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

Eugenio‐Pérez, Dianelena; Oca-Solano, Héctor Adolfo Montes de; Pedraza‐Chaverrí, José

doi:10.3109/13880209.2016.1150302

Cited by 44 publications

(38 citation statements)

References 126 publications

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“…Normally, the APAP is metabolized to non-toxic metabolites by glucuronides or sulfates in hepatocytes before it is finally excreted in the urine. However, once the capacity of normal metabolic pathways is saturated, surplus APAP will be metabolized by the cytochrome P450 (CYP) enzymes (most notably CYP2E1), producing a highly reactive and toxic intermediate N -acetyl- p -benzoquinone imine (NAPQI) and reactive oxygen species (ROS) [ 3 , 4 ]. Glutathione (GSH) could immediately metabolize and neutralize NAPQI to harmless mercapturic acid.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, the activation of the mitogen activated protein kinase (MAPK), c-Jun- N -terminal kinase (JNK), and the subsequent inflammatory responses result in the programmed injury [ 6 , 8 ]. It is evidenced that both oxidative stress [ 4 , 6 , 8 , 9 , 10 ] and inflammatory response [ 2 , 6 , 10 ] are involved in hepatic injury in APAP-induced liver injury model.…”

Section: Introductionmentioning

confidence: 99%

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Hepatoprotective Effect of Ugonin M, A Helminthostachys zeylanica Constituent, on Acetaminophen-Induced Acute Liver Injury in Mice

Kuo

et al. 2018

Molecules

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The present study aimed to discover the possible effectiveness of Ugonin M, a unique flavonoid isolated from Helminthostachys zeylanica—a traditional Chinese medicine used as anti-inflammatory medicine—and to elucidate the potential mechanisms of Ugonin M in the acute liver injury induced by acetaminophen (APAP). In this study, Ugonin M significantly ameliorated APAP-induced histopathological changes and the typical liver function biomarkers (i.e., alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (T-Bil)). It also affected APAP-induced abnormal lipid metabolism including total cholesterol (TC) and triglyceride (TG) in the serum. In inflammatory pharmacological action, Ugonin M suppressed the pro-inflammatory mediators such as nitric oxide (NO) and the lipid peroxidation indicator malondialdehyde (MDA). In addition, Ugonin M reinforced hemeoxygenase-1 (HO-1) protein expression and the production of antioxidant enzymes viz superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT). Furthermore, inflammation-associated cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β as well as proteins such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were decreased by the pretreatment of Ugonin M. Moreover, this study found that pretreatment of Ugonin M apparently decreased nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) activation via inhibition of the degradation of NF-κB, inhibitory κB-α (IκB-α), extracellular regulated kinase (ERK), c-Jun-N-terminal (JNK), and p38 active phosphorylation. In conclusion, Ugonin M significantly showed a protective effect against APAP-induced liver injury by reducing oxidative stress and inflammation. Thus, Ugonin M could be one of the effective components of H. zeylanica that plays a major role in the treatment of inflammatory disorders.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hepatoprotective Effect of Ugonin M, A Helminthostachys zeylanica Constituent, on Acetaminophen-Induced Acute Liver Injury in Mice

Kuo

et al. 2018

Molecules

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“…APAP-induced hepatotoxicity has been a significant issue for several years and different strategies have been studied, including the use of natural compounds with hepatoprotective effects [5, 6]. …”

Section: Introductionmentioning

confidence: 99%

Hepatoprotective Effect of Citral on Acetaminophen‐Induced Liver Toxicity in Mice

Uchida

Silva-Filho

Cardia

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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High doses of acetaminophen (APAP) lead to acute liver damage. In this study, we evaluated the effects of citral in a murine model of hepatotoxicity induced by APAP. The liver function markers alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyl transferase (γGT) were determined to evaluate the hepatoprotective effects of citral. The livers were used to determine myeloperoxidase (MPO) activity and nitric oxide (NO) production and in histological analysis. The effect of citral on leukocyte migration and antioxidant activity was evaluated in vitro. Citral pretreatment decreased significantly the levels of ALT, AST, ALP, and γGT, MPO activity, and NO production. The histopathological analysis showed an improvement of hepatic lesions in mice after citral pretreatment. Citral inhibited neutrophil migration and exhibited antioxidant activity. Our results suggest that citral protects the liver against liver toxicity induced by APAP.

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“…(Woolbright and Jaeschke, 2017). Paracetamol-induced liver toxicity has been a most important problem for many years, and various strategies have been investigated, together with the utilizing the natural bioactive compounds with hepatoprotective activity (Eugenio-Pérez et al, 2016;Ekpenyong et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the hepatoprotective activity of various extracts of Dyschoriste littoralis nees on paracetamol-induced hepatotoxicity rats

Balakrishnan²,

2020

ijrps

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The current investigation was to examine the hepatoprotective potential of D.littoralis Nees. (family Acanthaceae) On paracetamol-induced hepatotoxicity in rats. The aerial parts of D.littoralis Nees. The powder was concentrated with various solvents (PE, EA, and methanol) through Soxhlet concentrates and different crude concentrates utilized for hepatoprotective activity. Hepatotoxicity was induced by paracetamol (2g/kg b.wt.) on the 5th day of the investigational period and given orally. Paracetamol-induced rats to exhibit elevated activities of liver enzymes such as SGOT, SGPT, ALP, gamma-glutamyltranspeptidase (GGT), creatinine, urea, total bilirubin, total cholesterol & triglyc in serum. Furthermore, Oral administration of the ethyl acetate concentrates of D.littoralis (200 mg/ kgb.wt.) given rats were significant reduction the level of SGOT, SGPT, ALP, gamma-glutamyltranspeptidase (GGT) creatinine, urea, total bilirubin, total cholesterol & triglycerides when compared to other concentrates. They also significantly elevated the concentration of complete protein and albumin when compared to other concentrates. Thus, results suggested that ethyl acetate concentrates of D.littoralis could afford better hepatoprotective activity against paracetamol-induced hepatotoxicity rats.

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

Cited by 44 publications

References 126 publications

Hepatoprotective Effect of Ugonin M, A Helminthostachys zeylanica Constituent, on Acetaminophen-Induced Acute Liver Injury in Mice

Hepatoprotective Effect of Ugonin M, A Helminthostachys zeylanica Constituent, on Acetaminophen-Induced Acute Liver Injury in Mice

Hepatoprotective Effect of Citral on Acetaminophen‐Induced Liver Toxicity in Mice

Evaluation of the hepatoprotective activity of various extracts of Dyschoriste littoralis nees on paracetamol-induced hepatotoxicity rats

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