Protective effect of quercetin in the regression of ethanol-induced hepatotoxicity

Vidhya, A; Indira, M.

doi:10.4103/0250-474x.58186

Cited by 37 publications

(9 citation statements)

References 23 publications

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“…Ethanol may increase the activity of liver enzymes in mature organisms [50][51][52], but in the present study, the lowest activity was found in the group of animals receiving beer compared with the other groups. Therefore, it may be assumed that any component of beer may have simultaneously influenced the level of protein carbonyl groups and the activity of ALT in the liver of growing rats, but this should be confirmed by further studies.…”

Section: Discussioncontrasting

confidence: 65%

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

et al. 2020

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Typical alcohol consumption begins in the adolescence period, increasing the risk of alcoholic liver disease (ALD) in adolescents and young adults, and while the pathophysiology of ALD is still not completely understood, it is believed that oxidative stress may be the major contributor that initiates and promotes the progression of liver damage. The aim of the present study was to assess the influence of alcohol consumption on the markers of oxidative stress and liver inflammation in the animal model of prolonged alcohol consumption in adolescents using various alcoholic beverages. In a homogenic group of 24 male Wistar rats (4 groups—6 animals per group), since 30th day of life, in order to mimic the alcohol consumption since adolescence, animals received (1) no alcoholic beverage (control group), (2) ethanol solution, (3) red wine, or (4) beer (experimental groups) for 6 weeks. Afterwards, the activities of alcohol dehydrogenase (ADH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), as well as levels of cytochrome P450-2E1 (CYP2E1), thiobarbituric acid-reactive substances (TBARS), protein carbonyl groups, tumor necrosis factor-α (TNF-α), and interleukine-10 (IL-10) were measured in liver homogenates. The difference between studied groups was observed for CYP2E1 and protein carbonyl groups levels (increased levels for animals receiving beer compared with control group), as well as for ALT activity (decreased activity for animals receiving beer compared with other experimental groups) (p < 0.05). The results suggested that some components of beer, other than ethanol, are responsible for its influence on the markers of oxidative stress and liver inflammation observed in the animal model of prolonged alcohol consumption in adolescents. Taking this into account, beer consumption in adolescents, which is a serious public health issue, should be assessed in further studies to broaden the knowledge of the progression of liver damage caused by alcohol consumption in this group.

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Section: Discussioncontrasting

confidence: 65%

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

et al. 2020

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“…Alcohol feeding causes elevation in serum activities of AST, ALT, ALP, γGT and LDH enzymes which are markers of liver damage. In the study reported by Vidhya et al (2009) ethanol treated group resulted in significant increase in AST and ALT activities, which is an indication of hepatocellular damage in rats, whereas treatment with quercetin reduced ethanol -induced toxicity as indicated by the lowering of marker enzymes. In alcohol intoxication as a result of structural changes, an increase in the cell membrane permeability to ions results.…”

Section: Discussionmentioning

confidence: 90%

Hepatoprotective Activity of Herbal Preparation (Hp-4) against Alcohol Induced Hepatotoxicity in Mice

Jangle

2014

Int J Appl Sci Biotechnol

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Free radicals include both Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS).When free radicals are produced in a regulated manner in a healthy human body it is scavenged efficiently by antioxidant defense system. But excess generation of pro-oxidants by continuous chain reaction in the form of ROS and RNS cause several human diseases. The shift of the balance in the favour of pro-oxidants results in a condition called “oxidative stress”. Alcohol is primarily metabolized in the liver to generate ROS and RNS, leading to diseases such as cirrhosis, fatty liver and chronic hepatitis. Alcohol induced damage is associated with oxidative stress. The excess generation of prooxidants and reduced antioxidant levels provide an effective model of Hepatotoxicity which is noteworthy. Recent trend is to discover polyherbal formulation of medicinal plants which have hepatoprotective function. In the present study 80% alcoholic extract of leaves of Aloe vera, Bacopa monniera, Moringa oleifera and rhizome of Zingiber officinale were utilized to prepare Herbal Preparation or HP-4.Further the hepatoprotective effects of HP-4 was tested in alcohol induced Hepatotoxicity in mice. Silymarin is a well known hepatoprotective drug was used as a standard for comparison. Biochemical and histopathological studies provided ample evidence that HP-4 provided a hepatoprotective role in alcohol induced hepatotoxicity which was comparable to drug Silymarin. The presence of phytochemicals in HP-4 provided a synergistic, supra-additive and co-operative effects in the hepatoprotective function in alcohol induced hepatotoxicity mice model. DOI: http://dx.doi.org/10.3126/ijasbt.v2i1.9346 Int J Appl Sci Biotechnol, Vol 2(1): 50-58

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“…A recent report suggested that genistein or apigenin pretreatment could strengthen hepatic antioxidant ability, which contributed to inhibiting the production of CYP2E1-mediated reactive oxygen species, then downregulating the oxidative stress, and finally attenuating alcoholic liver injury [ 13 , 21 ]. Likewise, quercetin and EGCG supplementation could improve the inhibited antioxidant enzyme activity or block the MDA contents in liver resulting from chronic alcohol intake [ 24 , 32 ]. Our data denoted that, although quercetin was more effective at enhancing the HO-1 level ( Figure 4 B), apigenin, naringenin, and genistein had a more efficient effect in terms of increasing the activities of SOD, CAT, GSH, and GSH-Px ( Figure 4 C–F), in agreement with former results.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Five Structurally Diverse Flavonoid Subgroups against Chronic Alcohol-Induced Hepatic Damage in a Mouse Model

et al. 2018

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Alcoholic liver disease (ALD) has become one of the major global health problems, with augmented morbidity and mortality. Evidence indicates that flavonoids can reduce the risk of ALD owing to their biological properties. However, the effect of structurally different flavonoid subclasses on alleviating alcohol-induced liver damage in a same model has never been studied. In this study, mice were supplemented with five kinds of flavonoid subgroups, apigenin (flavone), quercetin (flavonol), naringenin (flavanone), (-)-epigallocatechin gallate (flavanol), and genistein (isoflavone), in the same dose (0.3 mmol kg−1 body weight) and then given 50% alcohol by gastric perfusion for five consecutive weeks. The results demonstrated that genistein and naringenin had greater benefits in terms of mitigating fibrosis and apoptosis, respectively, in the liver. Lipid deposition, partial inflammatory-related factors (nuclear factor kappa B p65, cyclooxygenase-2, and interleukin-6 levels), and hepatic histopathological alterations were similarly attenuated by five kinds of flavonoids. All the flavonoids also showed different degrees of influence on protecting against alcoholic liver injury on other aspects, such as serum biochemistry makers, hepatic lipid accumulation, lipid peroxidation, antioxidant capacities, and inflammation.

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Protective effect of quercetin in the regression of ethanol-induced hepatotoxicity

Cited by 37 publications

References 23 publications

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

Hepatoprotective Activity of Herbal Preparation (Hp-4) against Alcohol Induced Hepatotoxicity in Mice

Protective Effects of Five Structurally Diverse Flavonoid Subgroups against Chronic Alcohol-Induced Hepatic Damage in a Mouse Model

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