Ashif Iqubal

TL;DR: The fact that metabolites of CP are responsible for cardiotoxicity due to depletion of antioxidants/ATP level, altered contractility, damaged endothelium and enhanced pro‐inflammatory/pro‐apoptotic activities resulting into cardiomyopathy, myocardial infarction, and heart failure is supported.

TL;DR: In the current review, various sources of pollutants and exposure to the human population, developmental neurotoxicity, and molecular mechanism of different pollutants involved in the pathogenesis of different neurological disorders have been discussed.

TL;DR: This extensive review focuses on functional aspects governed by Silibinin in chemopreventive potential and clinical trials that are currently ongoing, at a single platform.

TL;DR: Findings of the study suggested that NER is a potential therapeutic molecule which can mitigate CP-induced neurotoxic manifestations via Nrf2 and NF-κB pathway, however, more detailed studies are needed to explicate the mechanism underlying its neuroprotective effect.

TL;DR: Nimodipine and vinpocetine both showed cardioprotection when given alone and their combination showed better restoration in terms of oxidative stress, cardiac membrane damage, haemodynamics, histopathology and ultrastructural changes in the heart.