The effect of melatonin on endotoxemia-induced intestinal apoptosis and oxidative stress in infant rats

Özdemir, Durgül; Uysal, Nazan; Tugyan, Kazim; Gönenç, Sevil; Açıkgöz, Osman; Aksu, İlkay; Özkan, Hasan

doi:10.1007/s00134-006-0492-z

Cited by 36 publications

(27 citation statements)

References 39 publications

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“…Coopersmith et al (2002a, b) found that decreasing intestinal apoptosis improved survival in septic mice subjected to cecal ligation and puncture. In the present study, we also found that administration of LPS into infant rats induced a significant apoptosis in both intestinal epithelium and lamina propria, which is consistent with previous studies (Cinel et al 2002;Ozdemir et al 2007).…”

Section: Discussionsupporting

confidence: 94%

“…This condition results in the mitochondrial damage, which leads to release of cytochrome C, caspase activation, and then apoptotic cell death (Leon et al 2004(Leon et al , 2005. We have previously demonstrated that endotoxemia induced lipid peroxidation in intestinal tissues and therapy strategies that protect oxidative stress attenuated intestinal apoptotic damage in infant rats (Ozdemir et al 2007). As mentioned above, Rho kinase demonstrated to play a regulatory role for apoptosis of various cell types (Shi and Wei 2007).…”

Section: Discussionmentioning

confidence: 96%

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The effect of Rho kinase inhibitor Y-27632 on endotoxemia-induced intestinal apoptosis in infant rats

et al. 2011

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The aim of this study was to evaluate the effect of Rho kinase inhibitor, Y-27632 on the intestinal apoptosis in endotoxemic infant rats. Wistar albino 15-17-day-old rat pups (n = 21) were randomized to three experimental groups: (1) controls; (2) endotoxemia (LPS); and (3) endotoxemia treated with Y-27632 (LPS + Y-27632). Endotoxemia was induced in rats by intraperitoneal (i.p) injection of lipopolysaccharide (Escherichia coli serotype 0111:B4; 10 mg/kg). Y-27632 was administered 5 mg/kg i.p at three times, just, 8 and 16 h after LPS injection. Twenty-four hours after LPS injection, intestinal apoptosis was assessed by hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and immunohistochemistry for active caspase-3. Endotoxemia induced extensive apoptotic injury in the intestinal tissues. The administration of Y-27632 to endotoxemic infant rats caused a marked decrease in the number of apoptotic cells in both intestinal epithelium and lamina propria. In conclusion, the inhibition of Rho kinase with Y-27632 diminished the intestinal apoptotic damage induced by endotoxemia in infant rats.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 96%

The effect of Rho kinase inhibitor Y-27632 on endotoxemia-induced intestinal apoptosis in infant rats

et al. 2011

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“…injections of melatonin and the other received vehicle. Melatonin (20 mg/kg) was dissolved in 5% ethanol in saline (Ozdemir et al, 2007, Olivier et al, 2009) and administered 5 minutes after LPS injection. A total of 72 rats from six litters were used in the present study.…”

Section: Methodsmentioning

confidence: 99%

Melatonin ameliorates brain injury induced by systemic lipopolysaccharide in neonatal rats

et al. 2014

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Our previous study showed that lipopolysaccharide (LPS)-induced brain injury in the neonatal rat is associated with nitrosative and oxidative stress. The present study was conducted to examine whether melatonin, an endogenous molecule with antioxidant properties, reduces systemic LPS-induced nitrosative and oxidative damage in the neonatal rat brain. Intraperitoneal (i.p.) injection of LPS (2 mg/kg) was administered to Sprague–Dawley rat pups on postnatal day 5 (P5), and i.p. administration of melatonin (20 mg/kg) or vehicle was performed 5 minutes after LPS injection. Sensorimotor behavioral tests were performed 24 h after LPS exposure, and brain injury was examined after these tests. The results show that systemic LPS exposure resulted in impaired sensorimotor behavioral performance, and acute brain injury, as indicated by the loss of oligodendrocyte immunoreactivity and a decrease in mitochondrial activity in the neonatal rat brain. Melatonin treatment significantly reduced LPS-induced neurobehavioral disturbances and brain damage in neonatal rats. The neuroprotective effect of melatonin was associated with attenuation of LPS-induced nitrosative and oxidative stress, as indicated by the decreased nitrotyrosine- and 4-hydroxynonenal-positive staining in the brain following melatonin and LPS exposure in neonatal rats. Further, melatonin significantly attenuated LPS-induced increases in the number of activated microglia in the neonatal rat brain. The protection provided by melatonin was also associated with a reduced number of inducible nitric oxide synthase (iNOS)+ cells, which were double-labeled with ED1 (microglia). Our results show that melatonin prevents the brain injury and neurobehavioral disturbances induced by systemic LPS exposure in neonatal rats, and its neuroprotective effects are associated with its impact on nitrosative and oxidative stress.

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“…Higher superoxide and lipid peroxide production including malondialdehyde (MDA), 4‐hydroxylalkenal and thiobarbituric acid reactive substances are a common result of LPS toxicity. These perturbations appear concomitantly with lower total antioxidant capacity levels including reduced activity of SOD and glutathione peroxidase (GPx) (Crespo et al , ; Paskaloglu et al , ; Wang et al , ; Yerer et al , ; Carrillo‐Vico et al , ; Sener et al , ; Escames et al , ; Ozdemir et al , ; Shang et al , ; Erbas et al , ). LPS‐induced oxidative damage is further confirmed by histological examination of the related tissues (Sener et al , ).…”

Section: Protective Mechanisms Of Melatonin Against Sepsismentioning

confidence: 99%

Utilizing melatonin to combat bacterial infections and septic injury

Deng

et al. 2017

British J Pharmacology

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*These authors contributed equally to this work.Melatonin, also known as N-acetyl-5-methoxytryptamine, is a ubiquitously acting molecule that is produced by the pineal gland and other organs of animals, including humans. As melatonin and its metabolites are potent antioxidants and free radical scavengers, they are protective against a variety of disorders. Moreover, multiple molecular targets of melatonin have been identified, and its actions are both receptor-mediated and receptor-independent. Recent studies have shown that melatonin may be useful in fighting against sepsis and septic injury due to its antioxidative and anti-inflammatory actions; the results generally indicate a promising therapeutic application for melatonin in the treatment of sepsis. To provide a comprehensive understanding regarding the protective effects of melatonin against septic injury, in the present review we have evaluated the published literature in which melatonin has been used to treat experimental and clinical sepsis. Firstly, we present the evidence from studies that have used melatonin to resist bacterial pathogens. Secondly, we illustrate the protective effect of melatonin against septic injury and discuss the possible mechanisms. Finally, the potential directions for future melatonin research against sepsis are summarized. AbbreviationsA-ADMSCs, adipose-derived mesenchymal stem cells; AA-NAT, arylalkylamine-N-acetyltransferase; ASMT, Nacetylserotonin O-methyltransferase; GPx, glutathione peroxidase; MDA, malondialdehyde; STAT1, signal transducer and activator of transcription 1; UPR, unfolded protein response

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The effect of melatonin on endotoxemia-induced intestinal apoptosis and oxidative stress in infant rats

Abstract: Melatonin diminished the intestinal oxidative stress and apoptotic damage induced by endotoxemia in infant rats.

Cited by 36 publications

References 39 publications

The effect of Rho kinase inhibitor Y-27632 on endotoxemia-induced intestinal apoptosis in infant rats

The effect of Rho kinase inhibitor Y-27632 on endotoxemia-induced intestinal apoptosis in infant rats

Melatonin ameliorates brain injury induced by systemic lipopolysaccharide in neonatal rats

Utilizing melatonin to combat bacterial infections and septic injury

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