Affiliations: [a] Department of Bioresources, Faculty of Biological Sciences, University of Kashmir, Srinagar, India
| [b] College of Applied Medical Sciences, Majmaah University, Almajmaah, Kingdom of Saudi Arabia
Correspondence:
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Correspondence to: Dr. Manzoor Ahmad Mir, Department of Bioresources, Faculty of Biological Sciences, University of Kashmir, Srinagar 190006, India and College of Applied Medical Sciences, Majmaah University, Almajmaah 11952, KSA. Mob: +919622901319; Tel./Fax: 01942434665; E-mail: [email protected]; [email protected]
Abstract: Much recent attention has been given to traditional medicines and natural products with potential and promising anti-inflammatory properties. Leaf extract of Ginkgo biloba GbE-761, possesses several clinical beneficial effects and is now used in a broad spectrum of pharmacological actions. However, mechanisms associated with its anti-inflammatory effect are not very much clear. Previously we established that GbE-761 exerts a neuroprotective effect against ischemic brain injury through an anti-apoptotic mechanism. In this study we investigated the anti-inflammatory effect of GbE-761 in LPS-activated murine macrophage. Our results demonstrate that GbE-761 potently inhibited LPS-induced NO and PGE2 production and these observations were consistent with the inhibition in the protein and mRNA expression levels of inducible iNOS and COX-2 enzymes in a dose dependent manner. Not only this, GbE-761 attenuated the production of pro-inflammatory cytokines like IL-1β, IL-6 and TNF-α in LPS-activated murine macrophages in concentration dependent manner. In addition we reported inhibition in the protein and mRNA expression levels of IL-1β, IL-6 and TNF-α. Furthermore, GbE-761 inhibited the NF-κB activation induced by LPS. Together these results suggest that anti-inflammatory properties of GbE-761 extract might be the results of inhibition of iNOS and COX-2 by upregulating anti-oxidative enzymes and inhibition of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) expression through the down-regulation of NF-kB activation in murine macrophages.
