Browsing by Author "Gourav Chandan"

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Acute Cardiac Events After ChAdOx1 nCoV-19 Corona Virus Vaccine: Report of Three Cases
(Lippincott Williams and Wilkins, 2022) Rohit Singh; Sankha Shubhra Chakrabarti; Indrajeet Singh Gambhir; Ashish Verma; Ishan Kumar; Soumik Ghosh; Ashutosh Tiwari; Gourav Chandan; Sasanka Chakrabarti; Upinder Kaur
[No abstract available]
Effectiveness of ChAdOx1 nCoV-19 vaccine during the delta (B.1.617.2) variant surge in India
(Elsevier Ltd, 2022) Sasanka Chakrabarti; Sankha Shubhra Chakrabarti; Gourav Chandan; Upinder Kaur; Bimal Kumar Agrawal
[No abstract available]
GLUT inhibitor WZB117 induces cytotoxicity with increased production of amyloid-beta peptide in SH-SY5Y cells preventable by beta-hydroxybutyrate: implications in Alzheimer’s disease
(Springer Science and Business Media Deutschland GmbH, 2023) Gourav Chandan; Upasana Ganguly; Soumya Pal; Sukhpal Singh; Reena V. Saini; Sankha Shubhra Chakrabarti; Adesh K. Saini; Sasanka Chakrabarti
Background: Inhibitors of glucose transporters are being explored as potential anti-cancer drugs. Decreased cerebral glucose utilization with reduced levels of several glucose transporters is also an important pathogenic signature of neurodegeneration of Alzheimer’s disease, but its exact role in the pathogenesis of this disease is not established. We explored in an experimental model if inhibitors of glucose transporters could lead to altered amyloid-beta homeostasis, mitochondrial dysfunction, and neuronal death, which are relevant in the pathogenesis of Alzheimer’s disease. Methods: SH-SY5Y cells (human neuroblastoma cell line) were exposed to an inhibitor (WZB117) of several types of glucose transporters. We examined the effects of glucose hypometabolism on SH-SY5Y cells in terms of mitochondrial functions, production of reactive oxygen species, amyloid-beta homeostasis, and neural cell death. The effect of β-hydroxybutyrate in ameliorating the effects of WZB117 on SH-SY5Y cells was also examined. Results: We observed that exposure of SH-SY5Y cells to WZB117 caused mitochondrial dysfunction, increased production of reactive oxygen species, loss of cell viability, increased expression of BACE 1, and intracellular accumulation of amyloid β peptide (Aβ42). All the effects of WZB117 could be markedly prevented by co-treatment with β-hydroxybutyrate. Cyclosporine A, a blocker of mitochondrial permeability transition pore (mPTP) activation, could not prevent cell death caused by WZB117. Conclusion: Results in this neuroblastoma model have implications for the pathogenesis of Alzheimer’s disease and warrant further explorations of WZB117 in primary cultures of neurons and experimental animal models. © 2023, The Author(s) under exclusive licence to Maj Institute of Pharmacology Polish Academy of Sciences.
Protective effects of cyclosporine A on neurodegeneration and motor impairment in rotenone-induced experimental models of Parkinson's disease
(Elsevier B.V., 2022) Sukhpal Singh; Upasana Ganguly; Soumya Pal; Gourav Chandan; Rahul Thakur; Reena V. Saini; Sankha Shubhra Chakrabarti; Bimal K. Agrawal; Sasanka Chakrabarti
The development of neuroprotective drugs targeting mitochondria could be an important strategy in combating the progressive clinical course of Parkinson's disease. In the current study, we demonstrated that in SH-SY5Y cells (human dopaminergic neuroblastoma cell line), rotenone caused a dose-dependent (0.25–1 μM) and time-dependent (up to 48 h) loss of cell viability and a loss of cellular ATP content with mitochondrial membrane depolarization and an increased formation of reactive oxygen species; all these processes were markedly prevented by the mitochondrial permeability transition pore blocker cyclosporine A, which did not affect complex I inhibition by rotenone. The nuclear morphology of rotenone-treated cells for 48 h indicated the presence of both necrosis and apoptosis. We then examined the effects of cyclosporine A on the rotenone-induced model of Parkinson's disease in Wistar rats. Cyclosporine A significantly improved the motor deficits and prevented the loss of nigral dopaminergic neurons projecting into the striatum in rotenone-treated rats. Being a marketed immuno-suppressive drug, cyclosporine A should be further evaluated for its putative neuroprotective action in Parkinson's disease. © 2022 Elsevier B.V.