alexa Neuroprotective Effects of Aframomum melegueta Extract after Experimental Traumatic Brain Injury
ISSN: 2329-6836

Natural Products Chemistry & Research
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Research Article

Neuroprotective Effects of Aframomum melegueta Extract after Experimental Traumatic Brain Injury

Aswathi Kumar, Deborah Kennedy-Boone, Harris A Weisz, Bridget A Capra, Tatsuo Uchida, Kristofer Jennings, Maria-Adelaide Micci, Margaret Parsley, Douglas S DeWitt, Donald S. Prough and Helen L Hellmich*
The University of Texas Medical Branch, 301 Harborside Drive, Galveston TX 77555-0830, USA
Corresponding Author : Helen L Hellmich
University of Texas Medical Branch
301 Harborside Drive, Galveston
TX 77555-0830, USA
Tel: 409-772-4216
Fax: 409-772-1224;
E-mail: [email protected]
Received November 24, 2014; Accepted December 22, 2014; Published February 01, 2015
Citation: Kumar A, Kennedy-Boone D, Weisz HA, Capra BA, Uchida T, et al. (2015) Neuroprotective Effects of Aframomum Melegueta Extract after Experimental Traumatic Brain Injury. Nat Prod Chem Res 3:167. doi: 10.4172/2329-6836.1000167
Copyright: © 2015 Kumar A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Aframomum melegueta is an herb in the ginger family that has been shown to have anti-inflammatory, antioxidative, anti-diabetic and antimicrobial properties. We investigated the possibility that the seeds of this herb, which are consumed by gorillas and used as a spice in West and North African cuisine, could have neuroprotective effects in a rat model of traumatic brain injury (TBI). Using Fluoro-Jade, an anionic fluorescent stain that is a well-established marker of degenerating neurons, we found that an extract of Aframomum, PMI-006, significantly reduced numbers of dying, Fluoro-Jade-positive neurons in the rat hippocampus 24 hr after TBI. We used an antibody to CD11b (Ox42), a microglial marker, to show that PMI almost completely reduced microglial activation-a hallmark of injury-induced inflammation- in the rat hippocampus and cortex. To elucidate the molecular mechanisms underlying the neuro protective effects of PMI-006, we used RT2 Profiler pathway-focused PCR arrays representing oxidative stress, cytokine & chemokines and NFκB cell signaling pathways to interrogate PMI-induced changes in hippocampal gene expression after TBI. We found that PMI treatment ameliorated the effects of brain injury and, in several cases, restored injuryinduced gene expression changes to sham control levels. PMI treatment did not significantly alter functional outcome in the Morris Water Maze, a neurobehavioral test of hippocampal-dependent spatial memory. However, because of its safety profile and because it mitigates the effects of TBI on stress and inflammatory signaling pathways that are associated with TBI pathology, PMI could be potentially beneficial in reducing neurodegeneration in TBI survivors.

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