https://www.selleckchem.com/products/phtpp.html In mice with IgE/OVA-induced asthma, oral administration of catalpol remarkably suppressed the production of OVA-specific IgE, the development of airway hyperresponsiveness (AHR), and the infiltration of eosinophils and neutrophils into the lungs. Histological studies demonstrated that catalpol substantially inhibited the recruitment of mast cells and increased mucus production in lung tissues. Catalpol-treated mice had significantly lower levels of helper T cell type 2 (Th2) cytokines (IL-4, IL-5, and IL-13), PGD2, eotaxin-1, and C-X-C chemokine ligand-1 (CXCL1) in bronchoalveolar lavage fluid (BALF) than did the allergic group. Collectively, these results indicated that the suppressive effects of catalpol on degranulation and mediator generation by mast cells were beneficial in treating allergic asthma. Lung cancer is one of the most frequently diagnosed cancers worldwide. However, the potential causes of lung cancer oncogenesis are still unclear. This study aims to explore the phenomenon and mechanism of NK cell exhaustion in lung cancer and lay the foundation for developing a targeting strategy to ameliorate immune cell exhaustion in cancer. NK cells were isolated from the blood samples of lung cancer patients and healthy volunteers. After culture in vitro, the colony forming ability, cytotoxicity, apoptosis and receptor expression of NK cells in the peripheral blood from the lung cancer patients and the volunteers were analyzed by flow cytometry and the corresponding methods. The correlation between the NK cell profile and lung cancer occurrence was analyzed as well. The colony formation and cytotoxicity of the NK cells from the lung cancer group were significantly decreased compared to whose of the NK cells from volunteers. The expression of NKG2A was upregulated and CD226 was downregulated significantly in the lung cancer group compared with the control group. Furthermore, through correlation analysis, the colon