Inhibition of carbon tetrachloride–mediated apoptosis and oxidative stress by melatonin in experimental liver fibrosis

2008 ◽  
Vol 24 (4) ◽  
pp. 201-208 ◽  
Author(s):  
M Ogeturk ◽  
I Kus ◽  
H Pekmez ◽  
H Yekeler ◽  
S Sahin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Radical Scavenger ◽  
Secretory Product ◽  
Protective Effects ◽  
Melatonin Treatment ◽  
Group I ◽  
Induced Apoptosis ◽  
Tissue Specimens ◽  
And Oxidative Stress

Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed both in vivo and in vitro. The aim of this experimental study was to investigate the protective effects of melatonin against carbon tetrachloride (CCl4)–induced apoptosis and oxidative stress in rat liver. Twenty-four male Wistar rats were divided in three equal groups. Group I was used as control. Rats in group II were injected every other day with CCl4 (0.5 mL/kg BW) for a month, whereas rats in group III were treated every other day with the same dose of CCl4 plus melatonin (25 mg/kg BW). At the end of the experiment, all animals were killed by decapitation and the livers were rapidly removed. Some of the liver tissue specimens were used for determination of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. The remaining tissue specimens were processed for immunohistochemical assessment, and the percentage rates of apoptotic liver cells stained with immunoreactive Bax were determined. Chronic administration of CCl4 significantly increased liver MDA contents, as an end product of lipid peroxidation, and also significantly decreased SOD and GSH-Px activities, emphasizing the generation of increased oxidative stress. Moreover, it caused an evident increase in apoptotic cells. Melatonin treatment significantly reduced MDA levels and elevated SOD and GSH-Px activities in rats received CCl4 plus melatonin. Furthermore, apoptotic changes caused by CCl4 were considerably decreased in these animals. The results of the present study indicate that melatonin treatment substantially prevents CCl4-induced apoptosis and oxidative damage in the liver. Thus, melatonin may serve as a drug for treating many clinical conditions that arise from inappropriate apoptosis.

Protective effects of various dosage of Curcumin against morphine induced apoptosis and oxidative stress in rat isolated hippocampus

2015 ◽  
Vol 67 (2) ◽  
pp. 230-235 ◽  
Author(s):  
Majid Motaghinejad ◽  
Morteza Karimian ◽  
Ozra Motaghinejad ◽  
Behnaz Shabab ◽  
Iraj Yazdani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effects ◽  
Induced Apoptosis ◽  
And Oxidative Stress

scholarly journals Melatonin protects the mouse testis against heat-induced damage

2020 ◽  
Vol 26 (2) ◽  
pp. 65-79 ◽  
Author(s):  
Pengfei Zhang ◽  
Yi Zheng ◽  
Yinghua Lv ◽  
Fuyuan Li ◽  
Lihong Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
Male Fertility ◽  
Reactive Oxygen Species Generation ◽  
Free Radical Scavenger ◽  
Testicular Atrophy ◽  
Therapeutic Drug ◽  
Radical Scavenger ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Abstract Spermatogenesis, an intricate process occurring in the testis, is responsible for ongoing production of spermatozoa and thus the cornerstone of lifelong male fertility. In the testis, spermatogenesis occurs optimally at a temperature 2–4°C lower than that of the core body. Increased scrotal temperature generates testicular heat stress and later causes testicular atrophy and spermatogenic arrest, resulting in a lower sperm yield and therefore impaired male fertility. Melatonin (N-acetyl-5-methoxytryptamine), a small neuro-hormone synthesized and secreted by the pineal gland and the testis, is widely known as a potent free-radical scavenger; it has been reported that melatonin protects the testis against inflammation and reactive oxygen species generation thereby playing anti-inflammatory, -oxidative and -apoptotic roles in the testis. Nevertheless, the role of melatonin in the testicular response to heat stress has not been studied. Here, by employing a mouse model of testicular hyperthermia, we systematically investigated the testicular response to heat stress as well as the occurrence of autophagy, apoptosis and oxidative stress in the testis. Importantly, we found that pre-treatment with melatonin attenuated heat-induced apoptosis and oxidative stress in the testis. Also, post-treatment with melatonin promoted recovery of the testes from heat-induced damage, probably by maintaining the integrity of the Sertoli cell tight-junction. Thus, we for the first time provide the proof of concept that melatonin can protect the testis against heat-induced damage, supporting the potential future use of melatonin as a therapeutic drug in men for sub/infertility incurred by various testicular hyperthermia factors.

scholarly journals Resveratrol and Montelukast Alleviate Paraquat-Induced Hepatic Injury in Mice: Modulation of Oxidative Stress, Inflammation, and Apoptosis

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Noha A. El-Boghdady ◽  
Nourtan F. Abdeltawab ◽  
Mohammed M. Nooh
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Antioxidant Properties ◽  
Protective Effects ◽  
Serum Total Protein ◽  
Stress Markers ◽  
Group I ◽  
Radical Generation ◽  
Anti Inflammatory ◽  
Induced Apoptosis

Paraquat (PQ) is one of the most used herbicide worldwide. Its cytotoxicity is attributed to reactive radical generation. Resveratrol (Res) and montelukast (MK) have anti-inflammatory and antioxidant properties. The protective effects of Res, MK, or their combination against PQ-induced acute liver injury have not been investigated before. Therefore, we explored the protective potential of Res and/or MK against PQ hepatic toxicity in a mouse model. Mice were randomly assigned to five groups: group I served as the normal control and group II received a single dose of PQ (50 mg/kg, i.p.). Groups III, IV, and V received PQ plus oral Res (5 mg/kg/day), MK (10 mg/kg/day), and Res/MK combination, respectively. Res and/or MK reduced PQ-induced liver injury, evidenced by normalization of serum total protein, ALT, and AST. Res and/or MK significantly reversed PQ-induced oxidative stress markers glutathione and malondialdehyde. Res and/or MK significantly reduced PQ-induced inflammation reflected in TNF-α levels. Furthermore, Res and/or MK reversed PQ-induced apoptosis assessed by differential expression of p53, Bax, and Bcl-2. Histopathologic examination supported the biochemical findings. Although Res and MK displayed antioxidative, anti-inflammatory, and antiapoptotic activities, their combination was not always synergistic.

scholarly journals Mechanisms of Protection With Melatonin By Hepatic Heme-Oxygenase-1 Activation In Burn

2017 ◽  
Vol 2 (1) ◽  
Keyword(s):  
Heme Oxygenase ◽  
Antioxidant Defense ◽  
Free Radical Scavenger ◽  
Model Material ◽  
Radical Scavenger ◽  
Heme Oxygenase 1 ◽  
Secretory Product ◽  
Protective Effects ◽  
Enhanced Expression ◽  
Induced Apoptosis

Background: Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed. Several studies show that heme-oxygenase-1 (HO-1) possesses antiapoptotic action and prevents hepatic damages. Recent studies indicate that heme-oxygenase-1(HO-1) inhibits apoptosis and exert hepatoprotective effect. The aim: of this experimental study was to investigate the protective effects of melatonin against burn-induced apoptotic injury and the association between the oxidative stress and the changed expression of hepatic HO-1 in burn rat model. Material and method: Melatonin was applied immediately after the burn. The expression of hepatic 4-hydroxynonenal (4-HNE), as marker of liver peroxidative injury, hepatic HO-1, marker of antioxidant defense and apoptosis-related genes Bcl-2 and Bax was evaluated using light immunоhistochemistry. Results: Burns caused an increased expression of HO-1, 4-HNE, Bax and Bax/Bcl-2 ratio and induced apoptosis of sinusoidal endothelial cells (SECs) in liver tissue. Melatonin treatment augmented the increase in HO-1 expression, decreased both burn-induced peroxidative damage and hepatic apoptosis as evidenced by reduced expression of Bax, enhanced expression of Bcl-2. Conclusion: Our present data suggest that melatonin suppresses burn-induced liver injury through HO-1 activation, attenuation of lipid peroxidation and modification of Bax/Bcl-2 ratio.

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