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Main and Health Science Campuses
Wolfe Hall room 1227, Phone: 419.530.2010
Frederic and Mary Wolfe Center room 155, Phone: 419.383.1904
Medicinal and Biological Chemistry
3000 Arlington Avenue, Toledo, OH 43614
B.S. 1996, University of Kashmir, India
M.S. 1998, Jamia Hamdard, India
Ph.D. 2002, Jamia Hamdard, India
Postdoctoral Fellow 2005, University of Louisville, Kentucky
Postdoctoral Fellow 2007, Johns Hopkins University, Baltimore
Instructor 2009, Johns Hopkins University, Baltimore
My laboratory is interested in developing neuroprotective agents targeting neurodegeneration associated with stroke and cerebrovascular diseases. We have previously shown that –(-)epicatechin, a polyphenolic compound found abundantly in dark chocolates, has neuroprotective properties and salvages dying neurons in the penumbra region of stroke, wherein cells are half dead and half alive and can be saved by timely intervention by targeting particular genes or molecules. To further delineate the mechanism of action of these potential neuroprotective agents, we are interested in evaluating how these compounds up-regulate antioxidant gene, Heme-oxygenase-1 (HO-1), which has been shown to provide neuroprotection in various ischemic models. We are also aware that HO1 is up-regulated by Nrf2, a transcription factor that has been shown to up-regulate a battery of antioxidant genes in stressful situations and strengthen defense mechanisms. Therefore, it is imperative to study the role of the HO1/Nrf2 pathway as a mechanism involved in the protection provided by these neuroprotective agents. To studying these novel compounds, we have developed in vivo [Middle Cerebral Artery Occlusion (t-MCAO); Permanent Distal Middle Cerebral Artery Occlusion (pMCAO); and Delayed Hippocampal Neuronal Death in global ischemia (BCCAO)] and in vitro [Oxygen-glucose deprivation (OGD); cell death models] working models of ischemia. These models simulate the conditions of human stroke and provide us alternatives to study the mechanism of stroke and test therapeutic potential of novel neuroprotective agents. These studies may provide a unique contribution for the treatment of stroke and ischemic brain injury and contribute to public health in the United States as well as globally.
1. Shah, Z.A, Gilani, R.A, Sharma, P, Vohora S.B. Cerebroprotective effect of Korean Ginseng Tea against global and focal models of ischemia in rats. Journal of Ethnopharmacology 2005, 101(1-3), 299-307.
2. Gozal, E, Shah Z.A, Pequignot J.M, Pequignot, J, Sachleben, L.R, Czyzyk-Krzeska, M.F, Li, R.C, Guo, S.Z, Gozal D. Tyrosine hydroxylase expression and activity in the rat brain: differential regulation following long term intermittent or sustained hypoxia. Journal of Applied Physiology 2005, 99(2), 642-649.
3. Shah, Z.A, Jortani, S.A, Tauman, R, Valdes Jr, R, Gozal, D. Serum proteomic patterns associated with sleep-disordered breathing in children. Pediatrics Research 2006, 59, 466-470.
4. Shah, Z.A, Klaus, J, Namiranian, K, Blizzard, K, Doré, S. Use of silicone-coated monofilament for inducing transient middle cerebral artery (MCA) occlusion in mice. Journal of stroke and Cerebrovascular Diseases 2006, 15, 133-138.
5. Shah, Z.A, Li, R, Thimmulappa, R.K, Biswal, S, Kensler T.W, Yamamoto, M, Doré, S (2007) Role of reactive oxygen species in modulation of Nrf2: Effect in transient ischemia. Neuroscience 2007, 147, 53-9.
6. Soukhova-O’Hare, G.K, Shah, Z.A, Lei, Z, Nozdrachev, A.D, Rao, C.V, Gozal, D. Erectile dysfunction in a murine model of sleep apnea. American Journal of Respiratory and Critical Care Medicine 2008, 15, 644-50.
7. Zeynalov, E, Shah, Z.A, Li, R, Dore, S. Heme Oxygenase 1 is associated with Ischemic Preconditioning-induced protection against brain ischemia. Neurobiology of Disease 2009, 35, 264-269.
8. Saleem, S, Shah, Z.A, Doré, S. Lipocalin-prostaglandin D synthase is a critical factor in transient and permanent focal cerebral ischemia. Neuroscience 2009, 160(3), 248-254.
9. Shah, Z.A, Li, R.C, Ahmad, A.S, Biswal, S, Kensler T.W, Yamamoto, M, Doré, S. (2010) Cocoa-derived flavonoid (-)-epicatechin is neuroprotective following transient focal ischemia: Effect mediated by Nrf-2 and HO-1. Journal of Cerebral Blood Flow and Metabolism 2010, 1-11.
10. Ahmad, M, Saleem S, Shah Z.A, Maruyama T, Narumiya S, Dore, S. (2010) The PGE2 EP2 receptor and its selective activation are beneficial against ischemic stroke. Experimental & Translational Stroke Medicine 2010, 2, 12-20.
11. Saleem, S, Shah, Z.A, Maruyama, T, Narumiya, S, Doré, S. (2010) Neuroprotective properties of prostaglandin I(2) IP receptor in focal cerebral ischemia. Neuroscience 2010, 170(1), 317-23.
12. Nada, S.E and Shah, Z.A. (2012) Preconditioning with Ginkgo biloba (EGb 761®) provides neuroprotection through HO1 and CRMP2. Neurobiology of Disease. Apr;46(1):180-189.