Zhike Pingchuan Granule suppresses interleukin (IL)-6 or the medium of M2 macrophages induced apoptosis in human bronchial epithelial cells

The aim of this study was to explore the effects and action mechanism of Zhike Pingchuan Granule in human bronchial epithelial cells induced by IL-6 or the supernatant of M2. Upon IL-6 stimulation at different doses, Cell Counting Kit-8 (CCK8) assay and flow cytometry were, respectively, utilized to detect the cell viability and apoptosis levels of 16-HBE cells. ELISA and Western blot were, respectively, used to analyze the inflammatory markers and JAK2/STAT3 signals. Immunofluorescence assay was performed to identify M0 and M2 cells. As shown in results, ZKPC perturbed the expression of IL-6 inducible genes important for apoptosis, oxidative and inflammatory response, which was enhanced by JAK2 inhibitor. Besides the inhibitory effects on the phosphorylation levels of JAK2/STAT3, ZKPC markedly increased cell viability and reduced apoptosis in human bronchial epithelial cells (16-HBE) cultured in the supernatant of M2 cells. Collectively, ZKPC could inhibit the IL-6-induced JAK/STAT3 signaling cascade, increase cell viability and decrease apoptosis induced by the supernatant of M2. A more comprehensive understanding of the action mechanism of ZKPC on JAK2/STAT3 signaling pathway in human bronchial epithelial cells induced by IL-6 or M2 supernatant will enable ZKPC development in the control of asthma.

Automated summary

The study aimed to investigate the effects and action mechanism of Zhike Pingchuan Granule in human bronchial epithelial cells induced by IL-6 or the supernatant of M2. Results showed that ZKPC disrupted important IL-6 inducible genes related to apoptosis, oxidative, and inflammatory responses, which was enhanced by JAK2 inhibitor. Additionally, ZKPC inhibited the IL-6-induced JAK2/STAT3 signaling cascade, increased cell viability, and decreased apoptosis in human bronchial epithelial cells cultured in the supernatant of M2.