Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
Advanced search 
Year : 2015  |  Volume : 11  |  Issue : 44  |  Page : 329-336

Apoptosis of AGS human gastric adenocarcinoma cells by methanolic extract of Dictamnus

1 Division of Longevity and Biofunctional Medicine, Healthy Aging Korean Medical Research Center, Yangsan 626-870, Korea
2 Division of Pharmacology, School of Korean Medicine, Pusan National University, Yangsan 626-870, Korea

Correspondence Address:
Byung Joo Kim
Division of Longevity and Biofunctional Medicine, School of Korean Medicine, Pusan National University, Yangsan 626-870
Login to access the Email id

Source of Support: This study was supported by The Korean National Research Foundation (NRF) funded by the Korean government (MSIP) (Grant no. 2014R1A5A2009936), Conflict of Interest: None

DOI: 10.4103/0973-1296.165994

Rights and Permissions

Background: The root bark of Dictamnus dasycarpusTurcz has traditionally been used in East Asia to treat skin diseases such as eczema, atopic dermatitis, and psoriasis. However, it has also been reported to exhibit an anti-proliferative effect on cancer cells. Objective: To investigate the anti-cancer effects of a methanol extract of Dictamnus dasycarpusroot bark (MEDD) on AGS cells (a human gastric adenocarcinoma cell-line). Materials and Methods: An 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium assay, a caspase activity assay, cell cycle analysis, mitochondrial membrane potential (MMP) measurements, and western blotting were used to investigate the anti-cancer effects of MEDD on AGS cells. Results: Treatment with MEDD significantly and concentration-dependently inhibited AGS cell growth. MEDD treatment in AGS cells led to increased accumulation of apoptotic sub-G1 phase cells in a concentration-dependent manner. Also, MEDD reduced the expressions of pro-caspase-3, -8 and -9, and increased the active form of caspase-3. Furthermore, subsequent Western blotting revealed elevated levels of poly (ADP-ribose) polymerase protein. MEDD treatment reduced levels of MMP and anti-apoptotic Bcl-2 and Bcl-xL proteins. Pretreatment with SB203580 (a specific inhibitor of p38 mitogen-activated protein kinases), SP600125 (a potent inhibitor of C-Jun N-terminal kinases), or PD98059 (a potent inhibitor of extracellular signal-regulated kinases) did not modify the effects of MEDD treatment. However, pretreatment with LY294002 (a specific inhibitor of Akt) significantly enhanced MEDD-induced cell death. Conclusion: These results suggest that MEDD-mediated cell death is associated with the intrinsic apoptotic pathway and that inhibition of Akt signaling contributes to apoptosis induction by MEDD.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded256    
    Comments [Add]    
    Cited by others 4    

Recommend this journal