Heat stress induces oxidative stress, and reduces body antioxidant metabolite levels, which can affect poultry production performance. Dietary antioxidants protect birds against the adverse effects of heat stress. The effects of increasing concentrations of dietary curcumin on the antioxidant parameters of layers maintained under high-temperature conditions for nine weeks were evaluated. Roman laying hens (n = 336, 22 weeks old, 1420 g BW) were divided into three treatment groups. The first group served as a thermoneutral control (kept at 25 ± 1 °C). The second group was exposed to high temperatures (32 ± 1 °C, 6 h/d), given a basal diet. The third group was further divided into five treatment groups (100, 150, 200, 250, 300 mg/kg Curcumin) fed a basal diet (treatments H1, H2, H3, H4, H5) under high temperatures conditions (32 ± 1 °C, 6 hours/day). As a result of this study, total superoxide dismutase activity was significantly higher in H2 and H3 groups, and total antioxidant capacity was higher in H2, H3, and H5 groups. Catalase and glutathione peroxidase activity was significantly higher in the H3 group. Malondialdehyde concentration was lowered in curcumin supplemented hens compared with control groups hens. Laying hens in all curcumin treatment groups had slightly higher activities of CAT, SOD, GSH-Px, and T-AOC in the liver, heart, and lungs, compared with heat stressed control group. It was concluded that dietary curcumin given to laying hens under heat stress may enhance their antioxidant status, and alleviate the detrimental effects of stressful environmental conditions.

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An animal model of Cd-induced kidney damage was designed to investigate the nephroprotective potential of the probiotic-fermented Ganoderma lucidum (served as FGL) via metabonomic analysis. The results showed that FGL...

MiR-146a plays as diverse roles in systemic malignancies, stimulating the tumor growth or blocking the tumor proliferation. However, its roles in breast cancer stem-like cells are barely known. We first identified the suppressive role of miR-146a in stem cells' renewal, promoting the asymmetric division of stem-like cells, and the expression of miR-146a was positively related with Let-7b level in vitro and in clinical specimens. Previous studies of Let-7 revealed its suppressive functions in stem-like cells expansion, and miR-146 was predicated to target and bind to the 3'UTR of LIN28, a negative regulator of Let-7 maturation. By using luc-assay and western, results showed that miR-146a increased the Let-7b level through degrading Lin28, and Lin28 is required for miR-146a induction of stem cells arresting and more asymmetric stem cells division. Moreover, Let-7 controlled Wnt signaling pathway activity is governed and strengthened by miR-146a, contributing to decrease the ratio of stem-like cells, forcing stem cells dividing asymmetrically. MiR-146a in turn formed negative feedback loop with Let-7 via the repression of NF-kB and Snai1 caused by Let-7b. Our results suggested the possible miR-146a/LIN28/Let-7/Snai1 signaling pathway in restraining the symmetric cells division, which was referred to the self-renewal capacity of breast cancer-stem like cells, and this axis helps to prohibit long–term tumor resistance and recurrence.MiR-146a plays as diverse roles in systemic malignancies, stimulating the tumor growth or blocking the tumor proliferation. However, its roles in breast cancer stem-like cells are barely known. We first identified the suppressive role of miR-146a in stem cells' renewal, promoting the asymmetric division of stem-like cells, and the expression of miR-146a was positively related with Let-7b level in vitro and in clinical specimens. Previous studies of Let-7 revealed its suppressive functions in stem-like cells expansion, and miR-146 was predicated to target and bind to the 3'UTR of LIN28, a negative regulator of Let-7 maturation. By using luc-assay and western, results showed that miR-146a increased the Let-7b level through degrading Lin28, and Lin28 is required for miR-146a induction of stem cells arresting and more asymmetric stem cells division. Moreover, Let-7 controlled Wnt signaling pathway activity is governed and strengthened by miR-146a, contributing to decrease the ratio of stem-like cells, forcing stem cells dividing asymmetrically. MiR-146a in turn formed negative feedback loop with Let-7 via the repression of NF-kB and Snai1 caused by Let-7b. Our results suggested the possible miR-146a/LIN28/Let-7/Snai1 signaling pathway in restraining the symmetric cells division, which was referred to the self-renewal capacity of breast cancer-stem like cells, and this axis helps to prohibit long–term tumor resistance and recurrence. Citation Format: Sun X, Du N, Li G, Zhang J, Zhang J, Xiao G, Wang J, Tang S-C, Ren H. MiR-146a functions as suppressive non-coding gene via indirect upregulation of Let-7 to promote asymmetric division and inhibit the self-renewal ability of breast cancer stem-like cells [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P5-07-10.