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1.
Natural Product Sciences ; : 281-286, 2023.
Artigo em Inglês | WPRIM | ID: wpr-1041783

RESUMO

The optimal condition for Moringa oleifera root barks extraction was determined using response surface methodology and Box-Behnken Design. The actual optimal condition of the factors was 65 o C, ethanol 60%, 40 (mL/g) liquid-to-solid ratio with 240 minutes extraction time. The enrichment of phenolic compounds sharply affected the antioxidant, and inhibitions of α-amylase enzyme, as well as, the anti-inflammatory effect of the extract from M. oleifera root barks. The extract in the optimal condition exhibited better 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging and α-amylase inhibitory activities than those of positive controls.Also, the extract showed weak hydroxyl free radical scavenging and nitric oxide (NO) production inhibitory effects. These revealed a simple and promising method for the preparation of bioactive products from the root bark of M. oleifera.

2.
Artigo em Chinês | WPRIM | ID: wpr-950389

RESUMO

Objective: To examine the in vitro and in vivo anti-inflammatory effects of the alkaloid enriched extract (ELA) from the roots of Eurycoma longifolia. Methods: The in vitro antiinflammatory effects of ELA were evaluated by examining its inhibitory activities against nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. The level of NO produced in the culture media was determined by Griess method. The iNOS and COX-2 protein expressions were analyzed by Western blot. The in vivo effect of ELA was evaluated on LPS-induced septic shock in mice model. Mice mortality was monitored for 5 days after injection of LPS. The chemical contents of the ELA were determined by using various chromatographic and spectroscopic techniques. Results: The ELA was found to exhibit a significant anti-inflammatory effect in both in vitro and in vivo models. The results demonstrated that ELA dose-dependently inhibited LPS-induced NO production as well as the protein iNOS and COX-2 expressions. In the septic shock model, ELA dose-dependently protected mice from LPS-induced mortality. Further study on the isolated components of ELA indicated that 9,10-dimethoxycanthin-6-one may contribute significantly to the anti-inflammatory effects of the extract. Conclusions: These results suggest that ELA exhibits the anti-inflammatory activity via suppression of pro-inflammatory mediators such as NO, iNOS, and COX-2 and protects mice from LPS-induced mortality in septic shock model.

3.
Artigo em Chinês | WPRIM | ID: wpr-733672

RESUMO

Objective:To examine the in vitro and in vivo anti-inflammatory effects of the alkaloid enriched extract (ELA) from the roots of Eurycoma longifolia.Methods:The in vitro anti-inflammatory effects of ELA were evaluated by examining its inhibitory activities against nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expressions in lipopolysaccharide (LPS)-stimulated RAW264.7 cells.The level of NO produced in the culture media was determined by Griess method.The iNOS and COX-2 protein expressions were analyzed by Western blot.The in vivo effect of ELA was evaluated on LPS-induced septic shock in mice model.Mice mortality was monitored for 5 days after injection of LPS.The chemical contents of the ELA were determined by using various chromatographic and spectroscopic techniques.Results:The ELA was found to exhibit a significant anti-inflammatory effect in both in vitro and in vio models.The results demonstrated that ELA dose-dependently inhibited LPS-induced NO production as well as the protein iNOS and COX-2 expressions.In the septic shock model,ELA dose-dependently protected mice from LPS-induced mortality.Further study on the isolated components of ELA indicated that 9,1 0-dimethoxycanthin-6-one may contribute significantly to the anti-inflammatory effects of the extract.Conclusions:These results suggest that ELA exhibits the anti-inflammatory activity via suppression of pro-inflammatory mediators such as NO, iNOS,and COX-2 and protects mice from LPS-induced mortality in septic shock model.

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