Dihydromyricetin (DHM) is a plant flavonoid and is the primary active ingredient isolated from the medicinal herb, Ampelopsis grossedentata. DHM has been shown to possess various pharmacological activities, including anti-inflammatory effects. However, the possible role of DHM in asthma treatment remains to be elucidated. The present study aimed to investigate its anti-inflammatory properties in mice with symptoms of allergic asthma. The C57BL/6 mice were sensitized and challenged with ovalbumin (OVA) to induce asthma. DHM or phosphate-buffered saline treatment was administered 1 h prior to the OVA challenge. The levels of interleukin (IL)-4, IL-5 and IL-13 in the bronchoalveolar lavage (BAL) fluid were measured by enzyme-linked immunosorbent assay (ELISA), and OVA-specific serum IgE and IgG1 levels were also determined by ELISA. Histopathological staining was performed to evaluate the infiltration of inflammatory cells into the BAL fluid, lung tissues and goblet cell hyperplasia. DHM treatment significantly reduced the total number of inflammatory cells, including eosinophils, neutrophils, lymphocytes and macrophages, in the BAL fluid. DHM also reduced the levels of IL-4, IL-5 and IL-13 in the BAL fluid, and reduced the secretion of OVA-specific IgE and IgG1 in the serum. The histological staining demonstrated that DHM treatment effectively suppressed the OVA-induced inflammatory cells in the lung tissues and in the mucus hypersecreted by goblet cells in the airway. These results showed that DHM had a potent anti-inflammatory effect in an OVA-induced mouse model of asthma, offering potential as an anti-inflammatory agent for the treatment of asthma.

The non-small-cell lung cancer (NSCLC) is the most common lung cancer which seriously threatens the human health. Xu Li’s experiential prescription (XLEP) can treat the NSCLC. However, whether XLEP can regulate the autophagy in the EGFR-positive NSCLC still remains unknown. We found that the cellular activity of drug-resistant cells and sensitive cells were all decreased in the TCM group and TCM + Gef group. The expression of autophagy-associated proteins (mTOR and Beclin1-Vps34) in drug-resistant cells was decreased in the TCM group, while the expression of autophagy-associated proteins in sensitive cells was all decreased in the TCM + Gef group. The ratio of M1/M2 macrophages was increased when IL-4-induced RAW264.7 was treated with TCM. TCM treatment promoted the expression of CCL2 and CCL3 while it downregulated the CCL22 level among A549, H1975, and PC9 cells. The expression of TNF-α and IL-6 was increased, and the expression of IL-10 and TGF-β was decreased in IL-4-induced RAW264.7 cells treated with TCM. And, TCM treatment also decreased the expression of Fizz1 and TGM2. In conclusion, this study indicated that XLEP could suppress the proliferation of EGFR-TKI-resistant cancer cells and increase the ratio of M1/M2 macrophages by inhibiting autophagy to treat the drug-resistant EGFR-positive NSCLC.

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