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Apelin‑36 is able to mediate a range of effects on various diseases, and is upregulated in lipopolysaccharide (LPS)‑induced acute lung injury (ALI). However, to the best of our knowledge, whether apelin‑36 is able to regulate LPS‑induced ALI has yet to be investigated. The present study aimed to investigate the role of apelin‑36 in LPS‑induced ALI, and the putative underlying mechanisms. Rats were assigned to one of four treatment groups The Control group, apelin‑36 group, LPS group and LPS + apelin‑36 group. At 4 h after intratracheal instillation of LPS (5 mg/kg), rats were intraperitoneally treated with 10 nmol/kg apelin‑36. Subsequently, pathological manifestations and the extent of inflammation and apoptosis of the lung tissues were assessed. Untransfected and apoptosis signal‑regulating kinase 1 (ASK1)‑overexpressing Beas‑2B cells were treated with LPS in the absence or presence of apelin‑36, and subsequently the levels of inflammation and apoptosis were assessed. The results obtained showed that the level of apelin‑36 was increased in the bronchoalveolar lavage fluid (BALF) of LPS‑treated rats. Co‑treatment with apelin‑36 alleviated LPS‑induced lung injury and pulmonary edema, reduced the levels of pro‑inflammatory cytokines, including interleukin‑6, monocyte chemoattractant protein‑1 and tumor necrosis factor‑α, in BALF, and inhibited apoptosis in the lung tissues. The presence of apelin‑36 also blocked the activation of LPS‑induced ASK1, p38, c‑Jun N‑terminal kinase and extracellular signal‑regulated kinase in lung tissues. , and these actions may be dependent on inhibition of the ASK1/mitogen‑activated protein kinase signaling pathway.In recent years, obesity has become a major public health concern. Obesity has been previously associated with low‑grade inflammation and TNF‑α induction in adipose tissue, which subsequently disrupts adipocyte metabolism. MicroRNAs (miRNAs/miRs) are important metabolic factors and their dysregulation has been associated with obesity‑related metabolic syndromes. In fact, it has been directly suggested that miR‑424 may be functionally associated with adipogenesis, although its exact role in this process remains unclear. The present study aimed to identify the function of miR‑424 in adipogenesis. In the present study, miR‑424 expression levels were analyzed during adipogenesis and the differential expression of this miRNA in the adipose tissue of obese and non‑obese children was also assessed. Furthermore, the interaction between miR‑424 and the adipocytokine TNF‑α was determined. Finally, miR‑424 target genes and downstream signaling pathways were predicted via bioinformatics and analyzed by performing a luciferase reporter assay to elucidate the functional mechanisms of miR‑424 in adipogenesis of visceral adipocytes. The results revealed that the expression levels of miR‑424 upregulated in the adipose tissue biopsies from obese children compared with the biopsies of non‑obese children. However, in cultured adipocytes, the expression levels of miR‑424 were discovered to be gradually downregulated during the adipogenesis process. TNF‑α treatment significantly downregulated the expression levels of miR‑424 via binding to its promoter region and reducing its transcriptional activity. Through bioinformatic prediction analysis, miR‑424 target genes were analyzed, of which several were identified to be involved in signaling pathways that are known to regulate adipogenesis, such as the Wnt signaling pathway. In conclusion, the present study indicated that miR‑424 was regulated by TNF‑α and served an important role in adipogenesis.Oxidative stress has been suggested to induce granulosa cell apoptosis, which contributes to follicular atresia. However, the mechanism via which oxidative stress mediates granulosa cell apoptosis remains elusive. Therefore, the aim of this study was to elucidate the molecular mechanisms regulating oxidative stress‑induced granulosa cell apoptosis. The present study demonstrated that reactive oxygen species induced by H2O2 resulted in human granulosa COV434 cell apoptosis via the regulation of sirtuin 1 (SIRT1)‑mediated p53 activity. Endogenous SIRT1 expression was alleviated by H2O2 treatment of COV434 cells in a time‑dependent manner. In addition, knockdown or inhibition of SIRT1 promoted H2O2‑induced poly(ADP‑ribose) polymerase (PARP) cleavage and p53 acetylation, which led to an increase in COV434 cell apoptosis. Treatment with H2O2 enhanced the expression levels of the p53‑dependent proteins, p53‑upregulated modulator of apoptosis (PUMA) and phorbol‑12‑myristate‑13‑acetate‑induced protein 1 (PMAIP1), as well as those of p53; however, knockdown of p53 decreased cleaved PARP, PUMA and PMAIP1 expression levels induced by H2O2 treatment. Moreover, knockdown of PUMA or PMAIP1 attenuated the H2O2 induction of PARP cleavage and COV434 cell apoptosis. In conclusion, the present findings suggested that H2O2‑induced oxidative stress causes granulosa COV434 cell apoptosis via the upregulation of p53 activity by SIRT1 suppression, indicating a mechanistic role of the SIRT1/p53 axis in H2O2‑induced granulosa cell apoptosis.The H19 long non‑coding RNA is involved in the development of tamoxifen resistance in breast cancer. However, the relationship between H19 and the metastatic potential and treatment options for tamoxifen‑resistant (TAMR) breast cancer is not completely understood. Curcumin inhibits cellular proliferation, migration and invasiveness in several cancer types, including pancreatic cancer, breast cancer and chronic myeloid leukemia. The present study aimed to investigate the role of H19 in MCF‑7/TAMR cell epithelial‑mesenchymal transition (EMT), migration and invasiveness, and to assess the ability of curcumin to inhibit H19‑mediated effects. Reverse transcription‑quantitative PCR and western blot analysis were conducted to detect the gene or protein expression. Cell Counting Kit‑8, wound healing and Transwell invasion assays were performed to estimate the capabilities of cell viability, invasion and migration. H19 overexpression enhanced MCF‑7/TAMR cell EMT, invasion and migration by upregulating Snail. DL-Buthionine-Sulfoximine price Furthermore, curcumin notably decreased the expression levels of epithelial marker E‑cadherin and markedly increased the expression levels of mesenchymal marker N‑cadherin in MCF‑7/TAMR cells compared with the control group.
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