The protective effects and mechanisms of myricetin on LPS-induced acute lung injury of BALB/c mice / 国际中医中药杂志

ABSTRACT

Objective To investigate whether myricetin (Myr) exert protective effects on acute lung injury induced by LPS and to explore its underlying mechanisms. Methods A total of 72 mice were divided into the control group, model group, myricetin group and active group, 18 in each group. Male BALB/c mice of the myricetin were given an intragastric injection of Myr (50 mg/kg), and the active group dexamethasone (Dex, 5 mg/kg) 1 h before intranasal instillation of LPS. While the other groups were given the same volum saline. 24 hours after LPS exposure, mice were sacrificed and various samples were collected for further analysis. Both levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the bronchoalveolar lavage fluid (BALF) were measured by ELISA kits. The numbers of total cells, macrophages, and neutrophils in the BALF were also determined using differential leukocyte cell count method. The phosphorylations of nuclear factor-kappa B (NF-κB) and IκB were further detected by western blot analysis. Results Compared with the model group, the levels of macrophages and neutrophils in BALF in the myricetin and active groups significantly decreased (P<0.01), while the total protein and W/D ratio of the lung tissue significantly decreased (P<0.05). Compared with the model group, the levels of TNF-α (5.47 ± 2.54 pg/ml, 4.19 ± 0.50 pg/ml vs. 15.28 ± 1.27 pg/ml), IL-1β(336.20 ± 41.06 pg/ml, 247.99 ± 25.12 pg/ml vs. 464.88 ± 34.51pg/ml), the MPO (0.74 ± 0.12 U/g, 0.61 ± 0.08 U/g vs. 1.66 ± 0.07U/g) in the myricetin and active groups significantly decreased (P<0.01). Compared with the model group, the expression of p-IκB/IκB (0.61 ± 0.01, 0.59 ± 0.01 vs. 0.95 ± 0.01), p-NF-κB/NF-κB (0.54 ± 0.01, 0.59 ± 0.03 vs. 0.96 ± 0.02) of the lung tissue in the myricetin and active groups significantly decreased (P<0.01). Conclusions Collectively, these findings revealed that Myr may alleviate the LPS-induced acute lung injury via relief of inflammatory reactions associated with blockage of the NF-κB signaling pathway.