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Sub-health has been described as a chronic condition of unexplained deteriorated physiological function, which falls between health and illness and includes fatigue as one of its principal manifestations. Mitochondrial dysfunctions have been discovered in fatigue-type sub-health such as impaired oxidative phosphorylation and mitochondrial damage. In the present study, we evaluated the effects of Lycium barbarum polysaccharide (LBP-4a), a polysaccharide fraction purified from Lycium barbarum, on anti-fatigue in sub-health mice, and the relevant mechanisms were studied. Forty mice were divided into control, model, LBP-4a(L) and LBP-4a(H) groups. Model mice were prepared through compound factors, including forced swim tests, sleep deprivation and wrapping restraint stress tests. After LBP-4a treatment for 4 weeks, the gastrocnemius muscles were obtained for morphological observation and the activities of SOD, GSH-Px and MDA content were detected. Furthermore, mitochondrial membrane potential and Ca(2+) content were measured in isolated skeletal muscle mitochondria. The results showed that LBP-4a could reduce skeletal muscle damage and MDA levels and enhance of SOD and GSH-Px activities compared with the model group. The levels of mitochondrial membrane potential and Ca(2+) were increased in LBP-4a-treated skeletal muscle mitochondria; moreover, the high-dosage group was better than that of the low dosage. In conclusion, LBP-4a exhibited anti-fatigue activity on sub-health mice, and the mechanism was closely correlated with a reduction in lipid peroxidation levels and an increase in antioxidant enzyme activities in skeletal muscle tissue, improving the intracellular calcium homeostasis imbalance and increasing mitochondrial membrane potential. These observations provided the background for the further development of LBP-4a as a type of anti-fatigue therapy used in sub-health treatment.

IntroductionOvarian cancer (OC) is one of the most common malignancies and the leading cause of cancer-related death among women. The long non-coding RNA Prostate cancer-associated transcript-1 (PCAT-1) has been reported to play important roles in multiple human cancers. However, the role of PCAT-1 in OC has never been investigated. The purpose of this study was to investigate the expression and roles of PCAT-1 in OC.Material and methodsExpression of PCAT-1 and miR-129-5p in OC tissues and cell lines was determined by qRT-PCR. Cell proliferation and apoptosis were analyzed by MTT assay and flow cytometry, respectively. The interaction between PCAT-1 and miR-129-5p was demonstrated by luciferase reporter assay.ResultsPCAT-1 is significantly upregulated in OC tissues and cell lines (p < 0.05). Overexpression of PCAT-1 promotes proliferation of OC cells and inhibits their apoptosis (p < 0.05). In addition, miR-129-5p is markedly downregulated in OC and its level is inversely correlated with PCAT-1 expression in OC tumor tissues (p < 0.05). miR-129-5p inhibits proliferation and induces apoptosis in OC cell lines (p < 0.05). Furthermore, it has been demonstrated that miR-129-5p is directly targeted by PCAT-1 and miR-129-5p overexpression can effectively attenuate the effects of PCAT-1 on the proliferation and apoptosis of OC cells.ConclusionsOur results suggest that PCAT-1 functions as an oncogene by inhibiting miR-129-5p in OC and silencing PCAT-1 may be a novel therapeutic strategy in the treatment of OC.

Diosmetin (DGVL) extracted from the traditional Chinese herb Galium verum L. has been found to have anticancer activity. In this study, the effects of DGVL on the thymus of U14-bearing mice were investigated. Using flow cytometry, peripheral blood lymphocytes were characterized based on the expression of surface markers for T helper cells (CD4(+)) and T suppressor cells (CD8(+)). Serum levels of tumor necrosis factor α (TNF-α), interleukin-2 (IL-2), IL-10, and transforming growth factor β1 (TGF-β1) and a cell proliferation assay were determined with an enzyme-linked immunosorbent assay. The expression of Fas and Fas ligand (FasL) on the thymus was determined by Western blotting. Our results showed that DGVL inhibited tumor growth and significantly increased the thymus weight compared with the control. Also, DGVL elevated serum levels of IL-2 and significantly reduced levels of TNF-α, TGF-β1, and IL-10 in a dose-dependent manner. Histological study and terminal dUTP nick end labeling staining results showed that DGVL protected thymus tissue against the onslaught of tumor growth by inhibiting thymus lymphocyte apoptosis. The cell proliferation assay revealed that DGVL might promote more thymus lymphocytes towards proliferation. Furthermore, the ratio of CD4(+)/CD8(+) T lymphocytes was significantly increased from 0.69 to 2.29 by treatment with DGVL. Immunoblotting analyses revealed that the expression of Fas and FasL on the thymus was lower in mice in the DGVL treatment group than in the control mice. In conclusion, DGVL can inhibit tumor growth and protect tumor-induced apoptosis of the thymus, and the mechanism is closely associated with reduced cell death in the thymus and a Fas-FasL-dependent pathway.