Catalpol Inhibits Tregs-to-Th17 Cell Transdifferentiation by Up-Regulating Let-7g-5p to Reduce STAT3 Protein Levels

Purpose@#Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease, and Th17 cells are key factors in the pathogenesis of human inflammatory conditions, such as RA. Catalpol (CAT), a component in Rehmanniae Radix (RR), has been found to regulate human immunity. However, the effects of CAT on Th17 cell differentiation and improvement of RA are not clear. @*Materials and Methods@#Collagen-induced arthritis (CIA) mice were constructed to detect the effects of CAT on arthritis and Th17 cells. The effect of CAT on Th17 differentiation was evaluated with let-7g-5p transfection experiments. Flow cytometry was used to detect the proportion of Th17 cells after CAT treatment. Levels of interleukin-17 and RORγt were assessed by qRT-PCR and enzyme-linked immunosorbent assay. The expression of signal transducer and activator of transcription 3 (STAT3) was determined by qRT-PCR and Western blot. @*Results@#We found that the proportion of Th17 cells was negatively associated with let-7g-5p expression in CIA mice. In in vitro experiments, CAT suppressed traditional differentiation of Th17 cells. Simultaneously, CAT significantly decreased Tregs-to-Th17 cells transdifferentiation. Our results demonstrated that CAT inhibited Tregs-to-Th17 cells transdifferentiation by up-regulating let-7g-5p and that the suppressive effect of CAT on traditional differentiation of Th17 cells is not related with let-7-5p. @*Conclusion@#Our data indicate that CAT may be a potential modulator of Tregs-to-Th17 cells transdifferentiation by up-regulating let-7g-5p to reduce the expression of STAT3. These results provide new directions for research into RA treatment.

SUICIDAL INTOXICATION WITH SEDATIVE SOPORIFIC DRUGS—AN ANALYSIS OF 6 CASES / 中国法医学杂志

Six cases of suicidal sedative-soporific drug poisoning is reported.The main clinical features were coma,respiratory depression,hypotension,disappearance of reflexes and peripherel circulatory failure.Thepathological fingdings were as follows:pulmonary congestion and edema;fatty degeneration of the liver;degeneration of the epithalial cells of the proximal convoluted tubules and cerebral edema.The severityof the pathological changes depend upon the duration between the drug administration and the time of deathThe longer the course,the more prominent the changes.The fatality rate related with the dose of drugadministration,the underlying deseases and the complications.