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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 487380, 13 pages
Research Article

Gallic Acid Enriched Fraction of Phyllanthus emblica Potentiates Indomethacin-Induced Gastric Ulcer Healing via e-NOS-Dependent Pathway

1Department of Biochemistry, University College of Medicine, I.P.G.M.E&R, 244B A.J.C. Bose Road, West Bengal, Kolkata 700020, India
2Central Research Laboratory, Department of Biochemistry, KPC Medical College and Hospital, 1F Raja S.C. Mullick Road, Jadavpur, West Bengal, Kolkata 700032, India
3Department of Pharmaceutical Chemistry, Central Drugs Laboratory, 3 Kyd Street, Kolkata-700016, India
4Bio-Organic Division, Bhabha Atomic Research Centre, Mumbai 400085, India

Received 31 March 2012; Revised 8 July 2012; Accepted 10 July 2012

Academic Editor: José Luis Ríos

Copyright © 2012 Ananya Chatterjee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The healing activity of gallic acid enriched ethanolic extract (GAE) of Phyllanthus emblica fruits (amla) against the indomethacin-induced gastric ulceration in mice was investigated. The activity was correlated with the ability of GAE to alter the cyclooxygenase- (COX-) dependent healing pathways. Histology of the stomach tissues revealed maximum ulceration on the 3rd day after indomethacin (18 mg/kg, single dose) administration that was associated with significant increase in inflammatory factors, namely, mucosal myeloperoxidase (MPO) activity and inducible nitric oxide synthase (i-NOS) expression. Proangiogenic parameters such as the levels of prostaglandin (PG) E2, vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), von Willebrand Factor VIII, and endothelial NOS (e-NOS) were downregulated by indomethacin. Treatment with GAE (5 mg/kg/day) and omeprazole (3 mg/kg/day) for 3 days led to effective healing of the acute ulceration, while GAE could reverse the indomethacin-induced proinflammatory changes of the designated biochemical parameters. The ulcer healing activity of GAE was, however, compromised by coadministration of the nonspecific NOS inhibitor, N-nitro-L-arginine methyl ester (L-NAME), but not the i-NOS-specific inhibitor, L-N6-(1-iminoethyl) lysine hydrochloride (L-NIL). Taken together, these results suggested that the GAE treatment accelerates ulcer healing by inducing PGE2 synthesis and augmenting e-NOS/i-NOS ratio.