The effect of dexmedetomidine on gastric ischemia reperfusion injury in rats. Biochemical and histopathological evaluation

Kuyrukluyıldız, Ufuk; Delen, Leman Acun; Önk, Didem; Yazıcı, Gülce Naz; Gülaboğlu, Mine; Süleyman, Halis

doi:10.1590/acb360104

Cited by 4 publications

(3 citation statements)

References 22 publications

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“…DEX promoted SOD activity by human blood [28]. It is also reported in studies that DEX also found to prevent oxidative damage by increasing antioxidant potential in ischemic reperfusion injury in rats [54,55]. DEX also reduces infammatory cell response by inhibiting the assembly of oxygen-free radical species and release of proinfammatory cytokines [56].…”

Section: Discussionmentioning

confidence: 92%

Protective Effects of Dexmedetomidine Infusion on Genotoxic Potential of Isoflurane in Patients Undergoing Emergency Surgery

Aroosa

Sattar

Javeed

et al. 2023

International Journal of Clinical Practice

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Background. Isoflurane (ISO) has been extensively uses in general anesthesia and reported to cause deoxyribonucleic acid (DNA) damage in prolonged surgical procedures. Dexmedetomidine (DEX) is an adrenergic agonist and having antioxidant activity that may reduce the genotoxic potential (DNA damage) and oxidative stress induced by ISO in patients undergoing major neurosurgical procedures. Methods and Findings. Twenty-four patients of ASA (American Society of Anesthesiologists) classes I and II were randomly divided into two groups (n = 12). Group A patients received ISO, while group B patients received DEX infusion for maintenance of anesthesia. Venous blood samples were collected at different time intervals and used to evaluate the oxidative stress marker malondialdehyde (MDA) and endogenous antioxidants superoxide dismutases (SOD) and catalases (CAT). A single-cell gel electrophoresis (SCGE)-comet assay was used to investigate the genotoxic potential of ISO. Conclusion. Increased level of antioxidants and decreased value of MDA and genetic damage index were seen in group B ( P < 0.001 ) in a time-dependent manner. Genetic damage was highest at point T2 (0.77 vs. 1.37), and continued to decrease till T3 (0.42 vs. 1.19), with respect to negative controls or baseline values following DEX infusion. Significantly, higher level of MDA was recorded in serum of group A ( P < 0.001 ) as compared to group B (1.60 ± 0.33 vs. 0.03 ± 0.001). Enzymatic activities of CAT and SOD were significantly higher in group B than group A (10.11 ± 2.18 vs. 5.71 ± 0.33), (1.04 ± 0.05 vs. 0.95 ± 0.01), respectively. It may play a contributing role in daily anesthesia practice and improve the toxic effects on patients as well as anesthesia personnel. Trial Registration. Ethical Committee of Post Graduate Medical Institute (PGMI), Lahore General Hospital approved the use of humans in this study vide human subject application number ANS-6466 dated February 04, 2019. Furthermore, as the clinical trials required registration from an appropriate registry approved by World Health Organization (WHO), this trail also retrospectively registered at Thai Clinical Trials Registry (an approved WHO registry for clinical trials registration) under reference ID TCTR20211230001 on December 30, 2021.

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Section: Discussionmentioning

confidence: 92%

Protective Effects of Dexmedetomidine Infusion on Genotoxic Potential of Isoflurane in Patients Undergoing Emergency Surgery

Aroosa

Sattar

Javeed

et al. 2023

International Journal of Clinical Practice

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“…While we found a decrease in another oxidative parameter, it also caused an increase in the levels of antioxidant parameters, such as tGSH. In the study by Kuyrukluyildiz et al (2021), investigating the protective effect of dexmedetomidine on the stomach, levels of oxidants such as MDA and MPO decreased in the dexmedetomidine-treated group; they found that tGSH and SOD decreased. Therefore, biochemically and histopathologically demonstrated that the I/R process causes oxidative damage in gastric tissues, and dexmedetomidine was found to prevent oxidative damage in the stomach by increasing antioxidant activity.…”

Section: Discussionmentioning

confidence: 99%

The effects of sugammadex on gastric ischemia-reperfusion injury in rats: Biochemical and histopathological evaluation

Koç

Kuyrukluyıldız²,

Gazi³

et al. 2023

gpb

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The primary sources of reactive oxygen species (ROS) that cause ischemia-reperfusion (I/R) injuries are enzymes xanthine oxidase (XO) and nicotinamide adenine dinucleotide phosphate oxidases (NOXs) in the literature, whereby one of the main ROS producing cells via NOX activity are polymophonuclear leukocytes (PNL). Sugammadex, the effect of which we plan to research against gastric I/R damage, is a modified gamma-cyclodextrin that antagonizes the action of steroidal neuromuscular blocking drugs. Previous studies have reported that sugammadex inhibits PNL infiltration. However, it is unknown whether an inhibitory effect on XO is present. We aimed to biochemically and histopathologically investigate the effects of sugammadex on I/R-induced stomach damage in rats. The animals were divided into groups that underwent gastric ischemia-reperfusion (GIR), 4 mg/kg sugammadex + gastric ischemia-reperfusion (SGIR), and a sham operation group (SG). The effect of sugammadex was evaluated by measuring oxidant-antioxidant and PNL parameters. There was no significant difference in XO levels between the SGIR and GIR groups. In the SGIR group, sugammadex inhibited the increase in myeloperoxidase (MPO) and malondialdehyde (MDA) levels (p < 0.001). The amount of MDA and MPO in the SGIR group was similar as in the SG group. Sugammadex significantly suppressed the decrease in tGSH levels in the SGIR group (p < 0.001). The difference between tGSH levels in the SG and SGIR groups was slight. In the SGIR group, sugammadex significantly suppressed the increase in tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL1-β) levels compared to the GIR group (p < 0.001). Additionally, sugammadex corrected histopathological modifications as much as sham group. In conclusion, sugammadex may be beneficial in preventing oxidative stress.

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“…the toxicity of excitatory amino acids, and inhibit neuronal apoptosis. [19][20][21] ROS are chemically reactive substances containing oxygen; their levels increase sharply in H 2 O 2 -induced PC12 cells, causing severe damage to the cell structure. 22 MDA is the final product of membrane lipid peroxidation, and the content change is one of the major signs of plasma membrane damage.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134

Zhang

Yang

et al. 2021

Hum Exp Toxicol

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Objective: To explore the mechanism of dexmedetomidine (DEX)-mediated miR-134 inhibition in hypoxia-induced damage in PC12 cells. Methods: Hydrogen peroxide (H2O2)-stimulated PC12 cells were divided into control, H2O2, DEX + H2O2, miR-NC/inhibitor + H2O2, and miR-NC/ mimic + DEX + H2O2 groups. Cell viability and apoptosis were assessed by the 3-(4,5-dimethylthiazol(-2-y1)-2,5-diphenytetrazolium bromide (MTT) assay and Annexin V-FITC/PI staining, while gene and protein expression levels were detected by qRT-PCR and western blotting. Reactive oxygen species (ROS) levels were tested by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining, and malondialdehyde (MDA) content was determined with a detection kit. Results: DEX treatment decreased H2O2-elevated miR-134 expression. H2O2-induced PC12 cell damage was improved by DEX and miR-134 inhibitor; additionally, cell viability was increased, while cell apoptosis was reduced. In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Inflammation and oxidative stress were increased in H2O2-induced PC12 cells but improved with DEX or miR-134 inhibitor treatment. However, this improvement of H2O2-induced inflammation and oxidative stress induced by DEX in PC12 cells could be reversed by the miR-134 mimic. Conclusion: DEX exerts protective effects to promote viability and reduce cell apoptosis, inflammation, and oxidative stress in H2O2-induced PC12 cells by inhibiting the expression of miR-134.

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The effect of dexmedetomidine on gastric ischemia reperfusion injury in rats. Biochemical and histopathological evaluation

Cited by 4 publications

References 22 publications

Protective Effects of Dexmedetomidine Infusion on Genotoxic Potential of Isoflurane in Patients Undergoing Emergency Surgery

Protective Effects of Dexmedetomidine Infusion on Genotoxic Potential of Isoflurane in Patients Undergoing Emergency Surgery

The effects of sugammadex on gastric ischemia-reperfusion injury in rats: Biochemical and histopathological evaluation

Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134

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