Mouse Ccl3 peptide

Thymoquinone (TQ) is an active ingredient of some medicinal herbs. Despite extensive studies on the biological and pharmacological properties of TQ, its effect on the characteristics of stem cells remains to be clarified. Therefore, this study was aimed to investigate the effect of TQ on viability, proliferation and immunomodulatory potential of mouse bone marrow-derived mesenchymal stem cells (BM-MSCs) in vitro. The BM-MSCs were isolated from young NMRI mice. The cytotoxic effect of TQ on the BM-MSCs was evaluated using MTT assay. Then, the effect of TQ on the proliferation of BM-MSCs and the mRNA expression of genes involved in self renewal and immunomodulatory potential of MSCs was assessed by the cell counting and real-time PCR assays. Results showed that TQ reduces the number of BM-MSCs in a dose- and time-dependent manner. In addition, the half-maximal inhibitory concentration values of TQ on the BM-MSCs were 8 mu g/ml at 24h and 4 mu g/ml at 48 and 72h after treatment. Furthermore, about 90% of the BM-MSCs were alive after treatment with concentrations 2 g mu/ml of TQ for 24h. The results of cell counting assay indicated that TQ at concentrations of 1-2 mu g/ml significantly enhanced the proliferation of BM-MSCs (P < 0.05). The gene expression analysis also showed that Tlr3, Tlr4, Ccl2, Ccl3, Sox2, and Rexi are overexpressed (Fold change z >= 1.5) in the TQ-treated BM-MSCs compared with the untreated samples. In conclusion, these findings propose that TQ may regulate self-renewal and immunomodulatory potential of MSCs. However, the exact mechanisms and the roles of this regulation are required to be elucidated in further study.

Background The effects of beta-glucan on colitis mice are contradictory in previous reports. As a result, it is still unclear whether there is an anti-colitis effect in Ganoderma lucidum polysaccharide (GLP), which is mainly composed of beta-glucan. Moreover, the association between GLP function and gut microbiota remains to be elucidated. Objective: This study aimed to investigate whether GLP consumption improved rat dextran sodium sulfate (DSS)-induced colitis by regulating gut microbiota and altering colonic epithelial expression. Design: The disease activity index (DAI) scores and the cecal short chain fatty acid (SCFA) levels of DSS-induced colitis rats fed with a GLP diet (Group GLP, n = 6) and a control diet (Group Con, n = 6) were investigated and analyzed. Moreover, the profiles of gut microbiota and colonic epithelial expression were analyzed using metagenomics and transcriptomics. Results: GLP consumption significantly lowered animal DAI scores by producing more SCFAs by increasing SCFA-producing bacteria such as Ruminococcus_l and reducing pathogens such as Escherichia-Shigella in both the small intestine and cecum of rat. Moreover, GLP consumption regulated 11 genes, including six upregulated (Ccl5, Cd3e, Cd8a, IL21r, Lck, and Trbv) and five downregulated (Ccl3, Gro, Il11, Mhc2. and Ptgs) genes enriched in six inflammation-related Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, resulting in enhancement of immunity and reduction of inflammatory response and colonic cancer risk. Conclusions: GLP consumption alleviated DSS-induced colitis and may have potential for ulcerative colitis relief.