1.Effect of Kechuanning Oral Liquid on Signal Transduction Pathway of PI3K in Asthma Rats Induced by Virus
Yinhe LUO ; Hua LI ; Jingyi YANG ; Mengqing WANG ; Sheng HUANG ; Ting HUANG ; Ping JIANG ; Luojia JIAO ; Ying LI
Chinese Journal of Information on Traditional Chinese Medicine 2013;(7):30-32
Objective To observe the effect of Kechuanning Oral liquid on the expression of P13K in CD4+and CD8+T cells of asthma rats induced by respiratory syncytial virus (RSV), and explore its mechanism of preventing and treating asthma induced by virus. Methods SD rats were randomly divided into phosphate-buffered saline (PBS) control group, model group, dexamethasone and salbutamol group (positive drug group), and Kechuanning oral liquid group. Ovalbumin asthma rats model was built and induced by RSV. CD4+and CD8+T cells were separated by magnetic beads method. The expressive level of PI3K-110αin T cells was detected by immumofluorescence method with flow cytometry. Results Compared with PBS control group, positive drug group and Kechuanning oral liquid group, the CD4+and CD8+T cells percentage and the expression level of PI3K-110α in CD4+ and CD8+T cells of model group were significantly higher. The differences were statistically significant (P<0.01). The CD4+and CD8+T cells percentage was not associated with the expression level of PI3K-110α in CD4+ and CD8+T cells of each group by Pearson correlation analysis. Conclusion The CD4+ and CD8+T cells involve in the asthma immunity balanced modulation, and the level of PI3K expressed by CD4+ and CD8+T cells increase distinctly. Kechuanning oral liquid can restrain the expression of PI3K in CD4+ and CD8+T cells, which might be one of the immunologic mechanisms of treating asthma.
2.IL-6 enhances the phagocytic function of mouse alveolar macrophages by activating the JAK2/STAT3 signaling pathway.
Mengqing HUA ; Peiyu GAO ; Fang FANG ; Haoyu SU ; Chuanwang SONG
Chinese Journal of Cellular and Molecular Immunology 2024;40(1):13-18
Objective To investigate the effect of interleukin-6 (IL-6) on the phagocytosis of MH-S alveolar macrophages and its related mechanisms. Methods A mouse acute lung injury (ALI) model was constructed by instilling lipopolysaccharide (LPS) into the airway. ELISA was used to detect the content of IL-6 in bronchoalveolar lavage fluid (BALF). In vitro cultured MH-S cells, in the presence or absence of signal transducer and activator 3 of transcription(STAT3) inhibitor Stattic (5 μmol/L), IL-6 (10 ng/mL~500 ng/mL) was added to stimulate for 6 hours, and then incubated with fluorescent microspheres for 2 hours. The phagocytosis of MH-S cells was detected by flow cytometry. Western blot analysis was used to detect the expression levels of phosphorylated Janus kinase 2 (p-JAK2), phosphorylated STAT3 (p-STAT3), actin-related protein 2 (Arp2) and filamentous actin (F-actin). Results The content of IL-6 in BALF was significantly increased after the mice were injected with LPS through the airway. With the increase of IL-6 stimulation concentration, the phagocytic function of MH-S cells was enhanced, and the expression levels of Arp2 and F-actin proteins in MH-S cells were increased. The expression levels of p-JAK2 and p-STAT3 proteins increased in MH-S cells stimulated with IL-6(100 ng/mL). After blocking STAT3 signaling, the effect of IL-6 in promoting phagocytosis of MH-S cells disappeared completely, and the increased expression of Arp2 and F-actin proteins in MH-S cells induced by IL-6 was also inhibited. Conclusion IL-6 promotes the expression of Arp2 and F-actin proteins by activating the JAK2/STAT3 signaling pathway, thereby enhancing the phagocytic function of MH-S cells.
Animals
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Mice
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Actins
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Disease Models, Animal
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Interleukin-6
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Janus Kinase 2
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Lipopolysaccharides
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Macrophages, Alveolar
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Signal Transduction