This study aimed to investigate the effects of total flavonoids of Fagopyrum dibotrys on acute lung injury induced by lipopolysaccharide (LPS) in mice.In this study, the total flavonoid extract of Fagopyrum dibotrys root was obtained with ethanol as an extraction solvent.Kunming mice were given intragastric administration of total flavonoid extract of buckwheat (25, 50, and 100 mg/kg) for 12 days, and acute lung injury was induced by intranasal 1 mg/kg LPS.The cell injury model was established by co-incubation of 20 μg/mL LPS and RAW 264.7 cells, and RAW 264.7 cells were treated with 10, 20, and 30 μg/mL of total flavonoids.The cytotoxicity of LPS and total flavonoids of Fagopyrum dibotrys was evaluated by the CCK-8 method and dehydrogenase (LDH) release.The contents of inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor (TNF-α), and interleukin-18 (IL-18) were detected by ELISA.The levels of oxidative biomarkers, including reactive oxygen (ROS), malonaldehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and H2O2 were detected by spectrophotometer and the apoptosis of RAW 264.7 cells was detected by Hoechst33342/PI double staining.Results showed that total flavonoids of Fagopyrum dibotrys could effectively inhibit the polarization of RAW 264.7 cells to M1 and reduce the secretion of pro-inflammatory mediators such as IL-1β, IL-6, IL-18, and TNF-α, reduce the release of LDH, eliminate accumulated ROS and MDA, increase the activity of SOD and CAT, increase the content of GSH, and resist apoptosis induced by LPS in a concentration-dependent manner.The effect of total flavonoid extract of Fagopyrum dibotrys was verified in mice with acute lung injury induced by LPS.It significantly decreased the secretion of IL-1β, IL-6, and TNF-α in serum and the levels of oxidative stress products MDA and H2O2, increased the activity of antioxidant enzyme CAT, and prevented the accumulation of edematous fluid in lung tissue.To sum up, total flavonoids of Fagopyrum dibotrys can effectively inhibit the production of pro-inflammatory mediators, reverse the expression of oxidative biomarkers, and resist apoptosis, thus inhibiting the polarization of macrophages to M1 and alleviating LPS-induced acute lung injury in mice by anti-inflammatory, antioxidant, and anti-apoptosis effects.
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