ATF6α, one of the sensor proteins in the stress signaling pathway of the endoplasmic reticulum, is located in the membrane of the endoplasmic reticulum. To date, the physiological function of ATF6α in the process of embryo implantation has not been reported. In this study, the expression pattern of ATF6α in the mouse uterus during peri-implantation and the estrous cycle was detected by real-time PCR, western blot and immunohistochemistry. ATF6α mRNA and protein levels were higher in the uterus near the implantation site on day 5 and were intensely expressed in the secondary decidual zone (SDZ) on days 7–8. In the uteri of pseudopregnant mice, ATF6α mRNA and protein levels were lower on day 5 than on other days. The activating blastocyst and artificial decidualization had an obvious effect of increasing the expression of ATF6α. In addition, the expression of ATF6α was affected by progesterone (P4) and estrogen (E2) in ovariectomized mice. This finding is further supported by evidence from mice during the estrous cycle. Thus, we have concluded that ATF6α may play an important role during embryo implantation and decidualization.

Ulcerative colitis (UC) is a relapsing and reoccurring inflammatory bowel disease. The treatment effect of Alhagi maurorum and stem cell extracts on UC remains unclear. The aim of the present study was to investigate the protective role of Alhagi maurorum combined with stem cell extract on the intestinal mucosal barrier in an intestinal inflammation mouse model. Sixty mice were randomly divided into a control group, model group, Alhagi group, MSC group, and MSC/Alhagi group. MSC and Alhagi extract were found to reduce the disease activity index (DAI) scores in mice with colitis, alleviate weight loss, improve intestinal inflammation in mice (p < 0.05), preserve the integrity of the ileal wall and increase the number of goblet cells and mucin in colon tissues. Little inflammatory cell infiltration was observed in the Alhagi, MSC, or MSC/Alhagi groups, and the degree of inflammation was significantly alleviated compared with that in the model group. The distribution of PCNA and TNF-alpha in the colonic tissues of the model group was more disperse than that in the normal group (p < 0.05), and the fluorescence intensity was lower. After MSC/Alhagi intervention, PCNA and TNF-alpha were distributed along the cellular membrane in the MSC/Alhagi group (p < 0.05). Compared with that in the normal control group, the intensity was slightly reduced, but it was still stronger than that in the model group. In conclusion, MSC/Alhagi can alleviate inflammatory reactions in mouse colonic tissue, possibly by strengthening the protective effect of the intestinal mucosal barrier.