Melatonin protects against cardiac damage induced by a combination of high fat diet and isoproterenol exacerbated oxidative stress in male Wistar rats

In the current study, it was found that high fat diet (60% of total kCal) (H) or/and isoproterenol (I) exacerbated oxidative stress and caused myocardial damage. This was indicated by increased levels of LPO, PCO, abnormal mitochondria and altered activities of metabolic as well as antioxidant enzymes in myocardium of rats. Melatonin at different doses (10, 20 and 40 mg/kg) effectively protected against myocardial damage induced by H or/and I and preserved all of these altered parameters. Morphological analyses showed that combination of H and I treatment led to the extensive myofibril disintegration and neutrophil infiltration. Melatonin at the dose of 40 mg/kg almost completely prevented these pathological alterations. The mechanistical studies have uncovered that the protective effects of melatonin on the myocardial damage induced by H and I are attributed to its direct and indirect antioxidative capacity, i.e., it directly scavenges free radicals and also regulates the gene expression of antioxidant enzymes. Collectively, based on the evidences gathered from the current study, it will not be unwise to suggest that melatonin can serve as an ideal therapeutic agent for those cardiovascular diseases caused by oxidative stress.

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Melatonin as a potential therapeutic molecule against myocardial damage caused by high fat diet (HFD)

Melatonin Research ◽

10.32794/mr11250030 ◽

2019 ◽

Vol 2 (3) ◽

pp. 37-56

Author(s):

Gargi Bose ◽

Auroma Ghosh ◽

Aindrila Chattopadhyay ◽

Palash K Pal ◽

Debasish Bandyopadhyay

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

High Fat Diet ◽

Molecular Mechanisms ◽

Myocardial Damage ◽

Dietary Fats ◽

Protective Effects ◽

High Fat ◽

Inflammatory Reactions ◽

Inflammatory Genes

High fat diet (HFD) has been implicated as an independent risk factor for cardiovascular diseases since the second half of the last century. The HFD causes various pathogeneses and progressions of cardiovascular diseases. The oxidative stress and pro-inflammatory reactions induced by the HFD are probably the major risk factors of myocardial damage. In this review we highlight the roles of different dietary fats on cardiovascular diseases and the protective effects of melatonin as a potent antioxidant and anti-inflammation molecule on the pathology induced by HFD. The focus will be given to the molecular mechanisms. The protective effects of melatonin on HFD induced myocardial damage are mediated by multiple pathways. These include that melatonin suppresses the oxidative stress, preserves the normal fat and glucose metabolisms and reduces the pro-inflammatory reactions. Melatonin downregulates the expressions of pro-inflammatory genes of TLR4, NF-κB and NLRP3-Caspase1 but upregulates the expressions of anti-inflammatory genes of Sirt3, CTRP3 and RISK. All of these render melatonin as a powerful protector against cardiovascular diseases caused by the HFD. This review suggests that melatonin can be used as a therapeutic agent in this specific condition.

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Antioxidant Properties of Fucoidan Alleviate Acceleration and Exacerbation of Hippocampal Neuronal Death Following Transient Global Cerebral Ischemia in High-Fat Diet-Induced Obese Gerbils

International Journal of Molecular Sciences ◽

10.3390/ijms20030554 ◽

2019 ◽

Vol 20 (3) ◽

pp. 554 ◽

Cited By ~ 13

Author(s):

Ji Ahn ◽

Myoung Shin ◽

Dae Kim ◽

Hyunjung Kim ◽

Minah Song ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Antioxidant Enzymes ◽

Cerebral Ischemia ◽

Neuronal Death ◽

High Fat Diet ◽

Antioxidant Properties ◽

Global Cerebral Ischemia ◽

High Fat ◽

Transient Global Cerebral Ischemia

Fucoidan, a natural sulfated polysaccharide, displays various biological activities including antioxidant properties. We examined the neuroprotective effect of fucoidan against transient global cerebral ischemia (tGCI) in high-fat diet (HFD)-induced obese gerbils and its related mechanisms. Gerbils received HFD for 12 weeks and fucoidan (50 mg/kg) daily for the last 5 days during HFD exposure, and they were subjected to 5-min tGCI. Pyramidal cell death was observed only in the CA 1 area (CA1) of the hippocampus in non-obese gerbils 5 days after tGCI. However, in obese gerbils, pyramidal cell death in the CA1 and CA2/3 occurred at 2 days and 5 days, respectively, after tGCI. In the obese gerbils, oxidative stress indicators (dihydroethidium, 8-hydroxyguanine and 4-hydroxy-2-nonenal) were significantly enhanced and antioxidant enzymes (SOD1 and SOD2) were significantly reduced in pre- and post-ischemic phases compared to the non-obese gerbils. Fucoidan treatment attenuated acceleration and exacerbation of tGCI-induced neuronal death in the CA1–3, showing that oxidative stress was significantly reduced, and antioxidant enzymes were significantly increased in pre- and post-ischemic phases. These findings indicate that pretreated fucoidan can relieve the acceleration and exacerbation of ischemic brain injury in an obese state via the attenuation of obesity-induced severe oxidative damage.

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Neural Protective Effects of Millet and Millet Polyphenols on High-Fat Diet-Induced Oxidative Stress in the Brain

Plant Foods for Human Nutrition ◽

10.1007/s11130-020-00802-6 ◽

2020 ◽

Vol 75 (2) ◽

pp. 208-214 ◽

Cited By ~ 1

Author(s):

Sen Li ◽

Furong Xian ◽

Xiao Guan ◽

Kai Huang ◽

Wenwen Yu ◽

...

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Protective Effects ◽

High Fat ◽

The Brain

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Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model

PLoS ONE ◽

10.1371/journal.pone.0260546 ◽

2021 ◽

Vol 16 (12) ◽

pp. e0260546

Author(s):

Mary J. Obayemi ◽

Christopher O. Akintayo ◽

Adesola A. Oniyide ◽

Ayodeji Aturamu ◽

Olabimpe C. Badejogbin ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Food Intake ◽

High Fat Diet ◽

Wistar Rats ◽

Liver Lipid ◽

Control Group ◽

Metabolic Dysfunction ◽

High Fat ◽

Male Wistar Rats

Background Adipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats. Materials and methods Twenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks. Results HFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin. Conclusion Taken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.

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Tempol, a Membrane-Permeable Radical Scavenger, Exhibits Anti-Inflammatory and Cardioprotective Effects in the Cerulein-Induced Pancreatitis Rat Model

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/4139851 ◽

2016 ◽

Vol 2016 ◽

pp. 1-7 ◽

Cited By ~ 16

Author(s):

Andrzej Marciniak ◽

Beata Walczyna ◽

Grażyna Rajtar ◽

Sebastian Marciniak ◽

Andrzej Wojtak ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiac Injury ◽

Myocardial Damage ◽

Morphological Evidence ◽

Radical Scavenger ◽

Protective Effects ◽

Cardiac Damage ◽

Stress Changes ◽

Sh Group ◽

Long Time

To date, it remains unclear whether mild form of acute pancreatitis (AP) may cause myocardial damage which may be asymptomatic for a long time. Pathogenesis of AP-related cardiac injury may be attributed in part to ROS/RNS overproduction. The aim of the present study was to evaluate the oxidative stress changes in both the pancreas and the heart and to estimate the protective effects of 1-oxyl-2,2,6,6-tetramethyl-4-hydroxypiperidine (tempol) at the early phase of AP. Cerulein-induced AP led to the development of acute edematous pancreatitis with a significant decrease in the level of sulfhydryl (–SH) groups (oxidation marker) both in heart and in pancreatic tissues as well as a substantial increase in plasma creatine kinase isoenzyme (CK-MB) activity (marker of the heart muscle lesion) which confirmed the role of oxidative stress in the pathogenesis of cardiac damage. The tempol treatment significantly reduced the intensity of inflammation and oxidative damage and decreased the morphological evidence of pancreas injury at early AP stages. Moreover, it markedly attenuated AP-induced cardiac damage revealed by normalization of the –SH group levels and CK-MB activity. On the basis of these studies, it is possible to conclude that tempol has a profound protective effect against cardiac and pancreatic damage induced by AP.

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High-Fat Diet Induces Oxidative Stress and MPK2 and HSP83 Gene Expression inDrosophila melanogaster

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/4018157 ◽

2016 ◽

Vol 2016 ◽

pp. 1-12 ◽

Cited By ~ 16

Author(s):

Mariane Trindade de Paula ◽

Márcia Rósula Poetini Silva ◽

Stífani Machado Araujo ◽

Vandreza Cardoso Bortolotto ◽

Luana Barreto Meichtry ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Antioxidant Enzymes ◽

High Fat Diet ◽

Saturated Fatty Acids ◽

Coconut Oil ◽

Damage Effect ◽

High Fat ◽

Normal Metabolism ◽

Hsp83 Gene

The consumption of a high-fat diet (HFD) causes alteration in normal metabolism affecting lifespan of flies; however molecular mechanism associated with this damage in flies is not well known. This study evaluates the effects of ingestion of a diet supplemented with 10% and 20% of coconut oil, which is rich in saturated fatty acids, on oxidative stress and cells stress signaling pathways. After exposure to the diet for seven days, cellular and mitochondrial viability, lipid peroxidation and antioxidant enzymes SOD and CAT activity, and mRNA expression of antioxidant enzymes HSP83 and MPK2 were analyzed. To confirm the damage effect of diet on flies, survival and lifespan were investigated. The results revealed that the HFD augmented the rate of lipid peroxidation and SOD and CAT activity and induced a higher expression of HSP83 and MPK2 mRNA. In parallel, levels of enzymes involved in lipid metabolism (ACSL1 and ACeCS1) were increased. Our data demonstrate that association among metabolic changes, oxidative stress, and protein signalization might be involved in shortening the lifespan of flies fed with a HFD.

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Alleviation of liver dysfunction, oxidative stress and inflammation underlines the protective effects of polysaccharides from Cordyceps cicadae on high sugar/high fat diet‐induced metabolic syndrome in rats

Chemistry & Biodiversity ◽

10.1002/cbdv.202100065 ◽

2021 ◽

Author(s):

Xiao Zhang ◽

Jinpeng Li ◽

Bo Yang ◽

Qina Leng ◽

Ji Li ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Liver Dysfunction ◽

High Fat Diet ◽

Protective Effects ◽

High Fat ◽

High Sugar ◽

Cordyceps Cicadae

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Lentinan Protects against Nonalcoholic Fatty Liver Disease by Reducing Oxidative Stress and Apoptosis via the PPARα Pathway

Metabolites ◽

10.3390/metabo12010055 ◽

2022 ◽

Vol 12 (1) ◽

pp. 55

Author(s):

Tingyi Du ◽

Qin Fang ◽

Zhihao Zhang ◽

Chuanmeng Zhu ◽

Renfan Xu ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Chow Diet ◽

Protective Effects ◽

High Fat ◽

Nonalcoholic Fatty Liver

Aim: Lentinan (LNT), a type of polysaccharide derived from Lentinus edodes, has manifested protective effects during liver injury and hepatocellular carcinoma, but little is known about its effects on nonalcoholic fatty liver disease (NAFLD). This study aimed to investigate whether LNT can affect the progression of NAFLD and the associated mechanisms. Methods: C57BL/6J mice were fed a normal chow diet or a high-fat diet (HFD) with or without LNT (6 mg/kg/d). AML12 cells were exposed to 200 μM palmitate acid (PA) with or without LNT (5 μg/mL). Results: After 21 wk of the high-fat diet, LNT significantly decreased plasma triglyceride levels and liver lipid accumulation, reduced excessive reactive oxygen species production, and subsequently attenuated hepatic apoptosis in NAFLD mice. These effects were associated with increased PPARα levels, a decreased Bax/Bcl-2 ratio, and enhancement of the antioxidant defense system in vivo. Similar effects were also observed in cultured cells. More importantly, these protective effects of LNT on palmitate acid-treated AML12 cells were almost abolished by PPARα knockdown. Conclusion: In conclusion, this study demonstrates that LNT may ameliorate hepatic steatosis and decrease oxidative stress and apoptosis by activating the PPARα pathway and is a potential drug target for NAFLD.

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