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.

Investigation of complement C4A and C4B deficiency in schizophrenia / 中国神经精神疾病杂志

Objective 　To assess the association between the gene of complement C4A, C4B deficiency and schizophrenia. Methods　192 patients with schizophrenia and 142 healthy controls were tested with the amplification restriction fragment length polymorphism (Amp-RFLP) technique.Results　The frequency of C4AQ0/C4AQ0 homozygote was higher in the patient group than in the control group (χ2=8.54, P＜0.01). The relative risk (RR) of C4AQ0/C4AQ0 homozygote for schizophrenia was 6.8. There was no increased frequency of C4B deficiency in patients with schizophrenia (χ2=0.11, P＞0.05, RR=0.73).Conclusions　These results indicate that there is a positive association between complement C4A dificiency and schizophrenia. Moreover, our study did not support a widespread association between a deficiency in complement component C4B and schizophrenia.