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Jagriti Bhatia

Researcher at All India Institute of Medical Sciences

Publications -  82
Citations -  2665

Jagriti Bhatia is an academic researcher from All India Institute of Medical Sciences. The author has contributed to research in topics: Oxidative stress & Nephrotoxicity. The author has an hindex of 29, co-authored 75 publications receiving 2050 citations. Previous affiliations of Jagriti Bhatia include University College of Medical Sciences.

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Preventive effect of crocin of Crocus sativus on hemodynamic, biochemical, histopathological and ultrastuctural alterations in isoproterenol-induced cardiotoxicity in rats.

TL;DR: The results suggest that crocin may have cardioprotective effect in ISO-induced cardiac toxicity through modulation of oxidative stress in such a way that maintains the redox status of the cell.
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Up-regulation of PPARγ, heat shock protein-27 and -72 by naringin attenuates insulin resistance, β-cell dysfunction, hepatic steatosis and kidney damage in a rat model of type 2 diabetes

TL;DR: This seminal study provides cogent evidence that naringin ameliorates IR, dyslipidaemia, β-cell dysfunction, hepatic steatosis and kidney damage in type 2 diabetic rats by partly regulating oxidative stress, inflammation and dysregulated adipocytokines production through up-regulation of PPARγ, HSP-27 and H SP-72.
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Apigenin ameliorates streptozotocin-induced diabetic nephropathy in rats via MAPK/NF-κB/TNF-α and TGF-β1/MAPK/Fibronectin pathways

TL;DR: Apigenin ameliorated renal damage due to DN by suppressing oxidative stress and fibrosis and by inhibiting MAPK pathway, which significantly prevented MAPK activation.
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Naringin protects against kainic acid-induced status epilepticus in rats: evidence for an antioxidant, anti-inflammatory and neuroprotective intervention.

TL;DR: The results of this study suggest that naringin has therapeutic potential since it suppresses KA-induced seizures, cognitive impairment and oxidative stress in the brain and is a result of its antioxidant and anti-inflammatory activity.
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Telmisartan ameliorates cisplatin-induced nephrotoxicity by inhibiting MAPK mediated inflammation and apoptosis

TL;DR: Investigating the protective effect of telmisartan in cisplatin-induced nephrotoxicity model in rats showed maximum nephroprotective effect which could be due to maintenance of cellular redox status and inhibition of MAPK activation.