Cocoa extract protects against early alcohol-induced liver injury in the rat

McKim, Stephen; Konno, Akira; Gäbele, Erwin; Uesugi, Takehiko; Froh, Mathias; Sies, Helmut; Thurman, Ronald G.; Arteel, Gavin E.

doi:10.1016/s0003-9861(02)00425-3

Cited by 71 publications

(42 citation statements)

References 29 publications

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“…One possible reason might be ultrasound diagnostic method, which could not as accurate as liver biopsy identify the histologic changes, and it may be a possible reason for abcense of significant differences between two groups in our trial. In contrast to our study, McKim et al found that Cocoaextract (400 mg/kg per day) continuously for 4 weeks improves liver function by blunting severe fat accumulation, mild inflammation, and necrosis in earlyalcoholinducedliverinjury in the mice [41] . The point that should be mentioned is that the pathogenesis of alcoholic fatty liver is not similar to NAFLD and this study is the first clinical trial that evaluated the effects of DC on NAFLD.…”

Section: Acknowledgmentcontrasting

confidence: 99%

The Effects of Dark Chocolate Consumption on Lipid Profile, Fasting Blood Sugar, Liver Enzymes, Inflammation, and Antioxidant Status in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized, Placebo-Controlled, Pilot study

Alavinejad

Farsi²,

Rezazadeh³

et al. 2015

Journal of Gastroenterology and Hepatology Research

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BACKGROUND: Nonalcoholic fatty liver disease (NAFLD)is an important health problem worldwide and despite the rising prevalence, there is currently no satisfying therapeutic strategy. Dark chocolate (DC) is a food rich in phenolic antioxidants, which may exert favorable and modifying effects on lipid profile, insulin resistance, oxidative stress, and metabolic effects. This study aims to investigate the possible effects of DC consumption on the lipid profile, fasting blood sugar (FBS), liver transaminases (ALT, and AST), inflammatory, and antioxidant status among NAFLD patients. METHODS: In this double-blind, placebo-controlled trial, 42 patients with NAFLD were randomly allocated to 2 groups: the treatment group (n=21) whom received 30 gr dark chocolate (83%) daily and the control group (n=21), for a 12 weeks period. RESULTS: During the intervention period, taking 30 gr DC (83%) daily resulted in a significant decrease in AST (P=0.012), body weight (P=0.027), and BMI (P=0.042) in the treatment group. In addition, patients who received DC had considerable changes in serum HDL (P=0.044). However, no significant changes occurred in serum levels of ALT, hs-CRP, anthropometric measures (WC, HC, and WHR), and grades of NAFLD in both groups (P>0.05). CONCLUSION: DC consumption can decrease the level of AST in patients with NAFLD and could be a potential therapeutic approach. We recommend more investigation about potential therapeutic effects of dark chocolate to be further clarified.

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Section: Acknowledgmentcontrasting

confidence: 99%

The Effects of Dark Chocolate Consumption on Lipid Profile, Fasting Blood Sugar, Liver Enzymes, Inflammation, and Antioxidant Status in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized, Placebo-Controlled, Pilot study

Alavinejad

Farsi²,

Rezazadeh³

et al. 2015

Journal of Gastroenterology and Hepatology Research

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“…16 Adducts of 4-hydroxynonenal (lipid peroxidation) were detected by immunohistochemistry as described previously. 17 Neutrophil accumulation in the livers was assessed by staining tissue sections for chloracetate esterase, a specific marker for neutrophils, using the naphthol AS-D chloracetate esterase kit (Sigma, St. Louis, MO). 18 Real-Time Polymerase Chain Reaction Analysis of messenger RNA Expression.…”

Section: Clinical Analyses and Histological Examinationmentioning

confidence: 99%

Role of the renin-angiotensin system in hepatic ischemia reperfusion injury in rats

et al. 2004

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It has been shown that the renin-angiotensin system (RAS) plays key roles in the development of fibrosis in numerous organs, including the liver. Other studies have suggested that the RAS also may play roles in diseases of chronic inflammation. However, whether the RAS also can mediate acute inflammation in liver is unclear. The purpose of this study therefore was to determine the effect of the RAS inhibitors captopril and losartan on acute liver damage and inflammation caused by hepatic ischemia and subsequent reperfusion. Accordingly, male rats were subjected to 1 hour of hepatic ischemia (70%) followed by reperfusion; animals were killed 3, 8, or 24 hours after reperfusion. The effect of captopril or losartan (100 or 5 mg/kg intragastrically, respectively) was compared with that of vehicle (saline). The expression of angiotensinogen in liver increased fivefold 3 hours after reperfusion. Indices of liver damage and inflammation (e.g., alanine aminotransferase levels, pathological features, tumor necrosis factor-␣ levels, and intercellular adhesion molecule-1 expression) all were significantly elevated in vehicle-treated animals after hepatic ischemia and subsequent reperfusion. Ischemia and reperfusion also caused an increase in the accumulation of protein adducts of 4-hydroxynonenal, an index of oxidative stress. Captopril or losartan treatment showed profound protective effects under these conditions, significantly blunting the increase in all these parameters caused by ischemia and reperfusion. In conclusion, RAS inhibitors prevent acute liver injury in a model of inflammation caused by ischemia and reperfusion. These data further suggest that the RAS may play a key role in mediating such responses in the liver and suggest a novel role for this system. (HEPATOLOGY 2004;40:583-589.)

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“…Antioxidant treatment in vitro has been demonstrated to protect hepatocytes overexpressing CYP2E1 from the synergistic toxicity of polyunsaturated fats such as arachidonic acid and iron [11]. Similarly, in vivo, feeding with the glutathione precursor L-oxothioazolidine-4-carboxylic acid and with dietary antioxidant extracts from cocoa and green tea, as well as gene therapy resulting in hepatic overexpression of either Cu/Zn or Mn superoxide dismutase has been shown to be protective against ALD [4,[12][13][14][15][16]. It is noteworthy that these later observations were performed in rat intragastric ethanol-infusion models such as that originally developed by Tsukamoto et al [5] where pathology is accompanied by endotoxemia and Kupffer cell activation as measured by increased production of oxidants via NADPH oxidase and increased expression of the endotoxin receptor CD14 [4,[12][13][14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Effects of N-acetylcysteine on ethanol-induced hepatotoxicity in rats fed via total enteral nutrition

Ronis

Butura

Sampey

et al. 2005

Free Radical Biology and Medicine

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The effects of the dietary antioxidant N-acetylcysteine (NAC) on alcoholic liver damage were examined in a total enteral nutrition (TEN) model of ethanol toxicity in which liver pathology occurs in the absence of endotoxemia. Ethanol treatment resulted in steatosis, inflammatory infiltrates, occasional foci of necrosis, and elevated ALT in the absence of increased expression of the endotoxin receptor CD14, a marker of Kupffer cell activation by LPS. In addition, ethanol treatment induced CYP2E1 and increased TNFα and TGFβ mRNA expression accompanied by suppressed hepatic IL-4 mRNA expression. Ethanol treatment also resulted in the hepatic accumulation of malondialdehyde (MDA) and hydroxynonenal (HNE) protein adducts, decreased antioxidant capacity, and increased antibody titers toward serum hydroxyethyl radical (HER), MDA, and HNE adducts. NAC treatment increased cytosolic antioxidant capacity, abolished ethanol-induced lipid peroxidation, and inhibited the formation of antibodies toward HNE and HER adducts without interfering with CYP2E1 induction. NAC also decreased ethanol-induced ALT release and inflammation and prevented significant loss of hepatic GSH content. However, the improvement in necrosis score and reduction of TNFα mRNA elevation did not reach statistical significance. Although a direct correlation was observed among hepatic MDA and HNE adduct content and TNFα mRNA expression, inflammation, and necrosis scores, no correlation was observed between oxidative stress markers or TNFα and steatosis score. These data suggest that ethanol-induced oxidative stress can contribute to inflammation and liver injury even in the absence of Kupffer cell activation by endotoxemia.

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Cocoa extract protects against early alcohol-induced liver injury in the rat

Cited by 71 publications

References 29 publications

The Effects of Dark Chocolate Consumption on Lipid Profile, Fasting Blood Sugar, Liver Enzymes, Inflammation, and Antioxidant Status in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized, Placebo-Controlled, Pilot study

The Effects of Dark Chocolate Consumption on Lipid Profile, Fasting Blood Sugar, Liver Enzymes, Inflammation, and Antioxidant Status in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized, Placebo-Controlled, Pilot study

Role of the renin-angiotensin system in hepatic ischemia reperfusion injury in rats

Effects of N-acetylcysteine on ethanol-induced hepatotoxicity in rats fed via total enteral nutrition

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