miR‐191‐5p and SATB1 (HGNC: 10541). The effects of miR‐191‐5p and SATB1 on cell proliferation and migration were examined through the CCK‐8 and Transwell assays. Subsequently, the binding relationships between miR‐191‐5p and SATB1 were confirmed by dual‐luciferase reporter gene assay. Finally, the potential mechanisms of action of miR‐191‐5p were explored through a serious of in vivo and in vitro experiments. Results Lung adenocarcinoma patients had a notably lower expression level of miR‐191‐5p than controls, patients with metastasis had a lower level than those without metastasis, and the level in patients with lung adenocarcinoma in stage III‐IV was lower than that in patients with lung adenocarcinoma in stage I‐II. Overexpression of miR‐191‐5p repressed the migration and proliferation of lung cancer A549/H1650 cells. According to the reporter gene assay, miR‐191‐5p could bind to SATB1. Besides, SATB1 was significantly overexpressed in cancer tissues of patients with lung adenocarcinoma, and SATB1 overexpression accelerated the migration and proliferation of A549/H1650 cells and reversed inhibition on cell migration and proliferation by miR‐191‐5p. Conclusion Overexpression of miR‐191‐5p is capable of blocking the migration and proliferation of lung cancer cells, and its mechanism may be through targeting SATB1 thus downregulating Wnt signaling.

Aims: This study aimed to evaluate the cardioprotective effects of ω-3 polyunsaturated fatty acids (PUFAs) postconditioning against ischemia-reperfusion (I/R) injury. Methods: Sixty Sprague-Dawley rats were randomly divided into 4 groups (n = 15 for each) and used to generate the Langendorff isolated perfused rat heart model. The sham group received a continuous perfusion of 150 min. The remaining three I/R-treated groups sequentially received a 30-min perfusion, a 30-min cardioplegia, and a 90-min reperfusion. The I/R-ischemic preconditioning (IP) group additionally received three cycles of 20-s reperfusion and 20-s coronary reocclusion preceded the 90 min of reperfusion. The I/R-ω group were perfused with ω-3 PUFAs for 15 min before the 90 min of reperfusion. The myocardial infarct size, the degree of mitochondrial damage, the antioxidant capacity of the myocardium, and the cardiac functions during reperfusion were compared among groups. Results: Compared with the I/R group, the I/R-ω group had significantly reduced myocardial infarct size, reduced levels of lactate dehydrogenase and malondialdehyde, elevated superoxide dismutase level, and elevated rising (+dp/dt_max) and descending (–dp/dt_max) rate of left ventricular pressure. The I/R-ω group had a significantly lower rate of mitochondrial damage in myocardial tissue compared with the I/R and I/R-IP groups. Conclusion: ω-3 PUFA postconditioning possesses good cardioprotective effects and may be developed into a therapeutic strategy for myocardial I/R injury.

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