Antioxidative effect of melatonin, ascorbic acid and<i>N</i>-acetylcysteine on caerulein-induced pancreatitis and associated liver injury in rats

Eşrefoğlu, Mukaddes; Gül, Mehmet; Ateş, Burhan; Batçıoğlu, Kadir; Selimoğlu, Mukadder Ayşe

doi:10.3748/wjg.v12.i2.259

Cited by 88 publications

(71 citation statements)

References 30 publications

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“…In AP, there is an excessive production of ROS due to the activation of leukocytes and the formation of proinflammatory interleukins (25). Several studies have reported an increase in MDA levels and a decrease in the activity of antioxidant enzymes (11,(22)(23)(24). In the present study, we observed higher tissue MDA levels and lower CAT and GPx enzyme activity levels in the cerulein group than in the control group.…”

Section: Resultssupporting

confidence: 64%

“…AP is considered to be an autodigestive disease. In addition to premature intracellular protease activation, other mechanisms such as oxidative stress have also been shown to be involved in the development of AP (11,12). In the present study, we investigated the possible protective effects of pentoxifylline, L-arginine and N G -nitro-L-arginine methyl ester (L-NAME) against cerulein-induced acute pancreatitis.…”

Section: Introductionmentioning

confidence: 99%

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Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Batçıoğlu

Gül

Uyumlu

et al. 2009

Braz J Med Biol Res

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The aim of this study was to evaluate the role of oxidative damage in pancreatitis-induced hepatic injury. Thirty-five rats were divided into five groups (each of 7 rats): control, cerulein (100 µg/kg body weight), cerulein and pentoxifylline (12 mg/kg body weight), cerulein plus L-NAME (10 mg/kg body weight) and cerulein plus L-arginine (160 mg/kg body weight). The degree of hepatic cell degeneration differed significantly between groups. Mean malondialdehyde levels were 7.00 ± 2.29, 20.89 ± 10.13, 11.52 ± 4.60, 18.69 ± 8.56, and 8.58 ± 3.68 nmol/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Mean catalase activity was 3.20 ± 0.83, 1.09 ± 0.35, 2.05 ± 0.91, 1.70 ± 0.60, and 2.85 ± 0.47 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively, and mean glutathione peroxidase activity was 0.72 ± 0.25, 0.33 ± 0.09, 0.37 ± 0.04, 0.34 ± 0.07 and 0.42 ± 0.1 U/mg protein for the control, cerulein, pentoxifylline, L-NAME, and L-arginine groups, respectively. Cerulein-induced liver damage was accompanied by a significant increase in tis sue malondialdehyde levels (P < 0.05) and a significant decrease in catalase (P < 0.05) and GPx activities (P < 0.05). L-arginine and pentoxifylline, but not L-NAME, protected against this damage. Oxidative injury plays an important role not only in the pathogenesis of AP but also in pancre atitis-induced hepatic damage.

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Section: Resultssupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Batçıoğlu

Gül

Uyumlu

et al. 2009

Braz J Med Biol Res

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“…Moreover, the overwhelming production of proinflammatory mediators, as well as oxidative injury, has also been involved in extending the inflammation to other organs different from the pancreas. Thus, inflammatory mediators, such as ICAM-1, could contribute to the exit of activated pancreatic enzymes from the circulation by increasing capillary permeability [52] and a reduction of hepatic dam age after antioxidant agentsadministration has been shown during experimental AP [53] .…”

Section: From Local Pancreatic Damage To Systemic Effectsmentioning

confidence: 99%

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

García

Calvo²

2010

WJGPT

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Acute pancreatitis (AP) is a common and potentially lethal acute inflammatory process. Although the majority of patients have a mild episode of AP, 10%-20% develop a severe acute pancreatitis (SAP) and suffer systemic inflammatory response syndrome (SIRS) and/or pancreatic necrosis. The main aim of this article is to review the set of events, first localized in the pancreas, that lead to pancreatic inflammation and to the spread to other organs contributing to multiorganic shock. The early pathogenic mechanisms in SAP are not completely understood but both premature activation of enzymes inside the pancreas, related to an impaired cytosolic Ca 2+ homeostasis, as well as release of pancreatic enzymes into the bloodstream are considered important events in the onset of pancreatitis disease. Moreover, afferent fibers within the pancreas release neurotransmitters in response to tissue damage. The vasodilator effects of these neurotransmitters and the activation of pro-inflammatory substances play a crucial role in amplifying the inflammatory response, which leads to systemic manifestation of AP. Damage extension to other organs leads to SIRS, which is usually associated with cardiocirculatory physiology impairment and a hypotensive state. Hypotension is a risk factor for death and is associated with a significant hyporesponsiveness to vasoconstrictors. This indicates that stabilization of the patient, once this pathological situation has been established, would be a very difficult task. Therefore, it seems particularly necessary to understand the pathological mechanisms involved in the first phases of AP to avoid damage beyond the pancreas. Moreover, efforts must also be directed to identify those patients who are at risk of developing SAP.

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“…'nın çalışmasında; iskemi-reperfüzyonun neden olduğu oksidatif stres, pankreasta azalmış enzimatik (süperoksit dismutaz, katalaz, glutatyon peroksidaz) ve nonenzimatik (GSH) antioksidanlar ile birlikte olup, melatonin tedavisi ile antioksidan enzimler artış göstermiştir [22]. Caerulein ile oluşturulan deneysel pankreatitte; melatonin uygulanmasının yük-selmiş MDA düzeyini azaltarak; pankreası oksidatif hasara karşı koruduğu bildirilmiştir [23]. Streptozotosin ve alloksan ile oluşturulan deneysel diabette melatonin uygulamasının pankreasta koruyucu etkisi olduğu gösterilmiştir [24].…”

Section: Discussionunclassified

The effects of melatonin on the oxidants and antioxidants in the pancreatic tissue during the aging process

Yüzüak

Akbulut²,

Yüzüak³

2014

J Clin Exp Invest

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Objective: To investigate the effect of melatonin on the levels of malondialdehyde (MDA), nitric oxide (NO) and glutathione (GSH) of pancreas tissues at young (4 months) and middle-aged (14 months) rats.Methods: Young and middle-age male Wistar albino rats were used in this experimental study. Rats were divided into two groups: melatonin applied; young rats , middle-aged rats and melatonin was not applied; young rats and middle-aged rats . Melatonin was administered at a dose of 10 mg/kg/ day in 0.2 cc-% 1 ethanol-phosphate buffered saline (PBS) solution via subcutan way for 7 days at 18:00 until surgery. In control group, 0.2 cc-%1 Ethanol-PBS was applied for 7 days at 18:00. At the end of seven days, MDA, NO levels which are indicators of oxidant stress and GSH were detected. Results:Although there were no significant difference between control and experiment group for the NO and MDA level of melatonin group of young rats, there were significantly difference in the GSH levels of pancreas tissues for melatonin levels. NO levels of the pancreas tissues were significantly reduced and GSH levels were significantly increased in the melatonin group of middle aged rats compared to the control group. The MDA levels of pancreas tissues were significantly increased in the middle aged control group compared to young control group. The MDA levels of pancreas tissues were not significantly different in melatonin group of middle-aged compared to control group. The NO and the GSH levels of the pancreas tissues were not significantly different between the control groups of young and middle aged rats. Conclusion:Aging may be related with an increase in free radicals and a reduction in the antioxidant capacity of the tissues and exogenous melatonin may play a protective role in aging by means of its action on free radicals. J Clin Exp Invest 2014; 5 (4): 583-588 Key words: Melatonin, pancreas, malondialdehyde, nitric oxide, glutathione, aging ÖZET Amaç: Melatoninin; genç (4 aylık) ve orta yaşlı (14 aylık) sı-çanlarda pankreas dokusunda malondialdehid (MDA), nitrik oksit (NO) ve glutatyon (GSH) düzeyleri üzerindeki etkisini araştırmak amaçlandı.Yöntemler: Bu deneysel çalışmada genç ve orta yaşlı erkek Wistar albino sıçanlar kullanıldı. Sıçanlar; melatonin verilen genç sıçanlar ve orta yaşlı sıçanlar, melatonin verilmeyen genç sıçanlar ve orta yaşlı sıçanlar şeklinde gruplandırıldı. Melatonin; 10 mg/kg/gün (% 1'lik etanol-phosphate buffered saline (PBS) çözeltisinde, 0,2 cc) olmak üzere, cerrahiye kadar 7 gün boyunca her gün saat 18:00'de subkutan olarak uygulandı. Kontrol grubundaki sıçanlara ise 7 gün süreyle 0,2 cc %1'lik Etanol-PBS, her gün saat 18:00'de subkutan olarak uygulandı. 7. günün sonunda sıçanların kalbinden kan alınıp takiben dekapite edilerek pankreas örnekleri alın-dı. Alınan örneklerde oksidan stresin göstergesi olarak MDA ve NO düzeyleri ve antioksidan etkinliği olan GSH düzeyi ölçüldü. Bulgular:Genç sıçanların kontrol ve deney grupları arasın-da NO ve MDA düzeyleri açısından istatistiksel olarak an...

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Antioxidative effect of melatonin, ascorbic acid andN-acetylcysteine on caerulein-induced pancreatitis and associated liver injury in rats

Cited by 88 publications

References 30 publications

Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Liver lipid peroxidation and antioxidant capacity in cerulein-induced acute pancreatitis

Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

The effects of melatonin on the oxidants and antioxidants in the pancreatic tissue during the aging process

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