Ms SARITA NEHRA, PhD - Defence Institute of Physiology and Allied Sciences.Defence Research and Development Organization

Ms SARITA NEHRA

PhD

Defence Institute of Physiology and Allied Sciences.Defence Research and Development Organization

NEW DELHI, DELHI | India

Main Specialties: Biology, Cardiovascular Disease, Internal Medicine, Interventional Cardiology, Pathology-Anatomic & Clinical

Additional Specialties: Heart Failure, Right Ventricular Hypertrophy, Pressure/Volume Overload, Cardiac Imaging, Cardio-immunology

ORCID logohttps://orcid.org/0000-0003-4410-9158


Top Author

Ms SARITA NEHRA, PhD - Defence Institute of Physiology and Allied Sciences.Defence Research and Development Organization

Ms SARITA NEHRA

PhD

Introduction

I have worked on research problems focusing on the modulation of cardiovascular physiology in ascendant to extremely high altitudes due to spontaneous failure of acclimatization including pulmonary hypertension and right heart failure. The core of the research problem relies upon establishing chronic stress-induced dilatory right ventricular hypertrophy and associated damages in the cardio-pulmonary system. The main translational focus of my research was to develop and evaluate a novel bio-nano-pharmaceutical for ameliorating hypoxia-induced cardiovascular disorders.

Primary Affiliation: Defence Institute of Physiology and Allied Sciences.Defence Research and Development Organization - NEW DELHI, DELHI , India

Specialties:

Additional Specialties:

Research Interests:


View Ms SARITA NEHRA’s Resume / CV

Education

Aug 2019
Davis Heart and Lung Research Institute, Wexner Medical Center, Ohio State Univeristy
Post-doc
DEPARTMENT OF PHYSIOLOGY AND CELL BIOLOGY
Aug 2019
Davis Heart and Lung Research Institute, Wexner Medical Center, Ohio State Univeristy
Post-doc
DEPARTMENT OF PHYSIOLOGY AND CELL BIOLOGY
Aug 2019
Davis Heart and Lung Research Institute, Wexner Medical Center, Ohio State Univeristy
Post-doc
DEPARTMENT OF PHYSIOLOGY AND CELL BIOLOGY
Jul 2013 - Aug 2017
DRDO Defence Institute of Physiology and Allied Sciences
DOCTORATE
DEPARTMENT OF EXPERIMENTAL BIOLOGY
Jun 2013
DCR UNIVERSITY OF SCIENCE AND TECHNOLOGY
MASTERS IN TECHNOLOGY
BIO-TECHNOLOGY
Jun 2013
DCR UNIVERSITY OF SCIENCE AND TECHNOLOGY
MASTERS IN TECHNOLOGY
BIO-TECHNOLOGY

Experience

Sep 2017 - Dec 2017
Rajiv Gandhi Cancer Institute and Research Centre
Research Officer
Research

Publications

9Publications

830Reads

2Profile Views

16PubMed Central Citations

Lingzhi or Reishi Medicinal Mushroom, Ganoderma lucidum (Agaricomycetes), as a Cardioprotectant in an Oxygen-Deficient Environment.

Int J Med Mushrooms 2017 ;19(11):1009-1021

Defence Institute of Physiology and Allied Sciences, DRDO, Timarpur, Delhi, India.

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http://dx.doi.org/10.1615/IntJMedMushrooms.2017024584DOI Listing
July 2018
7 Reads

Nanocurcumin-pyrroloquinoline formulation prevents hypertrophy-induced pathological damage by relieving mitochondrial stress in cardiomyocytes under hypoxic conditions.

Exp Mol Med 2017 12 1;49(12):e404. Epub 2017 Dec 1.

Experimental Biology Division, Department of Experimental Biology, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Timarpur, New Delhi, India.

This study investigates the therapeutic effect of a nanocurcumin formulation (NCF) containing nanocurcumin (NC) and pyrroloquinoline quinone (PQQ) on ameliorating hypoxia-induced stress in hypertrophied primary human ventricular cardiomyocytes (HVCM) under hypoxic conditions, as validated in a Sprague-Dawley rat model of chronic hypobaric hypoxia (cHH)-induced right ventricular hypertrophy (RVH). Based on our previous findings, here, we analyzed the improvement in the protective efficacy of NCF against mitochondrial damage. The electron transport chain Complexes' activities were analyzed as a chief operational center for mitochondrial homeostasis, along with key gene and protein markers for mitochondrial biogenesis, redox function, fatty acid oxidation, bio-energetic deficit and cell survival. NCF supplementation imparts cyto-protection from hypoxia-induced hypertrophy and damage in both in vitro and in vivo models while maintaining mitochondrial homeostasis better than NC and PQQ alone. This study proposes the use of NCF as a potential candidate molecule for imparting protection from high altitude-induced maladies in ascendants.

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http://dx.doi.org/10.1038/emm.2017.199DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5750470PMC
December 2017
138 Reads
1 Citation
5.063 Impact Factor

Chronic Hypobaric Hypoxia Induces Right Ventricular Hypertrophy and Apoptosis in Rats: Therapeutic Potential of Nanocurcumin in Improving Adaptation.

High Alt Med Biol 2016 Dec 14;17(4):342-352. Epub 2016 Sep 14.

1 Experimental Biology Division, Department of Experimental Biology, Defence Institute of Physiology and Allied Science , Defence Research and Development Organization, New Delhi, India .

Nehra, Sarita, Varun Bhardwaj, Santosh Kar, and Deepika Saraswat. Chronic hypobaric hypoxia induces right ventricular hypertrophy and apoptosis in rats: therapeutic potential of nanocurcumin in improving adaptation. High Alt Med Biol. 17:342-352, 2016.-a sustained work load on the right heart on ascent to high altitudes promotes right ventricular hypertrophy (RVH), which eventually undergoes decompensation and promotes pathological damage. However, the exact set of events leading to damage remains unidentified. Curcumin is a natural antioxidant and antihypertrophic agent, but it has poor biostability. Nanotized curcumin (nanocurcumin) has emerged as a promising agent with improved biostability while retaining the therapeutic properties of curcumin. The present study aimed at analyzing the therapeutic properties of nanocurcumin in ameliorating cardiac damage due to chronic hypobaric hypoxia (HH)-induced RVH in comparison to curcumin. Sprague-Dawley rats exposed to HH (25,000 feet, effective oxygen fraction in air [FO] ?0.08, temperature 28°C ± 1°C, relative humidity 55%?±?2% for 3, 7, 14, and 21 days) developed RVH with increased interstitial collagen content, Fulton's index, and cardiomyocyte cross-sectional area while upregulating atrial natriuretic peptide. Tissue damage due to apoptotic cell death was evident by cytochrome-c/caspase-3 activation and TUNEL assay. Concomitant modulation of cyclic guanosine monophosphate (cGMP)/cGK-1, calmodulin-dependent protein kinase II (CaMkinase II), and intracellular calcium levels with increased free radical-induced damage and lipid peroxidation further contributed to the right heart pathology. Nanocurcumin supplementation decreased HH-induced RVH and apoptosis while modulating cardiac cGMP/cGK-1 signaling, and maintaining CaMkinase II, intracellular calcium levels and redox status better than curcumin. Nanocurcumin-mediated antiapoptotic effects might have benefited residents and sojourners at high altitude in preventing hypoxic cardiac damage.

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http://dx.doi.org/10.1089/ham.2016.0032DOI Listing
December 2016
220 Reads
1.854 Impact Factor

Nanocurcumin accords protection against acute hypobaric hypoxia induced lung injury in rats.

J Physiol Biochem 2016 Dec 17;72(4):763-779. Epub 2016 Aug 17.

Experimental Biology Division, Department of Experimental Biology, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Lucknow Road, Timarpur, New Delhi-54, India.

Decline in oxygen availability experienced under hypobaric hypoxia (HH) mediates imbalance in lung fluid clearance and is a causative agent of acute lung injury. Here, we investigate the pathological events behind acute HH mediated lung injury and assess the therapeutic efficacy of nanocurcumin in its amelioration. We assess the protective efficacy of nanotized curcumin (nanocurcumin) in ameliorating HH induced lung injury and compare to curcumin. Rats exposed to acute HH (6, 12, 24, 48 and 72 h) were subjected to histopathology, blood-gas analysis and clinical biochemistry, cytokine response and redox damage. HH induced lung injury was analysed using markers of lung injury due to pulmonary vasoconstriction (ET-1/2/3 and endothelin receptors A and B) and trans-vascular fluid balance mediator (Na+/K+ ATPase). The protective efficacy of nanocurcumin was analysed by examination of Akt/Erk signalling cascade by western blot. HH induced lung injury was associated with discrete changes in blood analytes, differential circulatory cytokine response and severe pulmonary redox damages. Up-regulation of ET-1/2/3 and its receptors along with down-regulation of Na+/K+ ATPase confirmed defective pulmonary fluid clearance which promoted edema formation. Nanocurcumin treatment prevented lung edema formation and restored expression levels of ET-1/2/3 and its receptors while restoring the blood analytes, circulatory cytokines and pulmonary redox status better than curcumin. Modulation in Akt/Erk signalling pathway in rat lungs under HH confirmed the protective efficacy of nanocurcumin.

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http://dx.doi.org/10.1007/s13105-016-0515-3DOI Listing
December 2016
100 Reads
2.736 Impact Factor

Nanocurcumin Prevents Hypoxia Induced Stress in Primary Human Ventricular Cardiomyocytes by Maintaining Mitochondrial Homeostasis.

PLoS One 2015 25;10(9):e0139121. Epub 2015 Sep 25.

Experimental Biology Division, Department of Experimental Biology, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Timarpur, New Delhi, India.

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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0139121PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4583454PMC
June 2016
96 Reads
3.234 Impact Factor

Nanocurcumin protects cardiomyoblasts H9c2 from hypoxia-induced hypertrophy and apoptosis by improving oxidative balance.

J Physiol Biochem 2015 Jun 7;71(2):239-51. Epub 2015 Apr 7.

Experimental Biology Division, Department of Experimental Biology, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, Lucknow Road, Timarpur, New Delhi, India.

Hypoxia-induced cardiomyocyte hypertrophy is evident; however, the distinct molecular mechanism underlying the oxidative stress-mediated damages to cardiomyocytes remains unknown. Curcumin (diferuloylmethane) is known for anti-hypertrophic effects, but low bioavailability makes it unsuitable to exploit its pharmacological properties. We assessed the efficacy of nanotized curcumin, i.e. nanocurcumin, in ameliorating hypoxia-induced hypertrophy and apoptosis in H9c2 cardiomyoblasts and compared it to curcumin. H9c2 cardiomyoblasts were challenged with 0.5 % oxygen, for 24 h to assess hypoxia-induced oxidative damage, hypertrophy and consequent apoptosis. The molecular mechanism underlying the protective efficacy of nanocurcumin was evaluated in regulating Raf-1/Erk-1/2 apoptosis by caspase-3/-7 pathway and oxidative stress. Nanocurcumin ameliorated hypoxia-induced hypertrophy and apoptosis in H9c2 cells significantly (p???0.01), by downregulating atrial natriuretic factor expression, caspase-3/-7 activation, oxidative stress and stabilizing hypoxia-inducible factor-1? (HIF-1?) better than curcumin. Nanocurcumin provides insight into its use as a potential candidate in curing hypoxia-induced cardiac pathologies by restoring oxidative balance.

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http://dx.doi.org/10.1007/s13105-015-0405-0DOI Listing
June 2015
128 Reads
15 Citations
2.736 Impact Factor

Novel vascular endothelial growth factor blocker improves cellular viability and reduces hypobaric hypoxia-induced vascular leakage and oedema in rat brain.

Clin Exp Pharmacol Physiol 2015 May;42(5):475-84

Department of Experimental Biology, Defence Institute of Physiology and Allied Science, Defence Research and Development Organization, New Delhi, India.

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http://dx.doi.org/10.1111/1440-1681.12387DOI Listing
May 2015
101 Reads

Amlodipine protects rat ventricular cardiomyoblast H9c2 From hypoxia-induced apoptosis and restores oxidative balance by Akt-1-dependent manner.

J Cardiovasc Pharmacol 2014 Oct;64(4):375-84

*Defence Research and Development Organization, New Delhi, India; and †Department of Experimental Biology, Defence Institute of Physiology and Allied Science.

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http://pdfs.journals.lww.com/cardiovascularpharm/2014/10000/
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http://dx.doi.org/10.1097/FJC.0000000000000130DOI Listing
October 2014
14 Reads
2.135 Impact Factor

In-silico screening and in-vitro validation of Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2) inhibitors.

Bioinformation 2014 20;10(5):273-80. Epub 2014 May 20.

Division of Applied Sciences & IRCB, Indian Institute of Information Technology, Deoghat, Jhalwa, Allahabad-12, India.

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http://dx.doi.org/10.6026/97320630010273DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070036PMC
June 2014
26 Reads