Quercetin protects rat skeletal muscle from ischemia reperfusion injury

Akdemir, Fazile Nur Ekinci; Gülçın, İlhami; Karagöz, Berna; Soslu, Recep

doi:10.1080/14756366.2016.1193735

Cited by 45 publications

(26 citation statements)

References 80 publications

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“…The rats were given free access to a standard pellet diet and tap water ad libitum and were acclimated to the laboratory conditions for one week before starting the experiment [24]. They were maintained in standard housing facilities (temperature: 24 ± 1°C, relative humidity range: 45% ± 5%, and a 12 h light/12 h dark cycle).…”

Section: Methodsmentioning

confidence: 99%

Chrysin Protects Rat Kidney from Paracetamol-Induced Oxidative Stress, Inflammation, Apoptosis, and Autophagy: A Multi-Biomarker Approach

et al. 2017

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Paracetamol (PC) is a safe analgesic and antipyretic drug at therapeutic doses, and it is widely used in clinics. However, at high doses, it can induce hepatotoxicity and nephrotoxicity. Chrysin (CR) is a natural flavonoid that has biological activities that include being an antioxidant, an anti-inflammatory, and an anti-cancer agent. The main objective of this study was to investigate the efficacy of CR against PC-induced nephrotoxicity in rats. CR was given orally via feeding needle to male Sprague Dawley rats as a single daily dose of 25 or 50 mg/kg for six days. PC was administered orally via feeding needle as a single dose on the sixth day. PC caused significant glutathione depletion, lipid peroxidation, increased serum toxicity markers (serum urea and creatinine), and reductions in activities of antioxidant enzymes (superoxide dismutase — SOD, catalase — CAT, and glutathione peroxidase — GPx). The renal protective effect of CR was associated with decreasing the regulation of serum renal toxicity markers and increasing the regulation of antioxidant enzyme activities. Additionally, PC led to significant increases in the levels of inflammatory markers including tumour necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-33 (IL-33). Furthermore, PC induced apoptotic tissue damage by increasing cysteine aspartate-specific protease-3 (caspase-3) activity and autophagic tissue damage by increasing the expression of light chain 3B (LC3B). CR therapy significantly decreased these values in rats. This study demonstrated that CR has antioxidant, anti-apoptotic, anti-inflammatory and anti-autophagic effects on PC-induced kidney toxicity in rats.

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Section: Methodsmentioning

confidence: 99%

Chrysin Protects Rat Kidney from Paracetamol-Induced Oxidative Stress, Inflammation, Apoptosis, and Autophagy: A Multi-Biomarker Approach

et al. 2017

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“…PCA and CIS were applied in the PCA + CIS group. All animals were sacrificed under anaesthesia 24 h after CIS administration [34,35,36]. High dose anaesthesia was achieved using thiopental sodium (400 mg/kg b.w.…”

Section: Methodsmentioning

confidence: 99%

The Protective Effects of p-Coumaric Acid on Acute Liver and Kidney Damages Induced by Cisplatin

et al. 2017

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In this study, we aimed to investigate the effects of p-Coumaric acid (PCA) on cisplatin (CIS)-induced hepatotoxicity and nephrotoxicity in Wistar adult rats for 24 h compared to untreated control groups. In this experiment, 40 Wistar adult rats were utilized and divided randomly into five groups. After 24 h of CIS administration, liver and kidneys were harvested and assessed by H&E staining. Also, markers for oxidative stress and antioxidants were analyzed in theses tissues. Compared to the control group, accumulation of malondialdehyde was increased in groups treated CIS, whereas superoxide dismutase activities and glutathione levels were distinctly diminished in this group. The study’s histopathological findings such as hydropic degeneration, vascular congestion, sinusoidal dilatation in hepatocytes and tubular necrosis in kidneys were in accordance with the results of markers for oxidative stress. PCA may prevent hepatotoxicity and nephrotoxicity by increased antioxidant enzymes and reduced oxidant parameters.

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“…In recent years, several studies have demonstrated that H 2 S plays a role in the protection of multiple organs with IRI. H 2 S also effectively relieves IRI of the liver, kidney, lung, brain, and heart . The role of H 2 S in antagonising oxidative stress is increasingly appreciated.…”

Section: Discussionmentioning

confidence: 99%

Effect of hydrogen sulphide on inflammatory factors of the mitochondria after limb ischaemia‐reperfusion injury in rats

Cheng

Zhang

2019

International Wound Journal

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The goal of this study was to evaluate the effect of hydrogen sulphide on inflammatory factors and the energy metabolism of mitochondria after limb reperfusion injury in rats. Sixty Wistar rats were divided into three groups: the sham operated group, the control group (the ischaemia‐reperfusion injury [IRI] + normal saline group), and the experimental group (the IRI + H2S group). An experimental rat model of limb IRI was established. Skeletal muscle samples were collected to observe the content of necrotic products (including myoglobin (MB), lysophosphatidylcholine (LPC), and lipid peroxidation (LPO)); blood samples were collected to observe changes in the contents of interleukin‐1 (IL‐1), Interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α); and the mitochondria of skeletal muscle cells were extracted for mitochondrial transmembrane potential measurement and adenosine triphosphate (ATP) content determination. The results underwent further statistical analysis. The contents of MB, LPC, and LPO in the limb skeletal muscle, liver, lung, and kidney tissues of rats in the control group were significantly increased (P < 0.05) after IRI, which was markedly attenuated by treatment with hydrogen sulphide (P < 0.05). Ischaemia/reperfusion of the lower extremities in rats triggered a significant increase in serum levels of IL‐1, IL‐6, and TNF‐α, which was significantly inhibited by treatment with H2S during ischaemia/reperfusion. In addition, the inhibitory effect tended to be time‐dependent. After limb ischaemia/reperfusion, the mitochondrial transmembrane potential of skeletal muscle cells in the control group decreased significantly (P < 0.05), while the potential energy of the mitochondrial membrane in the experimental group was significantly higher than that in the control group (P < 0.05). The content of ATP in mitochondria of skeletal muscle cells of ischaemia‐reperfusion rats in the control group was significantly lower than that in the sham operated group (P < 0.05), while the content of ATP of mitochondria in the experimental group after H2S treatment was significantly higher than the control group (P < 0.05). Hydrogen sulphide can alleviate the injury of skeletal muscle and distal organs after limb ischaemia‐reperfusion and reduce local inflammatory reaction, which is essential in alleviating mitochondrial transmembrane potential and energy metabolism disorder during reperfusion injury. The purpose of the study is to summarise the available information and provide theoretical support for the application of hydrogen sulphide in the treatment of limb IRI in skeletal muscle and distal organs.

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Quercetin protects rat skeletal muscle from ischemia reperfusion injury

Cited by 45 publications

References 80 publications

Chrysin Protects Rat Kidney from Paracetamol-Induced Oxidative Stress, Inflammation, Apoptosis, and Autophagy: A Multi-Biomarker Approach

Chrysin Protects Rat Kidney from Paracetamol-Induced Oxidative Stress, Inflammation, Apoptosis, and Autophagy: A Multi-Biomarker Approach

The Protective Effects of p-Coumaric Acid on Acute Liver and Kidney Damages Induced by Cisplatin

Effect of hydrogen sulphide on inflammatory factors of the mitochondria after limb ischaemia‐reperfusion injury in rats

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