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Rami B. Kassab

Researcher at Al Baha University

Publications -  62
Citations -  1362

Rami B. Kassab is an academic researcher from Al Baha University. The author has contributed to research in topics: Oxidative stress & Glutathione peroxidase. The author has an hindex of 16, co-authored 47 publications receiving 678 citations. Previous affiliations of Rami B. Kassab include Helwan University & Modern Sciences and Arts University.

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The potential protective effect of Physalis peruviana L. against carbon tetrachloride-induced hepatotoxicity in rats is mediated by suppression of oxidative stress and downregulation of MMP-9 expression.

TL;DR: The results show that the potential hepatoprotective effects of Physalis peruviana may be due to physalis acts by promotion of processes that restore hepatolobular architecture and through the inhibition of oxidative stress pathway.
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Antagonistic Efficacy of Luteolin against Lead Acetate Exposure-Associated with Hepatotoxicity is Mediated via Antioxidant, Anti-Inflammatory, and Anti-Apoptotic Activities.

TL;DR: The findings describe the potential mechanisms involved in the alleviation of PbAc-induced liver injury by luteolin via its potent anti-inflammatory, antioxidant, and anti-apoptotic properties and how LUT supplementation significantly reversed all of the tested parameters in comparison with the Pb Ac-exposed group.
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Selenium Nanoparticles Pre-Treatment Reverse Behavioral, Oxidative Damage, Neuronal Loss and Neurochemical Alterations in Pentylenetetrazole-Induced Epileptic Seizures in Mice.

TL;DR: SeNPs were found to provide neuroprotection through preventing the development of oxidative challenge via the upregulation of Nrf2 and HO-1, inhibiting the inflammatory response and apoptotic cascade, and reversed the changes in the activity and levels of neuromodulators following the developing of epileptic seizures.
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The role of thymoquinone as a potent antioxidant in ameliorating the neurotoxic effect of sodium arsenate in female rat

TL;DR: Thymoquinone ameliorated the neurotoxic effect of arsenate and suppressed the oxidative stress induced in the nervous system through its antioxidant mechanism, in rats treated with TQ.
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The Neuroprotective Role of Coenzyme Q10 Against Lead Acetate-Induced Neurotoxicity Is Mediated by Antioxidant, Anti-Inflammatory and Anti-Apoptotic Activities

TL;DR: Treatment with CoQ10 rescued cortical neurons from PbAc-induced neurotoxicity by restoring the balance between oxidants and antioxidants, activating the Nrf2/HO-1 pathway, suppressing inflammation, inhibiting the apoptotic cascade, and modulating cortical neurotransmission and energy metabolism.