Hepatoprotective effect of curcumin in lipopolysaccharide/-galactosamine model of liver injury in rats: Relationship to HO-1/CO antioxidant system

Černý, Dalibor; Lekić, Nataša; Vanova, Katerina Hadrava; Muchová, Lucie; Hořínek, Aleš; Kmoníčková, Eva; Zı́dek, Zdeňek; Kameníková, L; Farghali, Hassan

doi:10.1016/j.fitote.2011.04.003

Cited by 46 publications

(13 citation statements)

References 40 publications

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“…There may be a causal association between increased peroxidation with elevated ASTs and the weight loss of ZnBG+L-treated pups. Other studies documented a positive correlation between LP and increased ASTs (33,34). Weight loss may be due to LP tissue damage, leading to alterations of membrane integrity.…”

Section: Discussionmentioning

confidence: 93%

Effect of light exposure on metalloporphyrin-treated newborn mice

et al. 2012

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Background: Neonatal hyperbilirubinemia arises from increased bilirubin production and decreased bilirubin elimination. Although phototherapy safely and effectively reduces bilirubin levels, recent evidence shows that it has adverse effects. Therefore, alternative treatments are warranted. Metalloporphyrins, competitive inhibitors of heme oxygenase (hO), the rate-limiting enzyme in bilirubin production, effectively reduce bilirubin formation; however, many are photoreactive. here, we investigated possible photosensitizing effects of chromium mesoporphyrin (crMP) and zinc deuteroporphyrin bis-glycol (ZnBG). Methods and results: Administration of crMP or ZnBG to 3-d-old mouse pups (3.75-30.0 µmol/kg intraperitoneally) and exposure to cool white (F20T12cW) and blue (TL20W/52) fluorescent lights (+L) for 3 h, resulted in a dose-dependent mortality (50% lethal dose (LD50) = 21.5 and 19.5 µmol/kg, respectively). In contrast to ZnBG, there was no significant difference in survival between the crMP+L and crMP groups. Following 30 µmol/kg ZnBG+L, we found significant weight loss, decreased liver antioxidant capacities, and increased aspartate aminotransaminase levels. At 6-d post-light exposure, ZnBG+L-treated pups showed gross and histologic skin changes at doses >7.5 µmol/kg. No lethality was observed following treatment with 30 µmol ZnBG/kg plus exposure to blue light-emitting diodes. Phototoxicity of ZnBG was dependent on light source, emission spectrum, and irradiance. conclusion: Low doses of ZnBG (<3.75 µmol/kg) retained maximal hO inhibitory potency without photosensitizing effects, and therefore are potentially useful in treating neonatal hyperbilirubinemia.

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Section: Discussionmentioning

confidence: 93%

Effect of light exposure on metalloporphyrin-treated newborn mice

et al. 2012

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“…Hepatoprotection of curcumin (single dose at 100 mg/kg intra peritoneal) against lipopolysaccharide-induced hepatitis in d -galactosamine-sensitized rats was clearly connected with the HO-1 up-regulation and the consequently bilirubin production. This protective effect accordingly impacted on nitric oxide synthase 2 (NOS-2) down-regulation and reduced the amounts of NO and lipid peroxidation products in liver [ 88 ].…”

Section: Cellular and Molecular Mechanisms Of Curcumin In The Prevmentioning

confidence: 99%

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

et al. 2018

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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.

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“…Recent studies have shown beneficial effects of curcumin in a liver injury model (Cerny et al, 2011), and curcumin treatment reduced radiation-induced lung fibrosis (Lee et al, 2010). …”

Section: Pharmacological Regulation Of Ho-1 and Its Effector Moleculementioning

confidence: 99%

Heme Oxygenase, Inflammation, and Fibrosis: The Good, the Bad, and the Ugly?

Lundvig¹,

Immenschuh²,

Wagener³

2012

Front. Pharmacol.

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Upon injury, prolonged inflammation and oxidative stress may cause pathological wound healing and fibrosis, leading to formation of excessive scar tissue. Fibrogenesis can occur in most organs and tissues and may ultimately lead to organ dysfunction and failure. The underlying mechanisms of pathological wound healing still remain unclear, and are considered to be multifactorial, but so far, no efficient anti-fibrotic therapies exist. Extra- and intracellular levels of free heme may be increased in a variety of pathological conditions due to release from hemoproteins. Free heme possesses pro-inflammatory and oxidative properties, and may act as a danger signal. Effects of free heme may be counteracted by heme-binding proteins or by heme degradation. Heme is degraded by heme oxygenase (HO) that exists as two isoforms: inducible HO-1 and constitutively expressed HO-2. HO generates the effector molecules biliverdin/bilirubin, carbon monoxide, and free iron/ferritin. HO deficiency in mouse and man leads to exaggerated inflammation following mild insults, and accumulating epidemiological and preclinical studies support the widely recognized notion of the cytoprotective, anti-oxidative, and anti-inflammatory effects of the activity of the HO system and its effector molecules. In this review, we address the potential effects of targeted HO-1 induction or administration of HO-effector molecules as therapeutic targets in fibrotic conditions to counteract inflammatory and oxidative insults. This is exemplified by various clinically relevant conditions, such as hypertrophic scarring, chronic inflammatory liver disease, chronic pancreatitis, and chronic graft rejection in transplantation.

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Hepatoprotective effect of curcumin in lipopolysaccharide/-galactosamine model of liver injury in rats: Relationship to HO-1/CO antioxidant system

Cited by 46 publications

References 40 publications

Effect of light exposure on metalloporphyrin-treated newborn mice

Effect of light exposure on metalloporphyrin-treated newborn mice

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

Heme Oxygenase, Inflammation, and Fibrosis: The Good, the Bad, and the Ugly?

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