P
Pabitra Bikash Pal
Researcher at Bose Institute
Publications - 21
Citations - 1962
Pabitra Bikash Pal is an academic researcher from Bose Institute. The author has contributed to research in topics: Oxidative stress & Apoptosis. The author has an hindex of 14, co-authored 18 publications receiving 1527 citations. Previous affiliations of Pabitra Bikash Pal include University of Texas Medical Branch.
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Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis
TL;DR: This review highlights the basic mechanisms of ROS production and their sites of formation; detail mechanism of both mitochondria-dependent and mitochondrial-independent pathways of apoptosis as well as their regulation by ROS and describes the involvement of oxidative stress under various environmental toxin- and drug-induced organ pathophysiology and diabetes-mediated apoptosis.
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Mangiferin Attenuates Diabetic Nephropathy by Inhibiting Oxidative Stress Mediated Signaling Cascade, TNFα Related and Mitochondrial Dependent Apoptotic Pathways in Streptozotocin-Induced Diabetic Rats
TL;DR: Mangiferin treatment, post to hyperglycemia, successfully inhibited all of these changes and protected the cells from apoptotic death and prevented oxidative stress related parameters, increased ROS production and decreased the intracellular antioxidant defenses in the kidney.
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Morin protects gastric mucosa from nonsteroidal anti-inflammatory drug, indomethacin induced inflammatory damage and apoptosis by modulating NF-κB pathway.
TL;DR: Morin reversed all the adverse effects to prevent IND-induced gastric ulceration in a PGE2 independent manner and is primarily attributed to its potent antioxidant nature that also helps in controlling severalIND-induced inflammatory responses.
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Mangiferin, a natural xanthone, protects murine liver in Pb(II) induced hepatic damage and cell death via MAP kinase, NF-κB and mitochondria dependent pathways.
TL;DR: Overall results demonstrate that mangiferin exhibit both antioxidative and antiapoptotic properties and protects the organ in Pb(II) induced hepatic dysfunction.
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Involvement of both intrinsic and extrinsic pathways in hepatoprotection of arjunolic acid against cadmium induced acute damage in vitro
TL;DR: Analysis of cytoprotective role of arjunolic acid against Cd induced oxidative impairment and cell death in murine hepatocytes suggests that Cd-induced hepatic dysfunction and apoptosis might be supported by the ROS formation and mediated via the activation of NF-κB.