Protective Effects and Mechanisms of Flavonoids in Renal Ischemia-Reperfusion Injury

Peng, Peng; Zou, Junrong; Zhong, B.; Zhang, Guoxi; Zou, Xiaofeng; Xie, Ting

doi:10.1159/000527262

Cited by 20 publications

(9 citation statements)

References 78 publications

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“…Administering RAL prior to ischemia induction resulted in a reduction in serum levels of urea and creatinine. This outcome is consistent with findings from other studies [34], which can be attributed to the anti-inflammatory impact of RAL, manifested by a significant downregulation of TNF-α and other cytokines in renal parenchymal cells [35].…”

Section: Discussionsupporting

confidence: 92%

The potential renoprotective effect of Raloxifene in renal ischemia-reperfusion injury in a male rat model

Hadi,

Ali,

Altimimi

2023

JMedLife

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Renal ischemia-reperfusion injury is caused by a temporary reduction in oxygen-carrying blood flow to the kidney, followed by reperfusion. During ischemia, kidney tissue damage induces overproduction of reactive oxygen species, which produces oxidative stress. The blood flow restoration during the reperfusion period causes further production of reactive oxygen species that ends with apoptosis and cell death. This study aimed to investigate the potential renoprotective effects of Raloxifene on bilateral renal ischemia-reperfusion injury in rats by looking into kidney function biomarkers, urea and creatinine, inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Additionally, antioxidant markers such as total antioxidant capacity (TAC) and the pro-apoptotic marker caspase-3 were assessed. Histopathological scores were also employed for evaluation. Our experimental design involved 20 rats divided into four groups: the sham group underwent median laparotomy without ischemia induction, the control group experienced bilateral renal ischemia for 30 minutes followed by 2 hours of reperfusion, the vehicle group received pretreatment with a mixture of corn oil and dimethyl sulfoxide (DMSO) before ischemia induction, and the Raloxifene-treated group was administered Raloxifene at a dose of 10 mg/kg before ischemia induction, followed by ischemia-reperfusion. Urea and creatinine, TNF-α, IL-1β, and caspase-3 in the Raloxifene group were significantly lower compared to the control and vehicle groups. On the other hand, TAC levels in the Raloxifene group were significantly higher than in the control and vehicle groups. This study concluded that Raloxifene had a renoprotective impact via multiple actions as an anti-inflammatory, anti-apoptotic, and antioxidant agent.

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Section: Discussionsupporting

confidence: 92%

The potential renoprotective effect of Raloxifene in renal ischemia-reperfusion injury in a male rat model

Hadi,

Ali,

Altimimi

2023

JMedLife

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“…The role of oxidative stress in the induction of organ damage following ischemia‒reperfusion has been thoroughly described in the literature [ 25 ]. However, the full molecular mechanisms underlying oxidative stress damage still need to be explored.…”

Section: Discussionmentioning

confidence: 99%

Impact of folic acid supplementation on ischemia‒reperfusion-induced kidney injury in rats: folic acid prophylactic role revisited

Hamed,

Khedr,

Ghonamy

et al. 2024

J Physiol Sci

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Folic acid (FA), with its anti-inflammatory and antioxidant properties, may offer protection against ischemia–reperfusion (IR) injury. This study investigated whether FA safeguards rat kidneys from IR by targeting high mobility group box-1 (HMGB1), a key inflammatory mediator. Fifty adult male Wistar rats were randomly allocated into four groups: control, IR, IR + FA pretreatment, and FA alone. Compared to controls, IR significantly impaired renal function and elevated levels of malondialdehyde, HMGB1, NF-κB, and caspase 3. FA pretreatment effectively reversed these detrimental changes, protecting renal function and minimizing tissue damage. The FA-alone group showed no significant differences compared to the control group, indicating no adverse effects of FA treatment. Mechanistically, FA inhibited HMGB1 expression and its downstream activation of NF-κB and caspase 3, thereby quelling inflammation and cell death. FA shields rat kidneys from IR-induced injury by suppressing HMGB1-mediated inflammation and apoptosis, suggesting a potential therapeutic avenue for IR-associated kidney damage.

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“…Furthermore, researchers reported that intraperitoneal administration of fisetin (20 mg/kg) 15 minutes before surgery attenuated I/R-induced mitochondrial dysfunction, restored mitochondrial copy number, modulated Pgc1 gene expression, reduced mitochondrial fission, enhanced mitochondrial fusion, and promoted mitochondrial autophagy. These actions collectively counteracted the I/R-related reduction in mitochondrial mass in renal tissue (72).…”

Section: Anothermentioning

confidence: 92%

Antioxidant Mechanisms in Myocardial Ischemia: Narrative Review

Sadeghi,

Abedi,

Atashpour

et al. 2023

Multidiscip Cardio Annal

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: Ischemia is a common condition in the population and has become one of the leading causes of mortality in recent years. It occurs due to a shortage of oxygen in the cell caused by inadequate blood flow, leading to the formation of free radicals. These free radicals can bind to the phospholipids in the cell membrane, resulting in proxy radicals and lipid hydroperoxidation. Malondialdehyde (MDA) is a cytotoxic byproduct of lipid peroxidation that causes cell damage and necrosis by rupturing the cell membrane. Subsequently, mitochondrial dysfunction related to fatty acid oxidation can develop, further exacerbating the damage caused by ischemia. Reactive oxygen species (ROS) produced in mitochondria have been shown to elevate oxidative phosphorylation disorder and disrupt the functioning of complexes I and IV. These enzyme activities can be restored to normal levels by activating antioxidant enzymes such as superoxide dismutase (Mn-SOD) and catalase, thereby strengthening the antioxidant defense system. Various antioxidants have been found to have protective effects. In this review, we compare the antioxidant effects of various plants and tannins that have been studied up to this point on myocardial ischemia. We also explain some of the cellular and molecular pathways that have been investigated to protect the myocardium against ischemia-reperfusion injury.

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Protective Effects and Mechanisms of Flavonoids in Renal Ischemia-Reperfusion Injury

Cited by 20 publications

References 78 publications

The potential renoprotective effect of Raloxifene in renal ischemia-reperfusion injury in a male rat model

The potential renoprotective effect of Raloxifene in renal ischemia-reperfusion injury in a male rat model

Impact of folic acid supplementation on ischemia‒reperfusion-induced kidney injury in rats: folic acid prophylactic role revisited

Antioxidant Mechanisms in Myocardial Ischemia: Narrative Review

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