A Study On The Mechanism Of MiR-146a Regulating TGF-β Secretion Via STAT5B In Jurkat Cell Line

Objectives Allergic rhinitis(AR),a common disease with a sharp rising trend,seriously affects the quality of life of patients.The research on the molecular regulatory mechanisms of AR has become a hot spot.In our essay,Jurkat cell line was used as the carrier to study the mechanism of mi R-146 a regulating the expression of anti-inflammatory factor TGF-β secreted by Treg cells through STST5 B,so as to provide reference for the clinical diagnosis and treatment of AR.Methods CD4+T cells were extracted from the peripheral blood of 14 patients with AR.In our study,the expression of mi R-146 a was over expressed by lentivirus infection,and the expression of mi R-146 a in Jurkat cells was knocked down at the same time.The regulatory relationship between mi R-146 a and STAT5 B was explored by Western blot,and the potential regulatory mechanism between mi R-146 a and cytokine TGF-β was verified by enzyme-linked immunosorbent assay(Elisa).Results CD4+T cell samples from 14 peripheral blood mononuclear cells were infected with mi R-146a-over-expression lentivirus and control virus respectively.QPCR showed that the expression of mi R-146 a in 8 samples of the overexpression group was higher than that of the control group,proving that the overexpression was successful.Western blot results showed that the expression of STAT5 B was increased in mi R-146a-over-expression cells.At the same time,Jurkat cells were infected with mi R-146 a knockdown virus and control virus.Western blot results showed that when the expression of mi R-146 a decreased,the expression level of STAT5 B protein decreased,while its phosphorylation level also decreased,and the expression level of FOXP3 also decreased significantly.The specific allergen Der p 2 was used to stimulate the peripheral blood monocyte CD4+T cells to induce inflammatory reaction.The expression level of TGF-β in the over expression group of mi R-146 a was higher than that of the control group by Elisa.The difference was statistically significant(P=0.0128).In Jurkat cell superserum,the expression level of anti-inflammatory factor TGF-β in mi R-146 a knockdown group decreased compared with the control group,and the difference was statistically significant(P=0.0123).Conclusions Mi R-146 a and STAT5B(/P-STAT5B)showed a positive regulatory relationship in AR.STAT5 B mediates the mechanism of mi R-146 a in regulating the secretion of anti-inflammatory factor TGF-β by Treg cells in AR patients.Mi R-146 a inhibits the inflammatory response of AR by promoting the expression of TGF-anti-inflammatory factors,providing a theoretical guidance for the clinical diagnosis and treatment of AR.