Carbenoxolone Attenuates Renal Ischemia-Reperfusion Injury in Rats by Modulating Inflammatory Cytokines, Oxidative Stress Markers, and Apoptotic Pathways
1
Collage of Pharmacy, The Islamic University, Najaf, Iraq, Iraq
2
Department of Pharmacology and Toxicology, College of Pharmacy, University of Babylon, Iraq, Iraq
Submission date: 2025-03-15
Final revision date: 2025-07-13
Acceptance date: 2025-08-29
Publication date: 2025-10-30
Corresponding author
Wiadomości Lekarskie 2025;(10):2034-2044
KEYWORDS
TOPICS
ABSTRACT
Aim:
Background: Ischemia/reperfusion injury (IRI) is a major cause of kidney damage, primarily driven by oxidative stress and inflammation. Aims: This study investigates the protective effects of Carbenoxolone (Cbx) in attenuating renal injury through the modulation of the FOXO3 gene.
Material and methods:
Materials and methods: Twenty-eight adult male Wistar Albino rats were randomly divided into four groups (N=7): Sham (laparotomy without ischemia), Control (bilateral renal ischemia for 30 min followed by 2 h reperfusion), Vehicle (DMSO injection prior to IRI), and Carbenoxolone-treated (Cbx injection three days before IRI).
Results:
Results: Tissue levels of TNF-α, IL-1β, MDA, Caspase-3, and KIM-1 were significantly elevated in the control and vehicle groups, while GSH levels were reduced. Cbx treatment significantly decreased TNF-α, IL-1β, MDA, Caspase-3, and KIM-1 while increasing GSH levels, indicating enhanced antioxidant defense. FOXO3 expression was notably lower in the Cbx group compared to the control and vehicle groups. Histopathological analysis further confirmed reduced renal damage in Cbx-treated rats. These findings suggest that Cbx exerts renoprotective effects by mitigating oxidative stress, inflammation, and apoptosis.
Conclusions:
Conclusion: Carbenoxolone significantly reduces RIRI-induced kidney damage, demonstrating its potential as a therapeutic agent for renal ischemic injuries.
Background: Ischemia/reperfusion injury (IRI) is a major cause of kidney damage, primarily driven by oxidative stress and inflammation. Aims: This study investigates the protective effects of Carbenoxolone (Cbx) in attenuating renal injury through the modulation of the FOXO3 gene.
Material and methods:
Materials and methods: Twenty-eight adult male Wistar Albino rats were randomly divided into four groups (N=7): Sham (laparotomy without ischemia), Control (bilateral renal ischemia for 30 min followed by 2 h reperfusion), Vehicle (DMSO injection prior to IRI), and Carbenoxolone-treated (Cbx injection three days before IRI).
Results:
Results: Tissue levels of TNF-α, IL-1β, MDA, Caspase-3, and KIM-1 were significantly elevated in the control and vehicle groups, while GSH levels were reduced. Cbx treatment significantly decreased TNF-α, IL-1β, MDA, Caspase-3, and KIM-1 while increasing GSH levels, indicating enhanced antioxidant defense. FOXO3 expression was notably lower in the Cbx group compared to the control and vehicle groups. Histopathological analysis further confirmed reduced renal damage in Cbx-treated rats. These findings suggest that Cbx exerts renoprotective effects by mitigating oxidative stress, inflammation, and apoptosis.
Conclusions:
Conclusion: Carbenoxolone significantly reduces RIRI-induced kidney damage, demonstrating its potential as a therapeutic agent for renal ischemic injuries.
| eISSN: | 2719-342X |
| ISSN: | 0043-5147 |
We process personal data collected when visiting the website. The function of obtaining information about users and their behavior is carried out by voluntarily entered information in forms and saving cookies in end devices. Data, including cookies, are used to provide services, improve the user experience and to analyze the traffic in accordance with the Privacy policy. Data are also collected and processed by Google Analytics tool (more).
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
You can change cookies settings in your browser. Restricted use of cookies in the browser configuration may affect some functionalities of the website.
