Berberine protects liver from ethanol-induced oxidative stress and steatosis in mice

Zhang, Pengcheng; Ma, Dongshen; Wang, Yongchen; Zhang, Miao; Xiao, Qiang; Liao, Min; Liu, Xie; Wu, Hui; Zhang, Yubin

doi:10.1016/j.fct.2014.10.005

Cited by 47 publications

(25 citation statements)

References 33 publications

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“…described the protective effects of berberine, an AMPK regulator, against alcohol‐induce oxidative stress and steatosis in mice. Blunted hepatic lipid accumulation, a decrease in oxidative stress by a reduction of LPO, GSH depletion and mitochondrial oxidative damage were found and attributed to the restoration of PPAR‐α by berberine …”

Section: Treatmentmentioning

confidence: 99%

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Molecular basis of alcoholic fatty liver disease: From incidence to treatment

Lívero

Acco

2015

Hepatology Research

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Alcoholic liver diseases have complex and multiple pathogenic mechanisms but still no effective treatment. Steatosis or alcoholic fatty liver disease (AFLD) has a widespread incidence and is the first step in the progression to more severe stages of alcoholic liver disease, with concomitant increases in morbidity and mortality rates. The ways in which this progression occurs and why some individuals are susceptible are still unanswered scientific questions. Research with animal models and clinical evidence have shown that it is a multifactorial disease that involves interactions between lipid metabolism, inflammation, the immune response and oxidative stress. Each of these pathways provides a better understanding of the pathogenesis of AFLD and contributes to the development of therapeutic strategies. This review emphasizes the importance of research on alcoholic steatosis based on incidence data, key pathogenic mechanisms and therapeutic interventions, and discusses perspectives on the progression of this disease.

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Section: Treatmentmentioning

confidence: 99%

“…Blunted hepatic lipid accumulation, a decrease in oxidative stress by a reduction of LPO, GSH depletion and mitochondrial oxidative damage were found and attributed to the restoration of PPAR-α by berberine. 134…”

Section: Nuclear Receptor Modulatorsmentioning

confidence: 99%

Molecular basis of alcoholic fatty liver disease: From incidence to treatment

Lívero

Acco

2015

Hepatology Research

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“…Two independent recent studies showed BBR protects the liver from ethanol-induced oxidative stress both in mice (Zhang et al, 2014) and rats (Patil et al, 2015). The neuroprotective effect of BBR against LD may result from diminished oxidative stress and inhibition of microglial activation.…”

Section: Discussionmentioning

confidence: 99%

Berberine protects against light-induced photoreceptor degeneration in the mouse retina

Song

Wang

et al. 2016

Experimental Eye Research

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Oxidative stress and inflammation play key roles in the light damage (LD) model of photoreceptor degeneration, as well as in age-related macular degeneration (AMD). We sought to investigate whether Berberine (BBR), an antioxidant herb extract, would protect the retina against light-induced degeneration. To accomplish this, Balb/c mice were treated with BBR or PBS via gavage for 7 days, and then were placed in constant cool white light-emitting diode (LED) light (10,000 lux) for 4 hours. Retinal function and degeneration were evaluated by histology, electroretinography (ERG) and optical coherence tomography (OCT) at 7d after LD. Additionally, mRNA levels of cell-type specific, antioxidant, and inflammatory genes were compared 7d after LD. Photoreceptor DNA fragmentation was assessed via the terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. LD resulted in substantial photoreceptor-specific cell death. Histological analysis using plastic sections showed dosing with BBR preserved photoreceptors. The ERG analysis demonstrated functional protection by BBR in rod-b, -a, and cone-b waves. In OCT images, mice receiving PBS showed severe thinning and disorganization of the photoreceptor layer 7 days after LD, whereas mice treated with BBR had significantly less thinning and disorganization. Consistent with OCT results, the mRNA levels of Rho in the NSR, and Rpe65 and Mct3 in the RPE, were significantly higher in mice treated with BBR. The numbers of TUNEL-positive photoreceptors were significantly decreased in BBR-treated mice. The retinal mRNA levels of oxidative stress genes, the number of microglia/macrophages, and the malondialdehyde (MDA) immunolabeling were significantly lower in BBR-treated mice compared to controls 48h after LD, which indicates oxidative stress was reduced by BBR in light-damaged eyes. In conclusion, systemic BBR is protective against light-induced retinal degeneration associated with diminished oxidative stress in the retina. These results suggest that BBR may be protective against retinal diseases involving oxidative stress.

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“…Accumulation of CYP2E1 in mitochondrial membrane leads to local and cellular oxidative stress and plays a vital pathogenic role in the development of alcoholic liver disease (ALD) [28] [29]. Generation of free radicals during ethanol oxidation by cytochrome P4502E1 is an important step in the pathogenesis of ethanol-associated liver injury [30]. CYP2E1 is likely to play a critical role in promoting the generation of ROS, resulting in hepatocyte damage, which is primarily blocked by anti-oxidant enzymes, especially at the pericentral area [31].…”

Section: Discussionmentioning

confidence: 99%

Ascorbic Acid Attenuates Acute Ethanol-Induced Liver Injury in SMP30 Knockout Mice

Cho¹,

Ullah²,

Elfadl³

et al. 2017

FNS

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Ascorbic acid (AA) is recognized as a free radical scavenger that protects cells from oxidative stress-induced damage. However, no studies have investigated the role of AA in acute alcoholic liver disease using senescence marker protein-30 (SMP30) knockout (KO) mice. SMP30 is a novel 34-kDa protein involved in AA biosynthesis. The present study aimed to elucidate the physiological functions of AA in acute ethanol-induced liver injury using SMP30 KO mice, which cannot synthesize AA in vivo. After a 4-week experimental period, mice were divided into six groups. The following three groups comprised the ethanol treatment groups: WT-E group (wild-type), KV-E group (AA-supplemented), and KT-E group (AA-deficient). Mice were exposed to an acute dose of ethanol (6 g ethanol/kg) administered by gavage once a day for three days. The other three control groups, namely, WT-C, KV-C, and KT-C control groups, received an equal volume of water via oral administration. Analysis of changes in body weight showed that mice in the KT-E group had significant loss of body weight compared to the control, KV-E, and WT-E groups. Behavioral analysis revealed that alcohol exposure significantly increased alcohol sensitivity in the KT-E group, whereas the WT-E, KV-E, and control groups developed ethanol tolerance. Aspartate transaminase (AST) levels in the KT-E group were significantly higher than those in the control, KV-E, and WT-E groups. The number of large and binucleated hepatocytes was significantly higher in the KT-E group than in the KV-E and WT-E groups. In addition, cytochrome P450 2E1 (CYP2E1) was over expressed in the central vein in the KT-E group when compared to the KV-E and WT-E groups. Our current findings indicate that AA supplementation in SMP30 KO mice can alleviate alcohol-induced liver damage by down regulating CYP2E1 expression. These results suggest that reduced CYP2E1 expression is a novel How to cite this paper:

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Berberine protects liver from ethanol-induced oxidative stress and steatosis in mice

Cited by 47 publications

References 33 publications

Molecular basis of alcoholic fatty liver disease: From incidence to treatment

Molecular basis of alcoholic fatty liver disease: From incidence to treatment

Berberine protects against light-induced photoreceptor degeneration in the mouse retina

Ascorbic Acid Attenuates Acute Ethanol-Induced Liver Injury in SMP30 Knockout Mice

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