Pallab Bhattacharya (India)
National Institute of Pharmaceutical Education and Research (NIPER),Ahmedabad.
Pharmacology and Toxicology
Dr. Bhattacharya is Associate Professor in Pharmacology and Toxicology at NIPER-A, India. He obtained his doctoral degree from Indian Institute of Technology (BHU), Varanasi, India and had his post-doctoral training at University of Miami Miller School of Medicine USA .He was a visiting scientist at Harvard Medical School, Boston, USA and Aarhus University, Denmark.His present research is to test the safety and efficacy of cell therapy in small and large animal model of ischemic stroke and further deciphering the related mechanisms of stem cell mediated mitoprotection and neuroprotection. His team also explores the cross talk between mitochondria and endoplasmic reticulum in stroke. His research interest also lies with the regulatory RNA mediated mesenchymal stem cell engineering and nanoparticle based targeted drug delivery to the brain.

Presenter of 2 Presentations

 Congress Calendar

Stroke in Sickle Cell Disease

Session Name
0590 - Teaching Course 01: Challenging Stroke Cases (Part 2) (ID 307)
Session Type
Clinical Manifestations
Date
Wed, 26.10.2022
Session Time
10:00 - 11:30
Room
Room 324-325
Presenter
Lecture Time
10:20 - 10:40

MITOCHONDRIAL DYSFUNCTION EXACERBATE ISCHEMIC STROKE PATHOLOGY IN CHRONIC KIDNEY DISEASE

Session Name
0150 - E-Poster Viewing: AS12 Basic Science and Translational Research (ID 423)
Session Type
E-Poster
Date
Wed, 26.10.2022
Session Time
07:00 - 23:59
Room
GALLERY
Presenter
Lecture Time
07:00 - 07:00

Abstract

Background and Aims

Stroke leads to disturbances in cerebral functions.Chronic kidney disease (CKD) is often correlated with an enhanced risk of stroke. The cerebro-renal interaction in stroke has been explored limitedly, hence, it is imperative to explore it in depth for developing therapeutic interventions.Present study aim to decipher the molecular mechanism by which Chronic Kidney Disease (CKD) may exacerbate
ischemic stroke pathology.

Methods

CKD was induced in Sprague Dawley Rats by 0.5% adenine diet for 28 days followed by a middle cerebral artery occlusion (MCAo) for ischemic stroke.LCMS/MS was performed to assess homocysteine levels in brain.Rats were evaluated for neurodeficits, motor functions and were sacrificed at 24 hours post MCAo. Brains were harvested for infarct size estimations, biochemical analysis, mitochondrial respiration and protein expression studies.

Results

Functional outcome was impaired to a greater extent in stroke+ CKD as compared to sham, stroke and CKD animals.Levels of MDA and nitrite were increased, and glutathione decreased in stroke+CKD animals as compared to sham, stroke and CKD. Mitochondrial respiration was compromised in stroke+CKD group as compared to other groups. Increased DRP1, calcineurin and caspase3 levels were observed. Increased brain homocysteine levels were detected in CKD and CKD+Stroke groups by LCMS/MS

Conclusions

Mitochondrial dysfunction following CKD contributes towards exacerbation of ischemic stroke pathology

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