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https://www.selleckchem.com/products/vps34-in1.html expression of macrophage polarization markers CD11c, CD16, CD206 and Arg1 in the LIRI group were significantly increased. Compared with the LIRI group, the expressions of CD11c and CD16 in the lung tissue of the DEX group were significantly decreased, and the expressions of CD206 and Arg1 were significantly increased. The intervention of PI3K/AKT signaling pathway inhibitor LY294002 significantly blocked the effect of dexamethasone on LIRI-mediated macrophage polarization (CD11c immunohistochemical score 7.20±0.36 vs. 5.00±0.34, CD16 immunohistochemical score 8.20±0.48 vs. 7.40±0.64, CD206 immunohistochemical score 5.80±0.59 vs. 7.40±0.28, Arg1 immunohistochemical score 7.20±0.72 vs. 8.80±0.48, all P less then 0.05). CONCLUSIONS Dexamethasone pretreatment can alleviate the intrapulmonary inflammatory response and lung injury caused by LIRI in rats. The mechanism of action is related to the polarization direction of pulmonary macrophagesvia activation of the PI3K/AKT pathway by dexamethasone.OBJECTIVE To analyze the differential gene expression of Shufeng Xuanfei Jiedu formula on whole expression profiles of the inflammation-related cytokines in mice infected with influenza virus by the gene chip technology. METHODS Male ICR mice were divided into normal group (N group), influenza virus pneumonia model group (M group), oseltamivir control group (C group) and Shufeng Xuanfei Jiedu formula high, medium and low dose groups (SH, SM, SL groups) according to the random number table method, with 10 mice in each group. A mouse model of influenza virus pneumonia was established by nasal drip of influenza virus strain FM1 (0.05 mL); in group N, 0.05 mL normal saline was used. In SH, SM and SL groups, Shufeng Xuanfei Jiedu formula was prescribed after 2 hours of intranasal infection (drug concentration approximately 3.8, 1.9 and 1.0 kg/L), 0.2 mL once a day for 4 days; in group C, the dosage of oseltamivir was 2.5 kg/L; in gro

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