Staff Members - Benha University
Coenzyme Q10 supplementation mitigates piroxicam-induced oxidative injury and apoptotic pathways in the stomach, liver, and kidney
biomedicine and pharmacotherapy • 2020
Publication Information
Authors
Ahmed Abdeen a,b,*, Afaf Abdelkader b,c, Dina Elgazzar d, Mohamed Aboubakr e,
Omnia A. Abdulah f, Khaled Shoghy g, Mohamed Abdel-Daim h,i, Hamed A. El-Serehy h,
Agnieszka Najda j, Amany El-Mleeh k
Keywords
NSAIDs
Nephrotoxicity
Hepatotoxicity
Gastric ulcer
Oxidative stress
COVID-19
Journal
biomedicine and pharmacotherapy
Publisher
Elsevier
Volume
130
Issue
Not Available
Pages
110627
publication.type
International
Paper Link
Open Link
Supplementary Materials
Not Available
Abstract
Piroxicam (PM) is an oxicam-NSAID commonly recommended for various pain and associated inflammatory
disorders. However, it is reported to have a gastric and hepato-renal toxic effect. Therefore, the current research
was planned to investigate the possible mechanisms behind the mitigating action of the coenzyme (CoQ10), a
natural, free radical scavenger, against PM tissue injury. Rats were assigned to five equal groups; Control, CoQ10
(10 mg/kg, orally), PM (7 mg/kg, i.p.), CoQ + PM L, and CoQ + PM H group. After 28 days, PM provoked severe
gastric ulceration and marked liver and kidney damage indicated by an elevated gastric ulcer index and
considerable alteration in liver and kidney biochemical tests. The toxic effects might be attributed to mitochondrial
dysfunction and excess generation of reactive oxygen species (ROS), as indicated by enhanced
malondialdehyde (MDA) levels along with decreased reduced-glutathione (GSH) levels and catalase (CAT) activity.
Apoptotic cell death also was demonstrated by increased regulation of activated caspase-3 in the stomach,
liver, and kidney tissues. Interestingly, external supplementation of CoQ10 attenuated the PM-inflicted deleterious
oxidative harm and apoptosis. This ameliorative action was ascribed to the free radical scavenging activity
of CoQ10.
disorders. However, it is reported to have a gastric and hepato-renal toxic effect. Therefore, the current research
was planned to investigate the possible mechanisms behind the mitigating action of the coenzyme (CoQ10), a
natural, free radical scavenger, against PM tissue injury. Rats were assigned to five equal groups; Control, CoQ10
(10 mg/kg, orally), PM (7 mg/kg, i.p.), CoQ + PM L, and CoQ + PM H group. After 28 days, PM provoked severe
gastric ulceration and marked liver and kidney damage indicated by an elevated gastric ulcer index and
considerable alteration in liver and kidney biochemical tests. The toxic effects might be attributed to mitochondrial
dysfunction and excess generation of reactive oxygen species (ROS), as indicated by enhanced
malondialdehyde (MDA) levels along with decreased reduced-glutathione (GSH) levels and catalase (CAT) activity.
Apoptotic cell death also was demonstrated by increased regulation of activated caspase-3 in the stomach,
liver, and kidney tissues. Interestingly, external supplementation of CoQ10 attenuated the PM-inflicted deleterious
oxidative harm and apoptosis. This ameliorative action was ascribed to the free radical scavenging activity
of CoQ10.