RESUMO
The main objective of this study is to establish the best preparation technology of the particles of Acanthopanax senticosus. First, take the reflux extraction method extract of Acanthopanax senticosus coarse powder, optimized by orthogonal experimental method, to flavonoids flavonoids extraction extraction rate as the indexes to determine the effects of extraction temperature, ethanol concentration, extraction time on flavonoids content. Then by a wet granulation of thorn slender acanthopanax particles, taste with granules, forming rate, melting rate as index to investigate the influences of materials adding amount of granules effect. The results showed that the ethanol water heating reflux extraction method to extract the temperature of 70â¯deg, the percentage of ethanol 75%, extraction time 2.5â¯h, the highest content of total flavonoids in the extract. Join the 5â¯ml and 10â¯g in the extract of acacia honey, dextrin, starch, sugar ratio for 3:4:8, the best taste of Acanthopanax granules. In the end, the best preparation technology of the granules is established, and the process is simple, which is suitable for the large-scale production of the factory.
RESUMO
BACKGROUND: Esculentoside A (EsA) is a saponin isolated from the Chinese herb Phytolacca esculenta. In our study, we sought to investigate the protective effects of EsA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. MATERIALS AND METHODS: To determine the effects of EsA on the reduction of histopathologic changes in mice with ALI, inflammatory cell count in bronchoalveolar lavage fluid (BALF) and lung wet-to-dry weight ratio were measured in LPS-challenged mice, and lung histopathologic changes observed via paraffin section were assessed. Next, cytokine production induced by LPS in BALF was measured by enzyme-linked immunosorbent assay. To further study the mechanism of EsA protective effects on ALI, IκBa, p38, and extracellular signal receptor-activated kinase pathways were investigated in lung tissue of mice with ALI. RESULTS: In the present investigation, EsA showed marked effects by reducing inflammatory infiltration, thickening of the alveolar wall, and pulmonary congestion. Levels of tumor necrosis factor α and interleukin 6 elevated by LPS were significantly decreased in BALF in EsA-pretreated ALI model. Furthermore, EsA significantly suppressed phosphorylation of IκBa, p38, and extracellular signal receptor-activated kinase. CONCLUSIONS: Taken together, our results suggest that EsA suppressed inflammatory responses in LPS-induced ALI through inhibition of the nuclear factor kappa B and mitogen activated protein kinase signaling pathways. EsA may be a promising potential preventive agent for ALI treatment.
