Idiopathic pulmonary fibrosis (IPF) is a common pulmonary interstitial disease with a high mortality rate. Adiponectin (APN) is reportedly an effective therapy for fibrosis-related diseases. This study aimed to investigate the potential effects of APN on IPF. Male BALB/c mice were injected with bleomycin (BLM) and treated with different doses of APN (0.1, 0.25, and 0.5 mg/kg). The body weights of the mice were recorded. Immunohistochemical, hematoxylin and eosin, and Masson staining were performed to evaluate pulmonary histopathological changes. Enzyme-linked immunosorbent assay (ELISA) and western blotting were performed to assess tissue inflammation. The human lung fibroblasts HELF were stimulated with TGF-β1 and treated with different doses of APN (2.5, 5, and 10 μg/ml). Cell proliferation, inflammation, and fibrosis were determined by MTT assay, EdU assay, colony formation assay, ELISA, and western blotting. APN significantly attenuated BLM-induced body weight loss, alveolar destruction, and collagen fiber accumulation in mice (p < 0.05). APN decreased the expression of α-SMA and collagen I and reduced the concentration of TNF-α, IL-6, IL-1β, and IL-18 in lung tissues (p < 0.05). In TGF-β1-treated HELF cells, cell proliferation and colony formation were inhibited by APN (p < 0.05). Additionally, the expression of α-SMA, collagen I, and pro-inflammatory cytokines were suppressed by APN (p < 0.05). APN inhibited the phosphorylation of IκB and nuclear translocation of p65. In conclusion, these findings suggest that APN is an effective agent for controlling IPF progression. The antifibrotic effects of APN might be mediated via inhibiting the NF-κB signaling pathway. Graphical Abstract

Major depression disorder (MDD) has become increasingly common in patients with ovarian cancer, which complicates the treatment course. The microRNA (miRNA)‑mRNA regulation network may help elucidate the potential mechanism of MDD in ovarian cancer. The differentially expressed microRNAs (DEmiRs) and mRNAs (DEmRNAs) were therefore identified from the GSE61741, GSE58105 and GSE9116 ovarian cancer datasets using GEO2R. The target genes of the DEmiRs were then obtained using the TargetScan, microRNAorg, microT‑CDS, miRDB and miRTarBase prediction tools. The DAVID program was used to identify the KEGG pathways of target genes, and the core genes of major depressive disorder (MDD) were identified using the Kaplan‑Meier Plotter for ovarian cancer. A total of 5 DEmiRs (miR‑23b‑3p, miR‑33b‑3p, miR‑1265, miR‑933 and miR‑629‑5p) were obtained from GSE61741 and GSE58105. The target genes of these DEmiRs were enriched in pathways that were considered high risk for developing MDD in ovarian cancer. A total of 11 risk genes were selected from these pathways as the core genes in the miRNA‑mRNA network of MDD in ovarian cancer, and eventually identified the following 12 miRNA‑mRNAs pairs: miR‑629‑5p‑FGF1, miR‑629‑5p‑AKT3, miR‑629‑5p‑MAGI2, miR‑933‑BDNF, miR‑933‑MEF2A, miR‑23b‑3p‑TJP1, miR‑23b‑3p‑JMJD1, miR‑23b‑3p‑APAF1, miR‑23b‑3p‑CAB39, miR‑1265‑CDKN1B, miR‑33b‑3p‑CDKN1B, and miR‑33b‑3p‑F2R. These results may provide novel insights into the mechanisms of developing MDD in ovarian cancer patients.