Objective Using serum pharmacology method to assess the optimal dose of Rhodiolasachalinensis extract (RSE)and Codonopsispilosula extract (CPE)combination as well as the effects of the combination on the immune function of mice.Methods Using the 3×3 facterial design,nine medicated serum of CPE and RSE mixture were made to assess the optimum combinational dose of CPE and RSE by detecting the T,B lymphocyte proliferation abilities and NK cell activity in vitro .Using the optimum combinational dose and reducing 2.5,5 and 10 times as high,middle and low doses of RSE+CPE groups,and the T,B lymphocyte proliferation abilities and the activity of NK cells in the mice were detected in vivo .Results The result of serum pharmacology indicates that compared with control group,the proliferation abilities of T,B lymphocytes and the activity of NK cells inducing by ConA and LPS in 200 mg· kg-1 RSE + 790 mg· kg-1 CPE group were increased (P < 0.05).The result of in vivo experiment indicated that compared with cyclophosphamide group,the spleen indexes (SI)in middle and high doses of RSE+CPE groups were significantly increased (P <0.05);compared with low dose of RSE+CPE group,the WBC number in middle dose of RSE + CPEgroup was significantly increased (P < 0.05 ). Compared with cyclophosphamide group,the T and B cell proliferation abilities induced with ConA and LPS and killing activities of NK cells in low,middle and high doses of RSE+CPE groups and positive drug CVT-200 group were significantly increased (P <0.05).Compared with CVT-200 group,low and high doses of RSE+CPE groups,the T and B cell proliferation abilities induced with ConA and LPS and the activity of NK cells in middle dose of RSE+CPE group were significantly increased (P <0.05).Conclusion RSE and CPE mixture can enhance the immune function of mice;RES 200 mg·kg-1 and CPE 790 mg·kg-1 are the optimal doses.

Objective To study the relationship between the expression of perforin, granzyme B and the cytotoxicity of NK cells, after NK cells were purified and expanded with different cytokines. Meth-otis It was detected that the mRNA expressions of perforin, ganzyme B from 8 donors, and the cytotoxcity of NK cells to target I(562 cells by competitive qualitative RT-PCR. Results The mRNA expressions of perforin, granzyme B by purified and expanded NK cells with different cytokines were markedly enhanced, and IL-2 +IL-15 group, IL-2 + IL-12 + IL-15 group were significantly higher than others. It is consistent that the relationship between the mRNA expressions of NK cells and the cytotoxicity of NK cells to I(562 cells. Conclusion The mRNA expressions of perforin, granzyme B of NK cells with different cytokines were obviously.

Objective: To study the expression of miRNA-181a in acute myeloid leukemia (AML) patients with normal karyotype to probe its prognosis significance. Methods: The expression level of miRNA-181a in bone marrow mononuclear cells of 120 de novo AML patients with normal karyotype was detected by real time fluorescence quantitative PCR. The direct sequencing method was used to detect IDH1, IDH2, NPM1, FLT3-ITD, DNMT3A and CEBPα mutations in CN-AML patients after PCR. The relationship between miRNA-181a expression and gene mutation, the clinical parameters and prognosis were analyzed. Results: The rates of overall surviva1 (OS) in high expression and low expression groups were 25.0 months and 15.0 months, respectively (P<0.05) . Relapse free survival (RFS) in high expression and low expression groups were 21.4 months and 11.2 months, respectively (P<0.05) . Significantly higher level hemoglobin, complete remission rate and proportion of wild type NPM1 expression in the high expression of miRNA-181a group were observed when compared with the lower expression of miRNA-181a group (P<0.05) . Multivariate Cox regression analysis showed miRNA-181a overexpression was an independent prognostic factor for CN-AML (HR=2.219, 95%CI 1.601~2.432, P=0.018) . Conclusion Higher expression of miRNA-181a was a good prognostic factor independent of clinical parameters and high frequency gene mutations, which implicated that the miRNA-181a expression level could be used as an important prognostic indicator of AML patients with normal karyotype.

Mycoplasma pneumoniae is the most common pathogen of respiratory tract infection in children and adults. Clinical observation shows that M. pneumoniae infection can cause massive mucus secretion in the respiratory tract, which makes the breathing of patients difficult. Studies have shown that M. pneumoniae infection can cause massive secretion of mucin 5AC (MUC5AC). Adhesin P1 plays an important role in the pathogenesis of M. pneumoniae infection by mediating the adhesion of pathogens to host cells, and the C-terminal residues of P1 (P1-C) are immunogenic. This study investigated the molecular mechanism of Wnt/β-catenin signaling pathway inhibitor Dickkopf-1 (DKK1) in the secretion of MUC5AC in mouse airway epithelial cells (MAECs) induced by P1-C. Scanning electron microscope and hematoxylin-eosin staining were used to observe the effect of P1-C on mucus secretion of MAECs. Protein chip was used to detect the secretion of cytokines and analyse the enrichment of related signaling pathways induced by P1-C in MAECs. Periodic acid schiff stain (PAS) staining, Tunel staining and Masson staining were used to detect the damage of the lungs of mouse exposed to P1-C. Immunohistochemistry was used to detect the secretion of MUC5AC expression, and Western blotting was used to reveal the molecular mechanism of DKK1-regulated secretion of MUC5AC induced by P1-C protein in MACES. The results showed that P1-C induced the massive secretion of mucus and inflammatory factors in MAECs. During P1-C infection, DKK1 down-regulated janus kinase 2 (JAK2), phosphorylation signaling and transcription activator 1 (p-STAT1) and phosphorylation signaling and activator of transcription 3 (p-STAT3) expression. Overexpression of DKK1 significantly up-regulated the expression of MUC5AC repressor transcription factor fork-head box protein A2 (FOXA2). At the same time, the expression of MUC5AC induced by P1-C was inhibited significantly. It is speculated that DKK1 can effectively reduce the secretion of MUC5AC in MAECs induced by P1-C by inhibiting the JAK/STAT1-STAT3 signaling pathway and up-regulating the expression of FOXA2.
Animals ; Mice ; Epithelial Cells ; Lung ; Mucin 5AC/metabolism* ; Mycoplasma pneumoniae/metabolism* ; Signal Transduction