Dr. Zahoor Shah
Assistant Professor of 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.
- Orbán-Gyapaia, O, Raghavan, A, Vasas, A, Forgo, A, Hohmann, J, Shah, ZA (2014). Flavonoids isolated from Rumex aquaticus exhibit neuroprotective and neurorestorative properties by enhancing neurite outgrowth and synaptophysin. CNS & Neurological Disorders - Drug Targets. In Press
- Nada, S.E, Tulsulkar, J, Shah, Z.A. (2014) Heme oxygenase 1-mediated neurogenesis is enhanced by Ginkgo biloba (EGb 761) after permanent ischemic stroke in mice. Molecular neurobiology. 49:945–956.
- Almaliti, J, Nada, S.E, Carter, B, Shah, Z.A, and Tillekeratne, L.M.V. (2013) Neuroprotective Agents Against H2O2-Induced Cell Death. Bioorg. Med. Chem Lett 2013 Mar 1;23(5):1232-7.
- Tulsulkar, J and Shah, Z.A. (2013) Ginkgo biloba prevents transient global ischemia-induced delayed hippocampal neuronal death through antioxidant and anti-inflammatory mechanism. Neurochemistry International 62 (2013) 189–197.
- Nada, S.E, Tulsulkar, J, Raghavan, A, Hensley, K, Shah, Z.A. (2012) A derivative of the CRMP2 binding compound lanthionine ketimine provides neuroprotection in a mouse model of cerebral ischemia. Neurochemistry International. Dec;61(8):1357-1363.
- Nesamony J, Singh, P.R, Nada, S.E, Shah, Z.A, Kolling, W.M. (2012) Calcium alginate nanoparticles synthesized through a novel interfacial cross-linking method as a potential protein drug delivery system. J Pharaceutical Sciences. 2012 Jun;101(6):2177-84.
- 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):180-9.
- Shah, Z.A Nada, S.E and Dore, S. (2011) Heme oxygenase 1, beneficial role in permanent ischemic stroke and in Gingko biloba (EGb 761) neuroprotection. Neuroscience 180, 248-255.
- 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. 1-11.
- Zeynalov, E, Shah, Z.A,Li, R, Dore, S. (2009) Heme Oxygenase 1 is associated with Ischemic Preconditioning-induced protection against brain ischemia. Neurobiology of Disease. 35(2): 264-269. (co-first author)
- Saleem, S, Shah, Z.A, Doré, S. (2009) Lipocalin-prostaglandin D synthase is a critical factor in transient and permanent focal cerebral ischemia. Neuroscience 160(3): 248-254. (Figure selected as a face page for the issue; co-first author)
- Soukhova-O’Hare, G.K, Shah, Z.A, Lei, Z, Nozdrachev, A.D, Rao, C.V, Gozal, D. (2008) Erectile dysfunction in a murine model of sleep apnea. American Journal of Respiratory and Critical Care Medicine. 15: 644-50.
- 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. 147(1): 53-9.
- Shah, Z.A, Klaus, J, Namiranian, K, Blizzard, K, Doré, S. (2006) Use of silicone-coated monofilament for inducing transient middle cerebral artery (MCA) occlusion in mice. Journal of stroke and Cerebrovascular Diseases. 15(4): 133-138.