Sreya Chattopadhyay

ORCID: 0000-0002-1898-4437
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About
Contact & Profiles
Research Areas
  • Nanoparticle-Based Drug Delivery
  • Nigella sativa pharmacological applications
  • Immune Cell Function and Interaction
  • Arsenic contamination and mitigation
  • Tea Polyphenols and Effects
  • Cell death mechanisms and regulation
  • Pomegranate: compositions and health benefits
  • Tryptophan and brain disorders
  • Exercise and Physiological Responses
  • Crystallization and Solubility Studies
  • X-ray Diffraction in Crystallography
  • Bioactive Compounds and Antitumor Agents
  • Cardiovascular and exercise physiology
  • Autophagy in Disease and Therapy
  • Nanoplatforms for cancer theranostics
  • Psoriasis: Treatment and Pathogenesis
  • RNA Interference and Gene Delivery
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Circadian rhythm and melatonin
  • Diet, Metabolism, and Disease
  • Chemotherapy-induced organ toxicity mitigation
  • Phytoestrogen effects and research
  • Immune Response and Inflammation
  • T-cell and B-cell Immunology
  • Heavy Metal Exposure and Toxicity

University of Calcutta
2016-2025

University of Engineering & Management
2018

Bose Institute
2000-2013

Indian Institute of Management Calcutta
2000-2002

Cationic Mesoporous silica Nanoparticle coated with hyaluronic acid conjugated polymer (HA-Dual miRNA Np) facilitated enhanced dual loading, efficient delivery and significantly inhibited tumor growth as well retarded metastasis in triple-negative breast cancer.

10.1039/d0bm00015a article EN Biomaterials Science 2020-01-01

The detailed molecular mechanism of transferrin-tagged thymoquinone nanoparticle mediated apoptotic induction in non-small cell lung carcinoma showing the involvement p53 dependent synergistic activation miR-34a and miR-16 pathway.

10.1039/c9bm00912d article EN Biomaterials Science 2019-01-01

Age-related macular degeneration (AMD) is a complex and progressive degenerative eye disease resulting in severe loss of central vision. Recent evidence indicates that immune system dysregulation could contribute to the development AMD. We hypothesize defective lysosome-mediated clearance causes accumulation waste products retinal pigmented epithelium (RPE), activating leading tissue injury have generated unique genetically engineered mice which (both by phagocytosis autophagy) RPE cells...

10.1002/path.4870 article EN The Journal of Pathology 2016-12-27

Pal, S, Chaki, B, Chattopadhyay, and Bandyopadhyay, A. High-intensity exercise induced oxidative stress skeletal muscle damage in post-pubertal boys girls: a comparative study. J Strength Cond Res 32(4): 1045-1052, 2018-The purpose of this study was to examine the sex variation high-intensity among 44 sedentary postpubertal girls through estimation postexercise release pattern markers like creatine kinase, lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate (AST) extent...

10.1519/jsc.0000000000002167 article EN The Journal of Strength and Conditioning Research 2017-08-01

The mechanistic target of rapamycin (mTOR) complexes 1 and 2 (mTORC1/2) are crucial for various physiological functions. Although the role mTORC1 in retinal pigmented epithelium (RPE) homeostasis age-related macular degeneration (AMD) pathogenesis is established, function mTORC2 remains unclear. We investigated both RPE health disease. Therefore, this study, we have attempted to demonstrate that specific overexpression mammalian lethal with Sec13 protein 8 (mLST8) mouse activates mTORC2,...

10.1111/acel.70018 article EN cc-by Aging Cell 2025-02-17

Failure of treatment for cancer in clinic by radio/chemotherapy is generally attributed to tumour resistance. Therefore, it important develop strategies increase the cytotoxicity cells radiation combination with unique selective cytotoxic agents. We evaluated potential ellagic acid (EA) as an enhancer oxidative stress cells. HepG2 were treated EA (10 µM) 12 h prior exposure single 7.5 Gy dose irradiation. Treatment and gamma showed increased reactive oxygen species generation, up regulation...

10.1038/s41598-017-14211-4 article EN cc-by Scientific Reports 2017-10-19

Tumor suppressor p53 plays the central role in regulating apoptosis response to genotoxic stress. From an evolutionary perspective, activity of has be backed up by other protein(s) case any functional impairment this protein, trigger DNA damage-induced cancer cells. We adopted multiple experimental approaches demonstrate that p53-impaired cells, damage caused accumulation paralogue p73 via Chk-1 strongly impacted Bax expression and p53-independent apoptosis. On contrary, when function was...

10.1074/jbc.m110.122705 article EN cc-by Journal of Biological Chemistry 2010-07-31
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