RESUMEN
Sishen pill (SSP) is an old Chinese medicine used to treat colitis with spleen-kidney-yang deficiency (SKYD) syndromes. However, its exact mechanism of action has not yet been fully elucidated. The aim of this study was to evaluate the effects and potential mechanisms of SSP on colitis with SKYD syndromes in mice. Colitis with SKYD syndromes was induced by rhubarb, hydrocortisone, and dextran sulfate sodium (DSS), and treatment was provided with SSP. Flow cytometry was performed to examine the inflammatory dendritic cell (infDC) regulations of SSP. The changes in the gut microbiota (GM) and fecal metabolites post-SSP treatment were investigated using the combination of 16S rRNA sequencing and untargeted metabolomics. Additionally, we also examined whether SSPs could regulate the infDCs by modifying TLR4/NF-κB signaling pathways. Compared with the DSS group, the disease activity index, colonic weight, index of colonic weight, and colonic injury scores, as well as the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, and IL-12p70 decreased significantly in the DSS + SSP group, while free triiodothyronine (FT3), free tetraiodothyronine (FT4), testosterone (TESTO), body weight change, colonic length, and the levels of IL-10 increased. Also, SSP decreased the amounts of CD103+CD11c+iNOS+, CD103+CD11c+TNF-α +, CD11c+CD103+CD324+, CD103+CD11c+MHC-II+, and CD103+CD11c+CD115+. Interestingly, 16S rRNA sequencing and untargeted metabolomics showed that SSP treatment restored the dysbiosis of GM and improved the dysfunction in fecal metabolism in colitis mice with SKYD syndromes. Correlation analysis indicated that the modulatory effects of SSP on FT3, FT4, IL-10, colonic weight index, CD103+CD11c+TNF-α +, CD103+CD11c+MHC-II+, and 13 common differential metabolites were related to alterations in the abundance of Parvibacter, Aerococcus, norank_f_Lachnospiraceae, Lachnospiraceae_UCG-006, Akkermansia, and Rhodococcus in the GM. In addition, SSP markedly inhibited the activation of the TLR4, MyD88, TRAF6, TAB2, and NF-κBp65 proteins and activated IκB. These results indicate that SSP can effectively alleviate colitis mice with SKYD syndrome by regulating infDCs, GM, fecal metabolites, and TLR4/NF-κB signaling pathways.
RESUMEN
The study aimed at introducing a digital method of locating the osteotomy position of the zygomatic arch during surgery and analyze the accuracy of this method. Patients with a prominent zygomatic bone who underwent zygomatic arch osteotomy and reduction in the orthognathic surgery department of our hospital were selected. Preoperative and postoperative computed tomography (CT) data of the patients were imported into modeling and analysis software Mimics 23.0 in DICOM format to construct 3D models of the zygomatic bone and zygomatic arch region. The data were obtained by locating the simulated osteotomy position of the zygomatic arch before the surgery, applying the digitally modeled osteotomy position of the zygomatic arch during the surgery, and locating the actual osteotomy position of the zygomatic arch after the surgery. The accuracy of the experimental method was verified by matching the preoperative simulation data with the postoperative osteotomy data. A Wilcoxon rank sum test was performed to compare the 20 cases' osteotomy positions obtained by preoperative simulation with the actual postoperative position. There was no significant difference in zygomatic arch osteotomy position between the preoperative simulation and the real postoperative position (Z=-1.867, P=0.062). The digital method to locate the zygomatic arch osteotomy seems to show an acceptable accuracy to achieve the proper osteotomy position and, therefore, should adopted whenever appropriate.
