Curcumin attenuated paracetamol overdose induced hepatitis

Somanawat, Kanjana; Thong-Ngam, Duangporn; Klaikeaw, Naruemon

doi:10.3748/wjg.v19.i12.1962

Cited by 49 publications

(52 citation statements)

References 25 publications

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“…Similarly, curcumin significantly inhibited the rise in AST, ALT and ALP by (52.8%, 37.08% and 41.8%) as compared to the relative acetaminophen group values. The previous results are in accordance with the results of previous researchers who demonstrated that these increases in liver enzymes were reduced by the administration of curcumin [38] and N-acetylcysteine [39].…”

Section: Discussionsupporting

confidence: 83%

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Protective Effect of Curcumin versus N-acetylcystein on Acetaminophen Induced Hepatotoxicity in Adult Albino Rats

AB¹,

HE²

2015

J Cytol Histol

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Curcumin exerted hepatoprotective influences on various animal models of liver injury such as carbon tetrachloride, endotoxin and thioacetamide. This Study aimed to investigate the protective effects of curcumin as compared to N-acetylcysteine in the rat model of acetaminophen induced hepatotoxicity. 55 albino rats were divided into four groups: group (control group). Group II received acetaminophen. Group III received both acetaminophen and N-acetylcysteine and Group IV received both acetaminophen and curcumin. At the end of the experiment, liver specimens were processed for histological study by light microscope and stained immunohistochemically for detection of apoptosis in hepatic cells by using anti p53 and the oxidative damage by anti-inducible nitric oxide synthase (anti iNOS). Serum levels of liver injury markers were assessed as well as the levels of malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) activity were determined in all dissected tissues. Histological examination of liver sections of acetaminophen treated group revealed degeneration, cytoplasmic vacuolation and hydropic necrosis of hepatocytes. The central and the portal veins were dilated and congested and invading infiltrative inflammatory cells were appeared in association with significant increase in p53 and iNOS positive cells. Significant rise in serum levels of liver injury markers and MDA in liver tissues were recorded. However, levels of GSH and SOD were significantly decreased. Both curcumin and N-acetylcysteine resolved most of these morphological, immunohistochemical and biochemical alterations. Curcumin has protective effect similar to N-acetylcysteine against liver damage induced by acetaminophen in rats by reducing oxidative stress and apoptosis.

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Section: Discussionsupporting

confidence: 83%

“…In this study the GSH consumption caused by acetaminophen overdose was significantly attenuated by administrating curcumin. The protective action of curcumin can be explained by GSH inducer through induction of glutathione reductase enzyme system [38,44].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Curcumin versus N-acetylcystein on Acetaminophen Induced Hepatotoxicity in Adult Albino Rats

AB¹,

HE²

2015

J Cytol Histol

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“…In the APAP-treated group, the liver showed extensive hemorrhagic hepatic necrosis at all zones. Curcumin supplementation caused the liver histopathology to improve (Somanawat et al 2013). Girish et al (2009) treated mice of either sex with curcumin (50 or 100 mg/kg) 7 d before APAP administration (500 mg/kg).…”

Section: Curcuminmentioning

confidence: 99%

“…The study of physical and chemical properties of these compounds as well as the mechanisms involved in hepatoprotection has led to the Curcumin prevented APAP-induced liver damage through the improvement of liver histopathology by reducing liver inflammation, restoring GSH, preventing the lipid peroxidation and augmenting the antioxidant defense system or regeneration of hepatocytes Bulku et al (2012), Somanawat et al (2013), Girish et al (2009) Honey Honey Pretreatment with honey prior to the administration of APAP significantly prevented the increase in the serum levels of hepatic enzyme markers, and reduced both oxidative stress and inflammatory cytokines. Histopathological evaluation of the livers also revealed that honey reduced the incidence of APAP-induced liver lesions Galal et al (2012) Silymarin Milk thistle Post-treatment with silymarin significantly normalized the body weight, histological damage, serum ALT, AST, BUN and creatinine levels.…”

Section: Concluding Remarks and Future Directionsmentioning

confidence: 99%

Role of food-derived antioxidant agents against acetaminophen-induced hepatotoxicity

Eugenio‐Pérez

Oca-Solano

Pedraza‐Chaverrí

2016

Pharmaceutical Biology

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Context Acetaminophen (APAP), also known as paracetamol and N-acetyl p-aminophenol, is one of the most frequently used drugs for analgesic and antipyretic purposes on a worldwide basis. It is safe and effective at recommended doses but has the potential for causing hepatotoxicity and acute liver failure (ALF) with overdose. To solve this problem, different strategies have been developed, including the use of compounds isolated from food, which have been studied to characterize their efficacy as natural dietary antioxidants. Objective The objective of this study is to show the beneficial effects of a variety of natural compounds and their use against acetaminophen-induced hepatotoxicity. Methods PubMed database was reviewed to compile data about natural compounds with hepatoprotective effects against APAP toxicity. Results and conclusion As a result, the health-promoting properties of 13 different food-derived compounds with protective effect against APAP-induced hepatotoxicity were described as well as the mechanisms involved in hepatoprotection.ARTICLE HISTORY

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“…Показано, что нарушения работы системы энергообеспечения выступают вторичным звеном патогенеза ряда заболеваний [4]. Учитывая рост числа регистрируемых побочных (токсических) эффектов лекарственных препаратов и зависимость функциональной активности печени от эффективности работы системы энергообеспечения гепатоцитов [5,6], исследование механизмов, определяющих развитие энергетического дисбаланса, особенно актуально. В контексте изучения биохимических механизмов нарушения функций печени при лекарственных или токсических гепатитах [7], удобным модельным токсином является ацетаминофен, который широко применяется в медицинской практике в качестве анальгетического и пиральгетического средства, а в случае передозировки вызывает существенные повреждения центральнолобулярных областей печени [8].…”

Section: Introductionunclassified

Activity of liver mitochondrial NAD+-dependent dehydrogenases of the krebs cycle in rats with acetaminophen-induced hepatitis developed under conditions of alimentary protein deficiency

Voloshchuk

Kopylchuk

2016

BIOMED KHIM

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Activity of isocitrate dehydrogenase, a-ketoglutarate dehydrogenase, malate dehydrogenase, and the NAD+/NADН ratio were studied in the liver mitochondrial fraction of rats with toxic hepatitis induced by acetaminophen under conditions of alimentary protein deprivation. Acetaminophen-induced hepatitis was characterized by a decrease of isocitrate dehydrogenase, a-ketoglutarate dehydrogenase and malate dehydrogenase activities, while the mitochondrial NAD+/NADН ratio remained at the control level. Modeling of acetaminophen-induced hepatitis in rats with alimentary protein caused a more pronounced decrease in the activity of NAD+-dependent dehydrogenases studied and a 2.2-fold increase of the mitochondrial NAD+/NADН ratio. This suggests that alimentary protein deprivation potentiated drug-induced liver damage

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Curcumin attenuated paracetamol overdose induced hepatitis

Abstract: APAP overdose can cause liver injury. Results indicate that curcumin prevents APAP-induced hepatitis through the improvement of liver histopathology by decreased oxidative stress, reduced liver inflammation, and restoration of GSH.

Cited by 49 publications

References 25 publications

Protective Effect of Curcumin versus N-acetylcystein on Acetaminophen Induced Hepatotoxicity in Adult Albino Rats

Protective Effect of Curcumin versus N-acetylcystein on Acetaminophen Induced Hepatotoxicity in Adult Albino Rats

Role of food-derived antioxidant agents against acetaminophen-induced hepatotoxicity

Activity of liver mitochondrial NAD+-dependent dehydrogenases of the krebs cycle in rats with acetaminophen-induced hepatitis developed under conditions of alimentary protein deficiency

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