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05). Between the PCOS‑IR and PCOS‑NIR groups, a total of 20&nbsp;differentially expressed protein spots were detected by 2D‑DIGE. Among these, 4&nbsp;proteins, namely afamin, serotransferrin, complement C3 and apolipoprotein&nbsp;C3 (APOC3), were also identified by MALDI‑TOF‑MS/MS. The alteration of APOC3 was further confirmed by western blot analysis and enzyme‑linked immunosorbent assay (ELISA). The present study also confirmed that the expression level of APOC3 was positively associated with the homeostasis model assessment of insulin resistance (HOMA‑IR). On the whole, the data indicate that APOC3 may be a potential diagnostic marker for PCOS‑IR patients.The aim of the present study was to determine whether curculigoside protects against myocardial ischemia‑reperfusion injury (MIRI) and to investigate the underlying mechanisms. An in&nbsp;vitro model of hypoxia/reoxygenation (H/R) was established by culturing H9c2 cells under hypoxic conditions for 12&nbsp;h, followed by reoxygenation for 1&nbsp;h. Cell Counting kit‑8 and lactate dehydrogenase (LDH) assays were subsequently used to examine cell viability and the degree of cell injury. In addition, isolated rat hearts were subjected to 30&nbsp;min of ischemia followed by 1&nbsp;h of reperfusion to establish a MIRI model. Triphenyltetrazolium chloride (TTC) staining was performed to measure the infarct size. Furthermore, TUNEL staining and flow cytometry were employed to evaluate cell apoptosis. The opening of the mitochondrial permeability transition pore (MPTP) and changes in the mitochondrial membrane potential (ΔΨm) were assessed. Reverse transcription‑quantitative PCR and western blot analysis were performed to investigate the expression levels of mitochondrial apoptosis‑related proteins. Curculigoside pre‑treatment significantly improved cell viability, decreased cell apoptosis and LDH activity, and reduced the infarct size and myocardial apoptosis in&nbsp;vitro and ex&nbsp;vivo, respectively. Moreover, curculigoside markedly inhibited MPTP opening and preserved the ΔΨm. [https://www.selleckchem.com/products/8-oh-dpat-8-hydroxy-dpat.html 8-OH-DPAT chemical structure] In addition, curculigoside significantly decreased the expression of cytochrome c, apoptotic protease activating factor‑1, cleaved caspase‑9 and cleaved caspase‑3. Notably, atractyloside, a known MPTP opener, abrogated the protective effects of curculigoside. On the whole, the present study demonstrated that curculigoside protected against MIRI, potentially by decreasing the levels of mitochondria‑mediated apoptosis via the inhibition of MPTP opening. Therefore, the results obtained in the present study may provide the theoretical basis for the future clinical application of curculigoside.Osteosarcoma is a common type of bone tumor that primarily occurs in children and young adults. MicroRNA (miRNA/miR) dysregulation is associated with the progression of osteosarcoma; therefore, the aim of the present study was to investigate the biological functions and molecular mechanisms of miR‑145‑5p in osteosarcoma. The expression of miR‑145‑5p in osteosarcoma tissues and cell lines was quantified using reverse transcription‑quantitative PCR (RT‑qPCR). The effect of miR‑145‑5p on the proliferation of osteosarcoma cells was detected using Cell Counting Kit‑8 and colony formation assays, as well as cell cycle distribution analysis. The effect of miR‑145‑5p on tumor growth was further investigated in&nbsp;vivo using a subcutaneous tumor model in nude mice. The interaction between miR‑145‑5p and E2F transcription factor 3 (E2F3) was determined using bioinformatics analysis, a luciferase assay, RT‑qPCR and western blotting. The results revealed that miR‑145‑5p expression was decreased in osteosarcoma cell lines and tissues compared with the corresponding normal controls. Increased miR‑145‑5p expression inhibited the proliferation and colony formation ability of osteosarcoma cells, and induced G1 phase arrest. Furthermore, mice injected with tumor cells overexpressing miR‑145‑5p exhibited smaller tumors than those in the control group. Further investigation revealed that miR‑145‑5p binds to and decreases the expression of E2F3. In addition, the mRNA levels of E2F3 were negatively associated with miR‑145‑5p in osteosarcoma tissues, and increasing E2F3 expression abrogated the inhibitory effects of miR‑145‑5p on osteosarcoma cells. Collectively, the results obtained in the present study suggest that miR‑145‑5p may suppress the progression of osteosarcoma, and may serve as a useful biomarker for the diagnosis of osteosarcoma, as well as a therapeutic target.Physical exercise has a neuroprotective effect and is an important treatment after ischemic stroke. Promoting neurogenesis and myelin repair in the penumbra is an important method for the treatment of ischemic stroke. However, the role and potential mechanism of exercise in neurogenesis and myelin repair still needs to be clarified. The goal of the present study was to ascertain the possible effect of treadmill training on the neuroprotective signaling pathway in juvenile rats after ischemic stroke. The model of middle cerebral artery occlusion (MCAO) in juvenile rats was established and then the rats were randomly divided into 9 groups. XAV939 (an inhibitor of the Wnt/β‑catenin pathway) was used to confirm the effects of the Wnt/β‑catenin signaling pathway on exercise‑mediated neurogenesis and myelin repair. Neurological deficits were detected by modified neurological severity score, the injury of brain tissue and the morphology of neurons was detected by hematoxylin‑eosin staining and Nissl staining, and themia/reperfusion.Human dental pulp stem cells (hDPSCs) present several advantages, including their ability to be non‑invasively harvested without ethical concern. The secretome of hDPSCs can promote the functional recovery of various tissue injuries. However, the protective effects on hypoxia‑induced skeletal muscle injury remain to be explored. The present study demonstrated that C2C12 myoblast coculture with hDPSCs attenuated CoCl2‑induced hypoxic injury compared with C2C12 alone. The hDPSC secretome increased cell viability and differentiation and decreased G2/M cell cycle arrest under hypoxic conditions. These results were further verified using hDPSC‑conditioned medium (hDPSC‑CM). The present data revealed that the protective effects of hDPSC‑CM depend on the concentration ratio of the CM. In terms of the underlying molecular mechanism, hDPSC‑CM activated the Wnt/β‑catenin pathway, which increased the protein levels of Wnt1, phosphorylated‑glycogen synthase kinase‑3β and β‑catenin and the mRNA levels of Wnt target genes.