Quercetin inhibits porcine intestinal inflammation in vitro

Purpose: To investigate the effect of Quercetin (Que) on inflammatory reaction in intestinal porcine enterocyte cells, IPEC-J2, induced by lipopolysaccharide (LPS).Methods: IPEC-J2 cells were pretreated with Que and then incubated with LPS. Cell viability, cell morphology, nitric oxide (NO) content, gene expression levels of interleukin-6 (IL-6) and interleukin-8 (IL-8), were then evaluated.Results: LPS incubation at 10 μg/mL for 24 h showed no effect on the viability and cell morphology of IPEC-J2, while Que pre-incubation significantly enhanced the viability of IPEC-J2 and improved cell morphology (p < 0.05). Que decreased the expression levels of pro-inflammatory cytokines IL-6 mRNA and IL-8 mRNA raised by LPS (p < 0.05). Interestingly, both LPS and Que demonstrated no influence on the release of NO.Conclusion: Pre-treatment of Que shows a positive effect on intestinal porcine enterocyte cells and inhibited porcine intestinal inflammation in vitro induced by LPS, but the mechanism may be not associated with NO-related signaling pathway. Therefore, Que might have a potential effect as a veterinary drug or feed additive for the treatment of enteritis in pigs.Keywords: Quercetin, Inflammatory cytokines, Intestinal porcine enterocyte cells, Lipopolysaccharid

Transcriptome Sequencing Investigated the Tumor-Related Factors Changes After T. gondii Infection

Toxoplasma gondii is an intracellular parasite and causes a global epidemic parasitic disease. T. gondii-infection could inhibit the growth of tumor. In this study, the transcriptomes of samples were detected by deep sequencing analysis. The transcriptome data was compared with reference genome to perform sequence alignment and the further analysis. The analyses of differential expression and the differentially expressed genes were performed in the present study. Genes involved in P53 signaling pathway, COLORECTAL cancer pathway, NON-SMALL CELL LUNG cancer signaling pathway, and BREAST cancer signaling pathway were up-regulated or down-regulated among the samples. The KEGG analysis indicated that the cancer pathways changed after infection of T. gondii. Furthermore, tumor-related mRNAs from different samples had a large difference, which suggested that the difference might provide important information in resisting cancer. The protein results indicated that tumor-related protein changes occurred after infection of T. gondii. In conclusion, the infection changed the cancer pathways, which could possibly inhibit the growth of tumor