Publications

Journal Article Review Ppublish 37 citations

PubMed: 36418600 DOI: 10.1007/s10787-022-01087-8

Targeting of neuroinflammation by glibenclamide in Covid-19: old weapon from arsenal.

Inflammopharmacology 31(1):1-7

Authors: Gaber El-Saber Batiha, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Mubarak Alruwaili, Raed AlRuwaili, Sarah M Albogami, Mohammed Alorabi, Hebatallah M Saad, Jesus Simal-Gandara

Affiliations

  • Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, AlBeheira, Egypt.
  • Professor in department of clinical pharmacology and medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
  • Department of Internal Medicine, College of Medicine, Jouf University, Sakaka, Saudi Arabia.
  • Department of Biotechnology, College of Science, Taif University, P.O.Box 11099, Taif, 21944, Saudi Arabia.
  • Department of Pathology, Faculty of Veterinary Medicine, Matrouh University, Marsa Matruh, 51744, Egypt.
  • Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Universidade de Vigo, E-32004, Ourense, Spain.

Abstract

In coronavirus disease 2019 (Covid-19) era, neuroinflammation may develop due to neuronal tropism of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) and/or associated immune activation, cytokine storm, and psychological stress. SARS-CoV-2 infection and linked cytokine storm may cause blood-brain barrier (BBB) injury through which activated immune cells and SARS-CoV-2 can pass into the brain causing activation of glial cells with subsequent neuroinflammation. Different therapeutic regimens were suggested to alleviate Covid-19-induced neuroinflammation. Since glibenclamide has anti-inflammatory and neuroprotective effects, it could be effective in mitigation of SARS-CoV-2 infection-induced neuroinflammation. Glibenclamide is a second-generation drug from the sulfonylurea family, which acts by inhibiting the adenosine triphosphate (ATP)-sensitive K channel in the regulatory subunit of type 1 sulfonylurea receptor (SUR-1) in pancreatic β cells. Glibenclamide reduces neuroinflammation and associated BBB injury by inhibiting the nod-like receptor pyrin 3 (NLRP3) inflammasome, oxidative stress, and microglial activation. Therefore, glibenclamide through inhibition of NLRP3 inflammasome, microglial activation, and oxidative stress may attenuate SARS-CoV-2-mediated neuroinflammation.

MeSH

Infections, Oxidative Stress, Stress, Physiological, Cells, Glyburide, Blood-Brain Barrier, Coronavirus, Weapons, Nlr Proteins, Covid-19, Sars-Cov-2

Cited by