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Liver, Oxidative Stress and Metabolic Syndromes

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A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (31 March 2019) | Viewed by 100728

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Special Issue Editor

Prof. Dr. Rita Rezzani

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Guest Editor

Anatomy and Physiopathology Division, Department of Clinical and Experimental Sciences, University of Brescia, 25123 Brescia, Italy
Interests: antioxidants; sex differences; skin; melatonin; oxidative stress and cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue “Liver, Oxidative Stress and Metabolic Syndromes” should shed light on different physiological hepatic functions, its several pathologies, and the mechanisms involved in these disorders. Moreover, it is focused on several therapeutic treatments considering also the different approaches, such as antioxidant, probiotic, prebiotics or a combination of both (symbiotics) substances.

The liver is a vital organ with numerous metabolic functions, including metabolism of both host and foreign molecules, glucose homeostasis, protein synthesis and detoxification. This organ is constantly exposed to viruses, pathogens and toxins, including gut microbiota. Moreover, this organ is often subjected to the injury related to overnutrition, obesity and metabolic syndrome. Lipid accumulation in hepatocytes has become one of the most frequent causes of liver abnormalities in Western countries. This pathology can cause histological abnormalities ranging from simple steatosis up to a progressive and chronic inflammation and, eventually, cirrhosis and hepatocellular carcinoma. It is known that many of these disorders are associated with hepatic changes in the enzymatic and non-enzymatic oxidative capacities. Thus, the oxidative stress, due to an increased reactive oxygen species (ROS) production, is one of the most important etiology of different liver disorders.

In conclusion, this Special Issue should review all aspects concerning the biological and biochemical mechanisms of hepatic physiological and pathological metabolism in order to ameliorate the therapeutic approaches of different disorders.

I encourage you to submit your manuscripts that fit with the objectives and topics of this Special Issue.

Prof. Rezzani Rita
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (14 papers)

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Editorial

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4 pages, 199 KiB

Open AccessEditorial

Liver, Oxidative Stress and Metabolic Syndromes

by Rita Rezzani and Caterina Franco

Nutrients 2021, 13(2), 301; https://doi.org/10.3390/nu13020301 - 21 Jan 2021

Cited by 23 | Viewed by 2455

Abstract

Today, talking about metabolic syndrome (MetS) and oxidative stress, can be risky [...] Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

Research

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23 pages, 4751 KiB

Open AccessArticle

Effects of Moderate Chronic Food Restriction on the Development of Postprandial Dyslipidemia with Ageing

by Alejandro Fernández, Lorena Mazuecos, Cristina Pintado, Blanca Rubio, Virginia López, Alain J. de Solís, María Rodríguez, Antonio Andrés and Nilda Gallardo

Nutrients 2019, 11(8), 1865; https://doi.org/10.3390/nu11081865 - 10 Aug 2019

Cited by 7 | Viewed by 3379

Abstract

Ageing is a major risk factor for the development of metabolic disorders linked to dyslipidemia, usually accompanied by increased adiposity. The goal of this work was to investigate whether avoiding an excessive increase in adiposity with ageing, via moderate chronic food restriction (FR), ameliorates postprandial dyslipidemia in a rat model of metabolic syndrome associated with ageing. Accordingly, we performed an oral lipid loading test (OLLT) in mature middle-aged (7 months) and middle-old-aged (24 months) Wistar rats fed ad libitum (AL) or under moderate FR for 3 months. Briefly, overnight fasted rats were orally administered a bolus of extra-virgin olive oil (1 mL/Kg of body weight) and blood samples were taken from the tail vein before fat load (t = 0) and 30, 60, 90, 120, 180, and 240 min after fat administration. Changes in serum lipids, glucose, insulin, and glucagon levels were measured at different time-points. Expression of liver and adipose tissue metabolic genes were also determined before (t = 0) and after the fat load (t = 240 min). Postprandial dyslipidemia progressively increased with ageing and this could be associated with hepatic ChREBP activity. Interestingly, moderate chronic FR reduced adiposity and avoided excessive postprandial hypertriglyceridemia in 7- and 24-month-old Wistar rats, strengthening the association between postprandial triglyceride levels and adiposity. The 24-month-old rats needed more insulin to maintain postprandial normoglycemia; nevertheless, hyperglycemia occurred at 240 min after fat administration. FR did not alter the fasted serum glucose levels but it markedly decreased glucagon excursion during the OLLT and the postprandial rise of glycemia in the 24-month-old rats, and FGF21 in the 7-month-old Wistar rats. Hence, our results pointed to an important role of FR in postprandial energy metabolism and insulin resistance in ageing. Lastly, our data support the idea that the vWAT might function as an ectopic site for fat deposition in 7-month-old and in 24-month-old Wistar rats that could increase their browning capacity in response to an acute fat load. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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14 pages, 2123 KiB

Open AccessArticle

A Mitochondrial Specific Antioxidant Reverses Metabolic Dysfunction and Fatty Liver Induced by Maternal Cigarette Smoke in Mice

by Gerard Li, Yik Lung Chan, Suporn Sukjamnong, Ayad G. Anwer, Howard Vindin, Matthew Padula, Razia Zakarya, Jacob George, Brian G. Oliver, Sonia Saad and Hui Chen

Nutrients 2019, 11(7), 1669; https://doi.org/10.3390/nu11071669 - 21 Jul 2019

Cited by 30 | Viewed by 4684

Abstract

Maternal smoking leads to glucose and lipid metabolic disorders and hepatic damage in the offspring, potentially due to mitochondrial oxidative stress. Mitoquinone mesylate (MitoQ) is a mitochondrial targeted antioxidant with high bioavailability. This study aimed to examine the impact of maternal cigarette smoke exposure (SE) on offspring’s metabolic profile and hepatic damage, and whether maternal MitoQ supplementation during gestation can affect these changes. Female Balb/c mice (eight weeks) were either exposed to air or SE for six weeks prior to mating and throughout gestation and lactation. A subset of the SE dams were supplied with MitoQ in the drinking water (500 µmol/L) during gestation and lactation. Intraperitoneal glucose tolerance test was performed in the male offspring at 12 weeks and the livers and plasma were collected at 13 weeks. Maternal SE induced glucose intolerance, hepatic steatosis, mitochondrial oxidative stress and related damage in the adult offspring. Maternal MitoQ supplementation reduced hepatic mitochondrial oxidative stress and improved markers of mitophagy and mitochondrial biogenesis. This may restore hepatic mitochondrial health and was associated with an amelioration of glucose intolerance, hepatic steatosis and pathological changes induced by maternal SE. MitoQ supplementation may potentially prevent metabolic dysfunction and hepatic pathology induced by intrauterine SE. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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14 pages, 2754 KiB

Open AccessArticle

Fatty Acid Desaturase Involvement in Non-Alcoholic Fatty Liver Disease Rat Models: Oxidative Stress Versus Metalloproteinases

by Giuseppina Palladini, Laura G. Di Pasqua, Clarissa Berardo, Veronica Siciliano, Plinio Richelmi, Barbara Mannucci, Anna Cleta Croce, Vittoria Rizzo, Stefano Perlini, Mariapia Vairetti and Andrea Ferrigno

Nutrients 2019, 11(4), 799; https://doi.org/10.3390/nu11040799 - 08 Apr 2019

Cited by 18 | Viewed by 3579

Abstract

We investigated changes in fatty acid desaturases, D5D, D6D, D9-16D and D9-18D, and their relationship with oxidative stress, matrix metalloproteinases (MMPs) and serum TNF-alpha in two rat models of non-alcoholic fatty liver disease NAFLD. Eight-week-old male Wistar rats fed for 3 weeks with methionine-choline–deficient (MCD) diet and eleven-week-old Obese male Zucker rats were used. Serum levels of hepatic enzymes and TNF-alpha were quantified. Hepatic oxidative stress (ROS, TBARS and GSH content) and MMP-2 and MMP-9 (protein expression and activity) were evaluated. Liver fatty acid profiling, performed by GC-MS, was used for the quantification of desaturase activities. Higher D5D and D9-16D were found in Obese Zucker rats as well as an increase in D9-18D in MCD rats. D6D was found only in MCD rats. A negative correlation between D5D and D9-16D versus TBARS, ROS and TNF-alpha and a positive correlation with GSH were shown in fatty livers besides a positive correlation between D9-18D versus TBARS, ROS and TNF-alpha and a negative correlation with GSH. A positive correlation between D5D or D9-16D or D9-18D versus protein expression and the activity of MMP-2 were found. NAFLD animal models showed comparable serum enzymes. These results reinforce and extend findings on the identification of therapeutic targets able to counteract NAFLD disorder. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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11 pages, 1966 KiB

Open AccessCommunication

Effects of Pharmacological Thermogenic Adipocyte Activation on Metabolism and Atherosclerotic Plaque Regression

by Anna Worthmann, Christian Schlein, Jimmy F. P. Berbée, Patrick C. N. Rensen, Joerg Heeren and Alexander Bartelt

Nutrients 2019, 11(2), 463; https://doi.org/10.3390/nu11020463 - 23 Feb 2019

Cited by 11 | Viewed by 4519

Abstract

Thermogenic adipocytes burn nutrients in order to produce heat. Upon activation, brown adipose tissue (BAT) clears vast amounts of lipids and glucose from the circulation and thus substantially lowers plasma lipid levels. As a consequence, BAT activation protects from the development of atherosclerosis. However, it is unclear if pharmacologic activation of BAT can be exploited therapeutically to reduce plaque burden in established atherosclerotic disease. Here we study the impact of thermogenic adipose tissues on plaque regression in a mouse model of atherosclerosis. Thermogenic adipocytes in atherosclerotic low-density lipoprotein (LDL) receptor (LDLR)-deficient mice were pharmacologically activated by dietary CL316,243 (CL) treatment for 4 weeks and the outcomes on metabolically active tissues, plasma lipids and atherosclerosis were analyzed. While the chronic activation of thermogenic adipocytes reduced adiposity, increased browning of white adipose tissue (WAT), altered liver gene expression, and reduced plasma triglyceride levels, atherosclerotic plaque burden remained unchanged. Our findings suggest that despite improving adiposity and plasma triglycerides, pharmacologic activation of thermogenic adipocytes is not able to reverse atherosclerosis in LDLR-deficient mice. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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17 pages, 3799 KiB

Open AccessArticle

Bamboo Stems (Phyllostachys nigra variety henosis) Containing Polyphenol Mixtures Activate Nrf2 and Attenuate Phenylhydrazine-Induced Oxidative Stress and Liver Injury

by Ji Hye Yang, Moon-Hee Choi, Chang-Su Na, Sam Seok Cho, Jae Hoon Kim, Sae Kwang Ku, Il Je Cho, Hyun-Jae Shin and Sung Hwan Ki

Nutrients 2019, 11(1), 114; https://doi.org/10.3390/nu11010114 - 08 Jan 2019

Cited by 16 | Viewed by 4461

Abstract

This study was designed to investigate the hepatoprotective effect of bamboo stems using in vitro and in vivo experimental liver damage models. Ethyl acetate fraction of 80% ethanol extract of Phyllostachys nigra stem (PN3) containing polyphenols had a higher NQO1-ARE reporter gene activity as monitored by the activity of the NF-E2-related factor (Nrf2) antioxidant pathway in cells in comparison to extracts from other species and under other conditions. The Nrf2 was translocated from the cytosol to the nucleus in response to PN3, followed by induction of the Nrf2 target gene expression, including HO-1, GCL, and NQO-1 in HepG2 cells. Phosphorylation of Nrf2 in HepG2 cells was enhanced in PN3, which was mediated by PKCδ, ERK, and p38 MAPK. Consequently, PN3 inhibited arachidonic acid (AA) + iron-induced reactive oxygen species generation and glutathione depletion, and, thus, highlighted their role in cytotoxicity. Treatment with major polyphenols of PN3, including catechin, chlorogenic acid, caffeic acid, and p-coumaric acid, also improved AA + iron-mediated oxidative stress and, thus, improved cell viability. Treatment with phenylhydrazine in mice, i.e., the iron overload liver injury model, increased plasma alanine aminotransferase and aspartate aminotransferase levels and changed histological features in mice—a response that was almost completely blocked by PN3 administration. Moreover, PN3 extract mitigated phenylhydrazine-induced oxidative stress and inflammatory responses. Conclusively, PN3 can exert a hepatoprotective effect against iron overload-induced acute liver damage due to its antioxidant properties. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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14 pages, 2314 KiB

Open AccessArticle

Effect of Wakame and Carob Pod Snacks on Non-Alcoholic Fatty Liver Disease

by Daniel Rico, Ana Belén Martin-Diana, Arrate Lasa, Leixuri Aguirre, Iñaki Milton-Laskibar, Daniel Antonio De Luis and Jonatan Miranda

Nutrients 2019, 11(1), 86; https://doi.org/10.3390/nu11010086 - 04 Jan 2019

Cited by 8 | Viewed by 3637

Abstract

Snacks combining different functional ingredients could represent a useful therapeutic strategy against NAFLD. The present study aimed to analyze the effect of two snack formulations based on carob and wakame flour in the treatment for NAFLD in rats. For this purpose, metabolic syndrome was induced in 50 adult rats by a high-fat high-fructose diet over eight weeks. After this period, rats were fed either normal calorie diets supplemented or not with snack A (1/50 wakame/carob pod) and snack B (1/5 wakame/carob pod) for four additional weeks. After sacrifice, liver composition and serum parameters were analyzed. Different pathways of triacylglycerol metabolism in liver were studied including fatty acid oxidation, fatty acid synthesis, triglyceride assembly and release, fatty acid uptake and glucose uptake. Oxidative stress was also measured. Snack treatment, and mainly B snack, reduced liver triacylglycerol levels by increasing fat oxidation. Moreover, this snack reduced oxidative stress. Therefore, this snack formulation could represent an interesting tool useful for fatty liver treatment. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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18 pages, 4870 KiB

Open AccessArticle

Pistachio Consumption Prevents and Improves Lipid Dysmetabolism by Reducing the Lipid Metabolizing Gene Expression in Diet-Induced Obese Mice

by Simona Terzo, Gaetano Felice Caldara, Vincenzo Ferrantelli, Roberto Puleio, Giovanni Cassata, Flavia Mulè and Antonella Amato

Nutrients 2018, 10(12), 1857; https://doi.org/10.3390/nu10121857 - 01 Dec 2018

Cited by 22 | Viewed by 4196

Abstract

Pistachios contain beneficial substances such as unsaturated fatty acids, phytosterols, and polyphenols. In the present study, we investigated if pistachio consumption is able to prevent or to revert hyperglycemia, dyslipidemia, hepatic steatosis, and adipose tissue morphological alterations caused by high fat diet (HFD) in the mouse. Moreover, the impact of pistachio intake on the mRNA expression of peroxisome proliferator-activated receptor γ (PPAR-γ), fatty acid transport proteins (FAT-P), fatty acid synthase (FAS), stearoyl-CoA desaturase (SCD1), and sterol regulatory element-binding transcription factor-1c (SREBP-1c) in liver and adipose tissue was also analyzed. No change in body weight, food intake, and hyperglycemia was observed between mice consuming pistachios (HFD-P) and HFD mice. Pistachio intake was able to prevent but not to reverse HFD-induced hypertriglyceridemia. Cholesterol plasma levels, steatosis grading, body fat mass, and adipocyte size were significantly lower in HFD-P group compared to HFD in both prevention and reversal protocol. Pistachio-diet was able to prevent HFD-induced overexpression of PPAR-γ, FAS, and SCD1 in the liver and SREBP-1c, PPAR-γ, and FAT-P in adipose tissue. Similarly, HFD-P significantly ameliorated the expression levels of FAT-P and SCD1 in the liver and SREBP-1c, FAS, and SCD1 in adipose tissue of obese mice. The present study shows that pistachio consumption is able to prevent and to ameliorate obesity-related dysfunctions by positively modulating the expression of genes linked to lipid metabolism. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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16 pages, 1085 KiB

Open AccessArticle

Association of Dietary Patterns with Metabolic Syndrome: Results from the Kardiovize Brno 2030 Study

by Antonella Agodi, Andrea Maugeri, Sarka Kunzova, Ondrej Sochor, Hana Bauerova, Nikola Kiacova, Martina Barchitta and Manlio Vinciguerra

Nutrients 2018, 10(7), 898; https://doi.org/10.3390/nu10070898 - 13 Jul 2018

Cited by 73 | Viewed by 5353

Abstract

Although metabolic syndrome (MetS) could be handled by lifestyle interventions, its relationship with dietary patterns remains unclear in populations from Central Europe. Using data from the Kardiovize Brno cohort, the present study aims to identify the main dietary patterns and to evaluate their association with MetS risk in a random urban sample from Brno, Czech Republic. In a cross-sectional study of 1934 subjects aged 25–65 years (44.3% male), dietary patterns were derived by food frequency questionnaire (FFQ) administration and principal component analysis. Metabolic syndrome was defined according to the International Diabetes Federation statement. Logistic regression models were applied. High adherence to the prudent dietary pattern was associated with lower odds of abdominal obesity, abnormal glucose concentration, and MetS. By contrast, high adherence to the western dietary pattern was associated with higher odds of abnormal glucose, triglycerides and blood pressure levels. Whilst our results confirm the deleterious effect of a western dietary pattern on several metabolic risk factors, they also indicate that the consumption of a diet rich in cereals, fish, fruit and vegetables is associated with a healthier metabolic profile. However, further prospective research is warranted to develop and validate novel potential preventive strategies against MetS and its complications. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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Review

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19 pages, 8575 KiB

Open AccessReview

The Role of Autophagy in Liver Epithelial Cells and Its Impact on Systemic Homeostasis

by Luana Tomaipitinca, Sara Mandatori, Romina Mancinelli, Federico Giulitti, Simonetta Petrungaro, Viviana Moresi, Antonio Facchiano, Elio Ziparo, Eugenio Gaudio and Claudia Giampietri

Nutrients 2019, 11(4), 827; https://doi.org/10.3390/nu11040827 - 11 Apr 2019

Cited by 20 | Viewed by 5705

Abstract

Autophagy plays a role in several physiological and pathological processes as it controls the turnover rate of cellular components and influences cellular homeostasis. The liver plays a central role in controlling organisms’ metabolism, regulating glucose storage, plasma proteins and bile synthesis and the removal of toxic substances. Liver functions are particularly sensitive to autophagy modulation. In this review we summarize studies investigating how autophagy influences the hepatic metabolism, focusing on fat accumulation and lipids turnover. We also describe how autophagy affects bile production and the scavenger function within the complex homeostasis of the liver. We underline the role of hepatic autophagy in counteracting the metabolic syndrome and the associated cardiovascular risk. Finally, we highlight recent reports demonstrating how the autophagy occurring within the liver may affect skeletal muscle homeostasis as well as different extrahepatic solid tumors, such as melanoma. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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25 pages, 1525 KiB

Open AccessReview

Impact of Nutritional Changes on Nonalcoholic Fatty Liver Disease

by Carolina M. Perdomo, Gema Frühbeck and Javier Escalada

Nutrients 2019, 11(3), 677; https://doi.org/10.3390/nu11030677 - 21 Mar 2019

Cited by 130 | Viewed by 16907

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a major global health threat due to its growing incidence and prevalence. It is becoming the leading cause of liver disease in addition to its strong association with cardio-metabolic disease. Therefore, its prevention and treatment are of strong public interest. Therapeutic approaches emphasize lifestyle modifications including physical activity and the adoption of healthy eating habits that intend to mainly control body weight and cardio-metabolic risk factors associated with the metabolic syndrome. Lifestyle interventions may be reinforced by pharmacological treatment in advanced stages, though there is still no registered drug for the specific treatment of NAFLD. The purpose of this review is to assess the evidence available regarding the impact of dietary recommendations against NAFLD, highlighting the effect of macronutrient diet composition and dietary patterns in the management of NAFLD. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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15 pages, 1930 KiB

Open AccessReview

Beta-Aminoisobutyric Acid as a Novel Regulator of Carbohydrate and Lipid Metabolism

by Dmitrii A. Tanianskii, Natalia Jarzebska, Andreas L. Birkenfeld, John F. O’Sullivan and Roman N. Rodionov

Nutrients 2019, 11(3), 524; https://doi.org/10.3390/nu11030524 - 28 Feb 2019

Cited by 74 | Viewed by 11301

Abstract

The prevalence and incidence of metabolic syndrome is reaching pandemic proportions worldwide, thus warranting an intensive search for novel preventive and treatment strategies. Recent studies have identified a number of soluble factors secreted by adipocytes and myocytes (adipo-/myokines), which link sedentary life style, abdominal obesity, and impairments in carbohydrate and lipid metabolism. In this review, we discuss the metabolic roles of the recently discovered myokine β-aminoisobutyric acid (BAIBA), which is produced by skeletal muscle during physical activity. In addition to physical activity, the circulating levels of BAIBA are controlled by the mitochondrial enzyme alanine: glyoxylate aminotransferase 2 (AGXT2), which is primarily expressed in the liver and kidneys. Recent studies have shown that BAIBA can protect from diet-induced obesity in animal models. It induces transition of white adipose tissue to a “beige” phenotype, which induces fatty acids oxidation and increases insulin sensitivity. While the exact mechanisms of BAIBA-induced metabolic effects are still not well understood, we discuss some of the proposed pathways. The reviewed data provide new insights into the connection between physical activity and energy metabolism and suggest that BAIBA might be a potential novel drug for treatment of the metabolic syndrome and its cardiovascular complications. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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25 pages, 884 KiB

Open AccessReview

Dietary Melatonin Supplementation Could Be a Promising Preventing/Therapeutic Approach for a Variety of Liver Diseases

by Francesca Bonomini, Elisa Borsani, Gaia Favero, Luigi F. Rodella and Rita Rezzani

Nutrients 2018, 10(9), 1135; https://doi.org/10.3390/nu10091135 - 21 Aug 2018

Cited by 38 | Viewed by 7490

Abstract

In the therapeutic strategies, the role of diet is a well-established factor that can also have an important role in liver diseases. Melatonin, identified in animals, has many antioxidant properties and it was after discovered also in plants, named phytomelatonin. These substances have a positive effect during aging and in pathological conditions too. In particular, it is important to underline that the amount of melatonin produced by pineal gland in human decreases during lifetime and its reduction in blood could be related to pathological conditions in which mitochondria and oxidative stress play a pivotal role. Moreover, it has been indicated that melatonin/phytomelatonin containing foods may provide dietary melatonin, so their ingestion through balanced diets could be sufficient to confer health benefits. In this review, the classification of liver diseases and an overview of the most important aspects of melatonin/phytomelatonin, concerning the differences among their synthesis, their presence in foods and their role in health and diseases, are summarized. The findings suggest that melatonin/phytomelatonin supplementation with diet should be considered important in preventing different disease settings, in particular in liver. Currently, more studies are needed to strengthen the potential beneficial effects of melatonin/phytomelatonin in liver diseases and to better clarify the molecular mechanisms of action. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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28 pages, 1244 KiB

Open AccessReview

Curcumin in Liver Diseases: A Systematic Review of the Cellular Mechanisms of Oxidative Stress and Clinical Perspective

by Mohammad Hosein Farzaei, Mahdi Zobeiri, Fatemeh Parvizi, Fardous F. El-Senduny, Ilias Marmouzi, Ericsson Coy-Barrera, Rozita Naseri, Seyed Mohammad Nabavi, Roja Rahimi and Mohammad Abdollahi

Nutrients 2018, 10(7), 855; https://doi.org/10.3390/nu10070855 - 01 Jul 2018

Cited by 268 | Viewed by 21927

Abstract

Oxidative stress has been considered a key causing factor of liver damage induced by a variety of agents, including alcohol, drugs, viral infections, environmental pollutants and dietary components, which in turn results in progression of liver injury, non-alcoholic steatohepatitis, non-alcoholic liver disease, liver fibrosis and cirrhosis. During the past 30 years and even after the major progress in the liver disease management, millions of people worldwide still suffer from an acute or chronic liver condition. Curcumin is one of the most commonly used indigenous molecules endowed by various shielding functionalities that protects the liver. The aim of the present study is to comprehensively review pharmacological effects and molecular mechanisms, as well as clinical evidence, of curcumin as a lead compound in the prevention and treatment of oxidative associated liver diseases. For this purpose, electronic databases including “Scopus,” “PubMed,” “Science Direct” and “Cochrane library” were extensively searched with the keywords “curcumin or curcuminoids” and “hepatoprotective or hepatotoxicity or liver” along with “oxidative or oxidant.” Results showed that curcumin exerts remarkable protective and therapeutic effects of oxidative associated liver diseases through various cellular and molecular mechanisms. Those mechanisms include suppressing the proinflammatory cytokines, lipid perodixation products, PI3K/Akt and hepatic stellate cells activation, as well as ameliorating cellular responses to oxidative stress such as the expression of Nrf2, SOD, CAT, GSH, GPx and GR. Taking together, curcumin itself acts as a free radical scavenger over the activity of different kinds of ROS via its phenolic, β-diketone and methoxy group. Further clinical studies are still needed in order to recognize the structure-activity relationships and molecular mechanisms of curcumin in oxidative associated liver diseases. Full article

(This article belongs to the Special Issue Liver, Oxidative Stress and Metabolic Syndromes)

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