- Author:
Dao Thi Thanh HIEN
1
;
Tran Phi LONG
2
;
Tran Phuong THAO
2
;
Jeong-Hyung LEE
2
;
Duong Thu TRANG
3
;
Nguyen Thi Thu MINH
3
;
Pham VAN CUONG
3
;
Nguyen Hai DANG
3
;
Do Thi Ngoc LAN
4
;
Nguyen Tien DAT
5
Author Information
- Publication Type:Journal Article
- Keywords: 10-dimethoxycanthin-6-one; Alkaloid,9; Anti-inflammation; Eurycoma longifolia
- From:Asian Pacific Journal of Tropical Biomedicine 2019;9(1):18-23
- CountryChina
- Language:Chinese
- Abstract: 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.