Anti-Allergic Rhinitis Mechanism of Bikangfu via Regulation of IL-35/STAT3， Inhibition of Eosinophil Activation and Improvement of Immune Function / 中国实验方剂学杂志

ObjectiveTo investigate the mechanism of interleukin-35（IL-35）/signal transducer and activator of transcription 3（STAT3）inhibition of eosinophil activation against allergic rhinitis（AR） by Bifukang. MethodOne hundred patients were randomly divided into a control group and a treatment group，50 cases in each group. The control group was given mometasone furoate nasal spray，and the treatment group was given Bifukang by nasal packing. The course of treatment was 28 days. The clinical efficacy，nasal classification and visual analogue scale（VAS） score of the two groups were observed before and after treatment. Enzyme linked immunosorbent assay（ELISA） was used to detect the expression levels of inflammatory factors ［interleukin（IL）-4，IL-10，IL-17，IL-35］ and Eotaxin and CC chemokine receptor-3（CCR3）in serum and nasal secretion of the two groups. The expression levels of STAT1，STAT3 and STAT4 were detected by real-time polymerase chain reaction（Real-time PCR）.The content of immunoglobulin G（IgG） and the ratio of CD4+/CD8+were detected by ELISA and flow cytometry. ResultAfter treatment， compared with before treatment， the levels of IL-4 and IL-17 in serum and nasal secretion in 2 groups were decreased， while the levels of IL-10 and IL-35 were increased （P<0.05， P<0.01）. The expression of STAT1， STAT2 and STAT3 in nasal secretions were significantly decreased （P<0.05）. IgG and CD4+/CD8+ were decreased， and the differences were statistically significant （P<0.05， P<0.01）.After treatment，compared with the control group，the levels of IL-4 and IL-17 in serum and nasal secretions of the treatment group were decreased，while the levels of IL-10 and IL-35 were increased （P<0.05）. The expression of STAT1，STAT3 and STAT4 in the treatment group was significantly inhibited compared with the control group after treatment （P<0.05）. In addition， the post-treatment serum CD4+/CD8+ and immunoglobulin G （IgG） levels were reduced in the treatment group compared with those of the control group （P<0.05， P<0.01）. During the treatment，there were no abnormal changes in heart，liver，kidney function and routine blood and urine tests in the two groups. ConclusionBifukang has a good effect on allergic rhinitis，and its mechanism may be related to the regulation of IL-35/STAT3 pathway，the inhibition of eosinophil activation and the improvement of related immune function.

Effect of Koumine on Proliferation and Apoptosis of Colorectal Cancer Cells via ROS/JNK/FoxO3a Signaling Pathway / 中国实验方剂学杂志

Objective:To explore the effect and underlying mechanism of koumine （Kou） at different concentrations （0， 100， 200， 400 μmol·L^-1） on the proliferation and apoptosis of colorectal cancer HCT-116 cells. Method:After 24 hours of<italic> in vitro</italic> intervention with HCT-116 cells by Kou， cell counting kit-8 （CCK-8） assay was used to detect its effect on cell proliferation. Flow cytometry was used to detect cell cycle， apoptosis， and reactive oxygen species （ROS） expression. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of forkhead box O3a （FoxO3a）. Cells were transfected with small interfering ribonucleic acid （siRNA）. Western blot was employed to detect the protein expression of the FoxO3a target gene. Result:Compared with the conditions in the blank group， Kou treatment reduced the proliferation rate of HCT-116 cells （<italic>P</italic><0.05， <italic>P</italic><0.01） in a dose-dependent manner， caused cell cycle arrest in the G₀/G₁ phase， and induced the apoptosis of HCT-116 cells （<italic>P</italic><0.05， <italic>P</italic><0.01）， which was positively correlated with the concentration of Kou. FoxO3a siRNA interference reduced the expression of FoxO3a and its downstream target genes cyclin-dependent kinase inhibitor 1A （p21）， cyclin-dependent kinase inhibitor 1B （p27）， and Bcl-2 interacting mediator of cell death （Bim） （<italic>P</italic><0.01）. Kou treatment induced the activation of c-Jun <italic>N</italic>-terminal kinase （JNK） in HCT116 cells. SP600125 （JNK specific inhibitor） treatment inhibited the Kou-induced FoxO3a activation and the expression of its downstream target genes. <italic>N</italic>-acetyl cysteine （NAC） treatment reduced Kou-induced ROS levels （<italic>P</italic><0.01） and JNK signal activation. The above results were significantly different from those in the blank group （<italic>P</italic><0.01）. Conclusion:Kou can effectively inhibit the proliferation of HCT-116 cells and promote apoptosis， and the mechanism may be related to the regulation of the ROS/JNK/FoxO3a pathway.