The present study was conducted to investigate the effect of Artemisia argyi on the production performance and intestinal barrier of rabbits. Weaned Hyla rabbits (30 d, n = 160) of similar body weight were divided into 4 groups (40 rabbits per treatment), and they were fed a control diet or fed an experimental diet supplemented with 3%, 6%, or 9% A. argyi. The results showed that the dietary supplementation with A. argyi did not affect the rabbits' food intake and body weight gain regardless of the inclusion level but decreased the diarrhea rate and diarrhea index (P < 0.05). Dietary addition of A. argyi increased the small intestine length and villus height/crypt depth, regardless of the inclusion level (P < 0.05). Compared with the control, the A. argyi supplementation increased the gene expression of zonula occludens 1 (ZO-1) and claudin 1 in all segments of the small intestine and regardless of the level of A. argyi (P < 0.05). In the duodenum, a dietary supplementation with 6% and 9% A. argyi increased the immunoglobulins A (IgA) content (P < 0.05). In the jejunum, the A. argyi supplementation decreased interleukin 2 (IL2) and IL6 content regardless of the inclusion level (P < 0.05). In the ileum, a 3% A. argyi addition decreased IL2 content, whereas a 6% A. argyi addition decreased IL6 content (P < 0.05). Furthermore, 6%-9% A. argyi supplementation increased the IgA content in the ileum (P < 0.05). In conclusion, dietary addition of A. argyi reduces diarrhea and modulates the gut immune function without affecting growth performances of rabbits.
miR-552 promotes tumor growth and metastasis in colorectal cancer. However, the function of miR-552 in osteosarcoma remains unclear. The current study investigated the role and mechanism of miR-552-5p in the proliferation, migration and invasion of osteosarcoma cells. miR-552-5p was significantly upregulated in osteosarcoma tissues and cell lines compared with adjacent normal tissues and normal osteoblast cells. Knockdown of miR-552-5p significantly reduced the proliferation of MG63 and U2OS cells, and inhibited cell migration and invasion. Wnt inhibitory factor 1 (WIF1) was the direct target gene of miR-552-5p in osteosarcoma cells. Overexpression of miR-552-5p markedly decreased the expression of WIF1 in MG63 and U2OS cells. A negative association was identified between the expression levels of miR-552-5p and WIF1 in osteosarcoma tissues. Furthermore, the expression of WIF1 was downregulated in osteosarcoma tissues and cell lines. Finally, knockdown of WIF1 in MG63 and U2OS cells treated with miR-552-5p inhibitors rescued their ability to proliferate, migrate and invade. Overall, the results indicated that miR-552-5p promoted osteosarcoma development and progression by inhibiting WIF1. Therefore, miR-552-5p may serve as a new therapeutic target for treatment of patients with osteosarcoma.
MiR-542-3p and its target gene integrin linked kinase (ILK) in human osteosarcoma together with the differentially expressed genes from osteosarcoma tissues was analyzed through bioinformatics analysis in this study. Real time quantitative polymerase chain reaction (qRT-PCR) and western blot showed that the miR-542-3p expression decreased while the ILK expression increased in the osteosarcoma tissues. The overexpressed miR-542-3p or silenced ILK restrained cell invasion, proliferation and migration and arrested cell cycle, facilitated cell apoptosis in U-2OS and 143B cells. The dual-luciferase assay confirmed the targeting relationship between miR-542-3p and ILK. MiR-542-3p overexpression inhibited osteosarcoma growth in vivo. In conclusion, miR-542-3p overexpression down-regulated its target gene ILK, promoted osteosarcoma cells apoptosis and inhibited their proliferation, migration and invasion.
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