Objective To investigate the correlation between the soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) and the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway in rats with abdominal sepsis.Methods Using a sepsis model produced by cecal ligation and puncture (CLP),Wistar rats were randomly (random number) divided into normal control group (n =6),sham-operated group (n =24,) CLP group (n =48),AG490 (JAK2 inhibitor) treatment group (n =48) and rapamycin (RPM,STAT3 inhibitor) treatment group (n =48).At different intervals,the rats in each group were sacrificed,then the peripheral blood cells were harvested to detect the percent of CD4 + CD25 + Treg cells in CD4 + cells by flow cytometry.Meanwhile,mRNA of sTREM-1 from the tissue samples of the liver was also measured by real-time reverse transcription-polymerase chain reaction (RT-PCR).Results Compared with the normal control group and the sham-operated group,expression of sTREM-1 in the CLP group was significantly higher,and it showed a gradually increased tendency over time.At 6 and 24 hours,there were no significant differences in the expressions of sTREM-1 between the AG490 group (1.572 ± 0.051,2.063 ± 0.025,respectively) and the CLP group (1.592 ±0.036,2.082 ±0.021,respectively).But the expression of sTREM-lin the AG490 group (2.522 ± 0.083,3.153 ± 0.021,respectively) was lower than those in the CLP group (2.592 ±0.055,3.204 ±0.013,respectively) during 48 and 72 hours.In addition,there was no significant difference in the expression of sTREM-1 between the RPM group (1.581 ± 0.017) and the CLP group (1.592 ±0.036) at 6 hours.And the expression of sTREM-1in the RPM group (1.486 ±0.019,1.263 0.011,1.115 ± 0.022,respectively) was significantly lower than those in the CLP group (2.082 ± 0.021,2.592 ±0.055,3.204 ± 0.013,respectively) during 24 to 72 hours.Conclusions These data proved that blocking JAK/STAT pathway could inhibit the expression of sTREM-1 and decelarate the progress of inflammatory reaction in rats with abdominal sepsis.

Objective To investigate the mechanism via which artesunate regulates the invasion and metastasis of colon cancer cells and the expression of members of the TGF-β1/Smad4 signaling pathway. Methods The cell counting kit 8 (CCK8), nude mouse xenograft model, Transwell invasion assay, and flow cytometry were used to investigate the effect of artesunate on the invasion and metastasis of colon cancer cells. Western blotting and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) were used to detect the expression of TGF-β1 and Smad4 proteins and mRNA, respectively. Results Artesunate inhibited the growth of transplanted tumor, cell proliferation, and invasion and promoted apoptosis. It inhibited TGF-β1 expression and promoted Smad4 expression. TGF-β1 inhibitors reversed the inhibitory effect of artesunate. Conclusion Artesunate can inhibit the growth of xenograft tumor in nude mice and its mode of action may be related to the TGF-β1/Smad4 signaling pathway.