The hepatoprotective potential of resveratrol in an experimental model of ruptured abdominal aortic aneurysm via oxidative stress and apoptosis

Abstract

The mortality rate in ruptured abdominal aortic aneurysms can today be reduced through cardiovascular surgery. However, ischemia and reperfusion‐induced tissue damage develop due to aortic cross‐clamping applied during surgery. The present study aimed to reduce oxidative stress‐induced hepatic damage resulting from ischemia and reperfusion due to aortic cross‐clamping during surgery by means of resveratrol administration. Forty male Sprague–Dawley rats were randomly assigned into four groups: control (healthy), glycerol+ischemia/reperfusion (I/R) (sham), I/R, and I/R + Resveratrol. In all groups scheduled for I/R, 60 min of shock was followed by 60 min of ischemia. In the I/R + Resveratrol group, 10 mg/kg of resveratrol was administered 15 min before ischemia and immediately before reperfusion via the intraperitoneal route. In addition, 120 min of reperfusion was applied under anesthesia after ischemia in all groups. Intralobar and interlobar necrosis, vascular congestion, and edematous fields resulting from aortic occlusion were present. Liver tissue malondialdehyde (MDA) levels and cleaved caspase‐3 positivity increased, while glutathione (GSH) levels decreased. However, resveratrol administration reduced intralobular and interlobar necrosis, vascular congestion and edematous fields, cleaved caspase‐3 positivity, and MDA levels, and increased GSH levels. Our findings suggest that resveratrol is effective against aortic occlusion‐induced liver injury by reducing oxidative stress and apoptosis.

Resveratrol inhibits the inflammatory response and oxidative stress induced by uterine ischemia reperfusion injury by activating PI3K-AKT pathway

“…Results of a previous study demonstrated that RSV may decrease the levels of peroxylipids, increase the activity of SOD and reduce the water content in rat brain tissues subjected to cerebral I/R, demonstrating a positive protective effect on cerebral I/R injury [31]. RSV administration also reduced the levels of cleaved caspase-3 and MDA, suggesting that RSV may be effective against liver I/R injury by reducing oxidative stress and apoptosis [32]. In addition, RSV demonstrated strong cardio-protective and anti-PLOS ONE arrhythmic effects following myocardial I/R, as indicated by the levels of CAT, SOD, MDA and glutathione peroxidase [33].…”

Cellular senescence and abdominal aortic aneurysm: From pathogenesis to therapeutics

“…to remove excessive ROS and reducing mitochondrial damage to protect cellular senescence and AAA (136,137). In addition, mdivi1, an inhibitor of Drp1, can also effectively maintain mitochondrial integrity and reduce vascular senescence (132,138).…”

“…The therapies that improve mitochondrial function by exogenous supplementation of their precursors, such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), have been demonstrated to be effective in the treatment of CVDs in vivo experiments ( 134 , 135 ). The natural compound resveratrol not only acts as an activator of SIRT1, but also acts as an antioxidant, helping to remove excessive ROS and reducing mitochondrial damage to protect cellular senescence and AAA ( 136 , 137 ). In addition, mdivi1, an inhibitor of Drp1, can also effectively maintain mitochondrial integrity and reduce vascular senescence ( 132 , 138 ).…”

Resveratrol Attenuates Degeneration and Apoptosis of Cardiomyocytes Induced by Aortic Clamping

“…No marked improvement has still been achieved in mortality rates in rAAA, which remains an important cause of mortality in men over 65 years old [ 1 ] . Also considering those patients who die with correct diagnoses before reaching the cardiovascular surgery team, rAAA is a much more important health problem than currently believed [ 2 ] . In rAAA, hypovolemic shock, which usually develops due to bleeding from the retroperitoneum, and sometimes into the abdomen, causes widespread perfusion disturbance in the entire body.…”

“…The essential mechanisms of IRI are free oxygen radical (FOR) formation, a decrease in antioxidant enzymes, lipid peroxidation, neutrophil activation, and caspase-3-induced apoptosis. Myocardial injury caused by IRI is one of the main causes of death in the early postoperative period in patients undergoing rAAA surgery [ 2 , 3 ] . It has been suggested that a significant proportion of problems emerging during intensive care follow-up immediately after surgery develop due to myocardial dysfunction and that myocardial functions, therefore, need to be preserved for recovery [ 3 ] .…”