The role of ghrelin on apoptosis, cell proliferation and oxidant‐antioxidant system in the liver of neonatal diabetic rats

Koyutürk, Meral; Saçan, Özlem; Karabulut, Sezin; Turk, Neslihan; Bolkent, Şehnaz; Yanardağ, Refiye

doi:10.1002/cbin.10464

Cited by 19 publications

(15 citation statements)

References 43 publications

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“…Gezginci-Oktayoglu et al (43) reported that a combination of selenium and vitamins C and E has a curative effect on hepatic damage. Ghrelin also improves the histopathological changes in the liver (44). Wild ginseng cambial meristematic cells protect the liver against GalN-induced inflammation, and sesamin ameliorates D-GaIN/lipopolysaccharide-induced hepatic damage (45,46).…”

Section: Discussionmentioning

confidence: 92%

An Antioxidant Combination Improves Histopathological Alterations and Biochemical Parameters in D-Galactosamine- Induced Hepatotoxicity in Rats

Çatal¹,

Tunalı²,

Bolkent³

et al. 2017

Eur J Biol

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The protective effects of a combination of antioxidants on histopathological changes and biochemical parameters were examined in D-galactosamine (D-GaIN)-induced hepatotoxicity in rats. Physiological saline solution was injected intraperitoneally into the control group, while D-GaIN (500 mg kg-1) was administered intraperitoneally into the experimental animals. The combination of 100 mg/kg/day ascorbic acid, 100 mg/kg/day alpha tocopherol, 15 mg/kg/day beta carotene, and 0.2 mg/kg/day sodium selenate was administered orally to intact control rats for 3 days. The same antioxidant combination was given to the D-GaIN group. Liver and blood samples were used for histopathological and biochemical assays. Liver tissues were significantly damaged by D-GaIN administration based on the histopathological findings. Serum aspartate and alanine transaminase, gamma glutamyl transpeptidase, alkaline phosphatase, lactate dehydrogenase, sialic acid, and uric acid levels increased. Serum and liver glutathione levels decreased, and serum superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase, catalase activities as well as lipid peroxidation values increased in the D-GaIN group. In contrast, administration of the antioxidants reversed the histopathological and biochemical changes in the liver of animals administered D-GaIN. In conclusion, the administration of a combination of antioxidants suppressed histopathological changes and biochemical parameters in rats given D-GaIN.

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Section: Discussionmentioning

confidence: 92%

An Antioxidant Combination Improves Histopathological Alterations and Biochemical Parameters in D-Galactosamine- Induced Hepatotoxicity in Rats

Çatal¹,

Tunalı²,

Bolkent³

et al. 2017

Eur J Biol

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“…Ghrelin has several biological actions, including regulating cell survival and proliferation, inhibiting inflammation, and exerting antioxidative effects [ 23 , 24 ]. Previous studies have indicated that the antioxidative effect of ghrelin is based on increasing the activity of endogenous antioxidant enzymes [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Ghrelin Protects Human Lens Epithelial Cells against Oxidative Stress‐Induced Damage

Bai

Yang

Liu

et al. 2017

Oxidative Medicine and Cellular Longevity

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Oxidative stress has been recognized as an important mediator in the pathogenesis of age-related cataracts; using antioxidant supplements is one plausible strategy to protect the antioxidative defense system against oxidative stress. Ghrelin administration is expected to reduce ROS, preventing the onset of different diseases. The role of ghrelin, if any, in protecting against oxidative stress in HLECs has never been examined. In the present study, we investigated the effects of ghrelin against H2O2-induced oxidative stress and the associated molecular mechanisms in HLECs and rat lenses. The results showed that pretreatment with ghrelin reduced H2O2-induced cellular apoptosis and ROS accumulation, increased the expression levels of SOD and CAT, and decreased the expression level of MDA. The morphological examination showed that the ghrelin-treated lens organ culture maintained transparency. This is the first report to show that ghrelin can protect HLECs from H2O2-induced oxidative stress. Our findings suggest that ghrelin may prevent the progression of cataracts, which has treatment value for ophthalmologists.

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“…In addition, the functions of ghrelin include improving ingestion, gastric acid secretion and gastrointestinal motility, and protecting the mucous membrane of the digestive system (9). Previous studies have reported that ghrelin exerts anti-inflammatory, antioxidative and neuroprotective effects (10)(11)(12). Therefore, the present study aimed to determine the protective effects of ghrelin against oxidative stress, inducible nitric oxide synthase (iNOS) and inflammation in MIRI mice, and to investigate the mechanisms underlying the cardioprotective effects of ghrelin.…”

Section: Introductionmentioning

confidence: 96%

“…Wang et al (20) demonstrated that ghrelin protects mice against endotoxemia-induced acute kidney injury via the suppression of nitric oxide, and inhibition of TNF-α, IL-1β and IL-6. Koyuturk et al (10) indicated that ghrelin inhibited apoptosis, cell proliferation and the oxidant-antioxidant system via caspase-8 and caspase-3 in the liver of neonatal diabetic rats. Furthermore, Ercan et al (21) suggested that ghrelin treatment suppressed sodium metabisulfite-induced oxidative stress and caspase-3 expression in rat gastric mucosa.…”

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confidence: 99%

Protective effects of ghrelin against oxidative stress, inducible nitric oxide synthase and inflammation in a mouse model of myocardial ischemia/reperfusion injury via the HMGB1 and TLR4/NF-κB pathway

Sun

Wang

2016

Molecular Medicine Reports

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The present study aimed to investigate the protective effects of ghrelin against oxidative stress, inducible nitric oxide synthase (iNOS) and inflammation in a mouse model of myocardial ischemia/reperfusion injury (MIRI). In addition, the study aimed to determine its underlying mechanisms. A mouse model of MIRI was used in vivo, in order to ascertain the protective effects of ghrelin on MIRI. Commercial kits were used to measure the serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH) in MIRI mice. Furthermore, Evan's Blue-triphenyltetrazolium chloride solution was used to analyze the protective effects of ghrelin against infarct size in MIRI mice. The underlying mechanisms were determined by measuring MIRI-induced tumor necrosis factor (TNF)‑α, interleukin (IL)‑6, superoxide dismutase (SOD), glutathione (GSH), GSH-peroxidase (GSH‑PX), malondialdehyde (MDA) and caspase‑3/caspase‑9 activities, and iNOS, high mobility group box 1 (HMGB1), Toll‑like receptor 4 (TLR4) and nuclear factor (NF)‑κB protein expression in MIRI mice. The results demonstrated that MIRI led to an increase in infarct size; CK, LDH, TNF‑α, IL‑6, MDA, caspase‑3 and caspase-9 serum levels; and iNOS protein expression. MIRI resulted in inhibition of SOD, FSH and GSH‑PX levels. Conversely, these alterations were significantly inhibited following treatment with ghrelin. In addition, the protective effects of ghrelin against MIRI suppressed HMGB1, TLR4 and NF‑κB protein expression in MIRI mice. The present study revealed that ghrelin exerted protective effects against oxidative stress, iNOS and inflammation in MIRI mice via the HMGB1/TLR4/NF-κB pathway.

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The role of ghrelin on apoptosis, cell proliferation and oxidant‐antioxidant system in the liver of neonatal diabetic rats

Cited by 19 publications

References 43 publications

An Antioxidant Combination Improves Histopathological Alterations and Biochemical Parameters in D-Galactosamine- Induced Hepatotoxicity in Rats

An Antioxidant Combination Improves Histopathological Alterations and Biochemical Parameters in D-Galactosamine- Induced Hepatotoxicity in Rats

Ghrelin Protects Human Lens Epithelial Cells against Oxidative Stress‐Induced Damage

Protective effects of ghrelin against oxidative stress, inducible nitric oxide synthase and inflammation in a mouse model of myocardial ischemia/reperfusion injury via the HMGB1 and TLR4/NF-κB pathway

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