Melatonin exhibit supportive effects on oxidants and anastomotic healing during intestinal ischemia reperfusion injury

Özkan, Nilüfer; Ersoy, Ömer Faik; Özsoy, Zeki; Çakır, Ebru

doi:10.5505/tjtes.2017.23539

Cited by 7 publications

(5 citation statements)

References 26 publications

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“…12 Of note, melatonin protects against ischemia-reperfusion injury in the kidney, intestine, and heart in normoglycemic animal models. [13][14][15] Recent studies have found the same beneficial effects in hyperglycemic rats' hearts and kidneys. 16,17 Emerging evidence demonstrates the neuroprotective effects of melatonin in normoglycemic animals with focal cerebral ischemia.…”

Section: Introductionmentioning

confidence: 76%

“…Melatonin can easily pass through the blood‐brain barrier and be tolerated in a wide range of doses without toxicity 12 . Of note, melatonin protects against ischemia‐reperfusion injury in the kidney, intestine, and heart in normoglycemic animal models 13–15 . Recent studies have found the same beneficial effects in hyperglycemic rats' hearts and kidneys 16,17 .…”

Section: Introductionmentioning

confidence: 99%

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Melatonin ameliorates cerebral ischemia‐reperfusion injury in diabetic mice by enhancing autophagy via the SIRT1‐BMAL1 pathway

et al. 2021

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Diabetic brains are more vulnerable to ischemia‐reperfusion injury. Previous studies have proved that melatonin could protect against cerebral ischemia‐reperfusion (CIR) injury in non‐diabetic stroke models; however, its roles and the underlying mechanisms against CIR injury in diabetic mice remain unknown. Streptozotocin‐induced diabetic mice and high‐glucose‐cultured HT22 cells were exposed to melatonin, with or without administration of the autophagy inhibitor 3‐methyladenine (3‐MA) and the specifically silent information regulator 1 (SIRT1) inhibitor EX527, and then subjected to CIR or oxygen‐glucose deprivation/reperfusion operation. We found that diabetic mice showed aggravated brain damage, increased apoptosis and oxidative stress, and deficient autophagy following CIR compared with non‐diabetic counterparts. Melatonin treatment exhibited improved histological damage, neurological outcomes, and cerebral infarct size. Intriguingly, melatonin markedly increased cell survival, anti‐oxidative and anti‐apoptosis effects, and significantly enhanced autophagy. However, these effects were largely attenuated by 3‐MA or EX527. Additionally, our cellular experiments demonstrated that melatonin increased the SIRT1‐BMAL1 pathway‐related proteins' expression in a dose‐dependent manner. In conclusion, these results indicate that melatonin treatment can protect against CIR‐induced brain damage in diabetic mice, which may be achieved by the autophagy enhancement mediated by the SIRT1‐BMAL1 pathway.

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Section: Introductionmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Melatonin ameliorates cerebral ischemia‐reperfusion injury in diabetic mice by enhancing autophagy via the SIRT1‐BMAL1 pathway

et al. 2021

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“…SOD protects cells from oxidative stress by converting the superoxide anion radical (O 2 – ) radicals to O 2 and H 2 O 2 [ 17 , 41 , 42 ]. In a recent study, SOD level was reported to increase after abdominal surgery [ 43 ]. GSH prevents oxidative damage by reducing ROS such as free radicals, peroxides, and lipid peroxides [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Improved motility in the gastrointestinal tract of a postoperative ileus rat model with ilaprazole

Kim

Sohn

Choi

et al. 2021

Korean J Physiol Pharmacol

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“…GSH is the major antioxidant sensitive to intracellular ROS ( Yu et al, 2019 ). SOD and CAT are the first line of defense against oxidative stress by directly scavenging ROS in the defense system ( Ozkan et al, 2018 ; Yu et al, 2019 ). MDA is the final product of lipid peroxidation and a biomarker indicating the level of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Inhibits Oxidative Stress and Apoptosis in Cryopreserved Ovarian Tissues via Nrf2/HO-1 Signaling Pathway

Sun

Liu

Yang

et al. 2020

Front. Mol. Biosci.

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In the field of assisted reproductive technology, female fertility preservation, particularly ovarian tissue cryopreservation in adolescent cancer patients, has attracted much attention. Melatonin (MLT) is well known for its antioxidative and anti-apoptotic properties; however, whether it can ameliorate the cryoinjury and inhibit the generation of reactive oxygen species (ROS) in cryopreserved ovarian tissues (OTs) has not yet been reported. Here, we demonstrated that MLT could protect follicular integrity; prevent cell apoptosis; decrease ROS, malondialdehyde (MDA), and nitric oxide (NO) levels; and increase activities of glutathione peroxidases (GSH-Px), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) in cryopreserved OTs. Furthermore, these effects may be related with the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, as evidenced by increased mRNA levels of Nrf2 downstream genes, including heme oxygenase-1 (HO-1), glutathione S-transferase M1 (GSTM1), SOD, and CAT. In summary, MLT can not only directly scavenge ROS but also significantly induce the activation of antioxidative enzymes via the Nrf2 signaling pathway, which is a new mechanism underlying the protection effects of MLT on cryopreserved OTs.

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Melatonin exhibit supportive effects on oxidants and anastomotic healing during intestinal ischemia reperfusion injury

Abstract: BACKGROUND:The aim of this study was to investigate the effects of melatonin on intestinal anastomosis after intestinal ischemia/ reperfusion injury (IRI).

Cited by 7 publications

References 26 publications

Melatonin ameliorates cerebral ischemia‐reperfusion injury in diabetic mice by enhancing autophagy via the SIRT1‐BMAL1 pathway

Melatonin ameliorates cerebral ischemia‐reperfusion injury in diabetic mice by enhancing autophagy via the SIRT1‐BMAL1 pathway

Improved motility in the gastrointestinal tract of a postoperative ileus rat model with ilaprazole

Melatonin Inhibits Oxidative Stress and Apoptosis in Cryopreserved Ovarian Tissues via Nrf2/HO-1 Signaling Pathway

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