-To establish the anti-inflammatory activity of the total flavonoid fraction of the root barks of Broussonetia papyrifera (EBP) and a new formula, the ethanol extract of the root barks of B. papyrifera was fractionated with ethylacetate, yielding the hydrophobic prenylated flavonoid-enriched fraction. EBP and the ethanol extract of the whole Lonicera japonica (ELJ) plant were then mixed at a ratio of 1:1 (w/w) to give a new preparation (BL) in the hope of obtaining an optimal formula with a higher anti-inflammatory activity. Evaluation of the effects of these preparations on A23187-treated rat basophilic leukemia (RBL-1) cells revealed that EBP potently inhibited 5-lipoxygenase (5-LOX), while ELJ showed weak inhibition. Additionally, the mixture (BL) clearly showed stronger inhibitory effects against 5-LOX than either preparation alone. These preparations also inhibited cyclooxygenase-2-catalyzed PGE2 and inducible nitric oxide (NO) synthase-catalyzed NO production by lipopolysaccharide-treated RAW 264.7 cells. When tested against arachidonic acid-induced mouse ear edema, EBP showed strong inhibitory activity at doses of 5-200 mg/kg when administered orally, but BL had obviously stronger inhibitory effects. When tested against λ-carrageenaninduced paw edema in mice, BL showed a potent and synergistic anti-inflammatory effect. In addition, in the acetic acid-induced writhing test, BL was found to have strong analgesic activity at 50-400 mg/kg. Taken together, these results indicate that each of these preparations exert anti-inflammatory activity in vitro and in vivo. In particular, BL showed stronger anti-inflammatory activity than EBP, and these anti-inflammatory effects were partially related to the inhibition of eicosanoid and NO production. BL may be useful for the treatment of human inflammatory disorders.
Investigations into the development of new therapeutic agents for lung inflammatory disorders have led to the discovery of plant-based alternatives. The rhizomes of Anemarrhena asphodeloides have a long history of use against lung inflammatory disorders in traditional herbal medicine. However, the therapeutic potential of this plant material in animal models of lung inflammation has yet to be evaluated. In the present study, we prepared the alcoholic extract and derived the saponin-enriched fraction from the rhizomes of A. asphodeloides and isolated timosaponin A-III, a major constituent. Lung inflammation was induced by intranasal administration of lipopolysaccharide (LPS) to mice, representing an animal model of acute lung injury (ALI). The alcoholic extract (50–200 mg/kg) inhibited the development of ALI. Especially, the oral administration of the saponin-enriched fraction (10–50 mg/kg) potently inhibited the lung inflammatory index. It reduced the total number of inflammatory cells in the bronchoalveolar lavage fluid (BALF). Histological changes in alveolar wall thickness and the number of infiltrated cells of the lung tissue also indicated that the saponin-enriched fraction strongly inhibited lung inflammation. Most importantly, the oral administration of timosaponin A-III at 25–50 mg/kg significantly inhibited the inflammatory markers observed in LPS-induced ALI mice. All these findings, for the first time, provide evidence supporting the effectiveness of A. asphodeloides and its major constituent, timosaponin A-III, in alleviating lung inflammation.
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