Associate Professor
Anatomy and Neurobiology

MEMPHIS TN 381632103
Tel: (901) 448-2178


  •  PhD Institution: Hamdard University, Department of Toxicology, New Delhi, India.
  • Postdoctoral: Emory University, School of Medicine, Department of Emergency Medicine, Atlanta, GA: University of Georgia, College of Pharmacy, Department of Clinical and Experimental Therapeutics, Augusta, GA

Research Description

The broad goal of our lab is to understand, at a cellular and molecular level, the interplay between inflammation and oxidative stress in neurovascular injury after stroke, and to develop novel therapeutic strategies. We integrate cellular, molecular, genetic, and pharmacological approaches to elucidate the mechanisms that control the progression of neurovascular brain injury after stroke.

Stroke is a major cause of long-term disability worldwide and there is no treatment for it except recombinant tissue type plasminogen activator (rtPA). rtPA can be administered only within a short time window (4.5 hours) after stroke onset, and it often leads to rupturing of the cerebrovascular system, leading to hemorrhage, oxidative stress and inflammation. We believe that treatment of acute stroke with rtPA in combination with certain potent neuroprotectants/ small molecules can combat oxidative stress and inflammation and will prove to be a good strategy to prevent secondary injury.

Our laboratory uses a multidisciplinary approach to examine the molecular mechanisms and therapeutic targets involving in neurovascular injury including, Western blotting, PCR, immunocytochemistry, and cutting edge neuroscience techniques. In addition, we incorporate a broad variety of functional behavioral tests useful for investigating experimental manipulations including, the Morris water maze, Beam walk open field apparatus, passive avoidance, CatWalk, rotarod apparatus, and Grip strength test, Novel Object recognition.

Hyperglycemia and Stroke

Clinical and experimental investigations demonstrate that post-stroke hyperglycemia (HG)/diabetes significantly increases the risk and severity of neurovascular complications in acute stroke. Further, these conditions reduce the efficacy of reperfusion therapies and increase the likelihood of neurovascular complications, including blood-brain barrier-BBB leakage, edema and hemorrhage. The limited understanding of the molecular mechanisms by which HG contribute to reperfusion injury is a critical barrier to progress in the development of new therapies for stroke. Our group has been leading studies that elucidated the pivotal role of vascular protection in stroke and HG/diabetes. However, there is still a gap in understanding how inflammasome activation and redox changes affect the neurovascular unit, particularly in HG/diabetes, to sustain neuronal injury and worsen stroke outcome. Thioredoxin-interacting protein (TXNIP) is a central signaling hub that links oxidative/glucose stress and inflammation to cellular injury, making it a “multiple pathways” target and thus a promising new approach for stroke therapy. Our long-term goal is to identify suitable drug targets to aid in the discovery of novel and clinically applicable therapies to improve stroke outcome.

View references (pubmed link)