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Cardiovascular disease is a high incidence and mortality rate disease worldwide. Exercise training has become an established evidence-based treatment strategy that is beneficial for many cardiovascular diseases. This study aimed to investigate the effects of exercise on hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient (ApoE−/−) mice. Male ApoE−/− mice were randomly divided into the following four groups: normal diet (ND), normal diet + exercise training (ND + E), high-fat diet (HFD), and high-fat diet + exercise training (HFD + E). Exercise training consisted of swimming for 40 min, 5 days/week for 12 weeks. After 12 weeks, histopathological alterations in cardiac tissue and the serum were measured. Furthermore, the NOX4, NRF2, SIRT1, TGF-β, HO-1, collagen III, Smad3, Bax, Bak, Bcl-2, Bcl-xl, IL-1β, IL-6, and IL-18 expression levels were evaluated using immunohistochemistry and western blotting; Results: the serum levels of SIRT1, GSH-Px, and SOD were lower in ApoE−/− HFD mice compared with those in ApoE−/− HFD + E mice. Significant pathological changes were observed in the ApoE−/− HFD + E group compared with those in the ApoE−/− HFD group. Increased levels of oxidative stress, fibrosis, and apoptosis, and decreased antioxidant expression in the ApoE−/− HFD group compared with those in ApoE−/− HFD + E mice. Exercise exerts protective effects against cardiac damage caused by hyperlipidemia.

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Abstract. Cytokine-induced killer (CIK) cells have been used as adoptive immunotherapy in cancer. The present study evaluated the effect of CIK cells on immune function in patients with lung cancer. Patients were divided into three groups, according to the treatment received prior to CIK cell treatment: CIK group (no prior treatment), Che-Sur group (prior chemotherapy and surgery) and Che-Rad group (prior chemotherapy and radiotherapy). Following treatment, the average percentage of cluster of differentiation (CD)3 + CD4 + , CD3 + , natural killer (NK) and NKT cells in peripheral blood was significantly higher than that prior to CIK treatment in the Che-Sur and CIK groups, and the levels of interferon-γ in serum were significantly higher than those prior to CIK treatment in the Che-Sur and CIK groups. On the contrary, the levels of interleukin-10 had decreased in these groups following CIK treatment. Subsequently, patients were divided into three groups according to the percentage of CD3 + CD56 + CIK cells that were administered to the patients. The number of NK and NKT cells increased with increasing number of CD3 + CD56 + cells. The patients in the CIK and Che-Sur groups were the most benefited ones following CIK treatment, contrarily to those in the Che-Rad group, since the increase in the number of CD3 + CD56 + CIK cells in the aforementioned patients enhanced the number of NK cells, which exhibit antitumor activity.

Background: Tumor initiating cells (TICs) were confirmed to drive the therapeutic resistance of hepatocellular carcinoma (HCC), but the mechanism by which tumor microenvironment maintains the HCC stemness is not fully understood. This study aims to investigate the effect of regulatory T cells (Tregs) on the TICs characteristics of HCC. Methods: Immunocytochemistry, flow cytometry, real-time PCR, western blot, in vitro sphere-formation, and in vivo tumorigenesis assay were used to detect HCC TIC characteristics. Additionally, the association between FoxP3 expression, Wnt/β-catenin pathway activation, and HCC stemness were analyzed by forced expression or inhibition of FoxP3. Results: It was showed Tregs enhanced the stemness of HCC cells by upregulation of TIC-related markers CD133, Oct3/4, Sox2, c-Myc, Klf4, Nanog, CD13, EpCAM, and induction of epithelial to mesenchymal transition (EMT), increase of TICs ratio, as well as promotion of tumorigenic ability. Moreover, β-catenin and c-Myc were upregulated in HCC cells when co-cultured with Tregs. After Wnt/β-catenin pathway inhibition, HCC stemness was also inhibited. In addition, Tregs-derived exosomes played the same role as Tregs in enhancing HCC TIC properties, and exosome inhibition led to decreased TIC ratio as well as TIC markers expression. Furthermore, Tregs-derived exosomes down-regulate FoxP3 and GSK3β of HCC cells. Forced expression of FoxP3 resulted in increased GSK3β, decreased β-catenin and TIC ratio of HCC. In contrast, FoxP3 interference reduced GSK3β, increased β-catenin and TIC ratio. Conclusions: This study, for the first time, demonstrated Tregs enhanced HCC stemness through Wnt//β-catenin pathway by down-regulating FoxP3.