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Year : 2019  |  Volume : 9  |  Issue : 1  |  Page : 18-23

Anti-inflammatory effects of alkaloid enriched extract from roots of Eurycoma longifolia Jack

1 Deparment of Traditional Pharmacy, Hanoi University of Pharmacy, 13-Le Thanh Tong, Hoan Kiem, Hanoi, Vietnam
2 Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, Gangwon-Do 200-701, Republic of Korea
3 Advanced Center for Bio-organic Chemistry, Institute of Marine Biochemistry, Vietnam Academy of Science and Technology, 18 Hoang Quoc Viet, Cau Giay, Hanoi, Vietnam
4 National Institute of Drug Quality Control, 48-Hai Ba Trung, Hoan Kiem, Hanoi, Vietnam
5 Center for Research and Technology Transfers, VAST, 18 Hoang Quoc Viet, Cau Giay, Hanoi, Vietnam

Correspondence Address:
Nguyen Tien Dat
Center for Research and Technology Transfers, Vietnam Academy of Science and Technology, 18 Hoang Quoc Viet, Cau Giay, Hanoi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2221-1691.250265

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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.

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