Protective effects of Cholestin on ethanol induced oxidative stress in rats

Hsieh, You Liang; Yeh, Yen Hung; Lee, Ya Ting; Huang, Chih Yang

doi:10.1002/jsfa.6904

Cited by 12 publications

(7 citation statements)

References 35 publications

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“…Because of varying hepatic cell damages, such as chronic alcohol intake, the levels of ALT and AST are elevated in the plasma. Thus, the increase in AST and ALT are often employed as indicators of cellular damages and hepatic functional impairments [36]. ALT and AST levels in ALD model significantly increased compared with control.…”

Section: Discussionmentioning

confidence: 99%

The hepato-protective effect of eupatilin on an alcoholic liver disease model of rats

Lee

Nam

Choi

et al. 2020

Korean J Physiol Pharmacol

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Eupatilin is known to possess anti-apoptotic, anti-oxidative, and antiinflammatory properties. We report here that eupatilin has a protective effect on the ethanol-induced injury in rats. Sprague-Dawley rats were divided into 6 groups: control, vehicle, silymarin, eupatilin 10 mg/kg, eupatilin 30 mg/kg, and eupatilin 100 mg/kg. Plasma levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were analyzed to determine the extent of liver damage. Total cholesterol (TC) and triglycerides (TG) were analyzed to determine the level of liver steatosis. Malondialdehyde level, superoxide dismutase (SOD) activity, and glutathione (GSH) level were analyzed to determine the extent of oxidative stress. Tumor necrosis factor (TNF)- and interleukin (IL)-1 were quantified to verify the degree of inflammation. Based on our findings, chronic alcohol treatment significantly changed the serum indexes and liver indicators of the model rats, which were significantly improved by eupatilin treatment. Rats in the eupatilin-treatment group showed reduced levels of AST, ALT, TG, TC, TNF-, and IL-1, increased SOD activity and GSH levels, and improved overall physiology compared to the alcoholic liver disease model rats. H&E staining also verified the eupatilin-mediated improvement in liver injury. In conclusion, eupatilin inhibits alcohol-induced liver injury via its antioxidant and anti-inflammatory effects.

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Section: Discussionmentioning

confidence: 99%

The hepato-protective effect of eupatilin on an alcoholic liver disease model of rats

Lee

Nam

Choi

et al. 2020

Korean J Physiol Pharmacol

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“…Serum AST, ALT, ALP, and LDH are among the most sensitive biochemical markers employed in the assessment of liver function. It is proved that AST, AST, ALP, and LDH can be expressed in the liver and that abnormal upregulation of these enzymes would cause damage and necrosis of hepatic cells [ 25 , 26 ]. When the permeability of hepatocellular membrane is enhanced under pathological conditions, these cellular enzymes are released into the bloodstream, resulting in an elevation of serum enzyme levels.…”

Section: Discussionmentioning

confidence: 99%

“…Surprisingly, PD administration further augmented the activities of these two enzymes as compared with ethanol group. The enhancement of this compensatory mechanism by PD might contribute to its hepatoprotective effects by stimulating ethanol metabolism [ 26 , 38 ]. Additionally, our results also demonstrated that the increase of ALDH level was much more potent than that of the ADH level, suggesting that PD is able to avoid acetaldehyde accumulation.…”

Section: Discussionmentioning

confidence: 99%

Polydatin Protects Rat Liver against Ethanol‐Induced Injury: Involvement of CYP2E1/ROS/Nrf2 and TLR4/NF‐κB p65 Pathway

Huang

Liu

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Excessive alcohol consumption leads to serious liver injury, associating with oxidative stress and inflammatory response. Previous study has demonstrated that polydatin (PD) exerted antioxidant and anti-inflammatory effects and attenuated ethanol-induced liver damage, but the research remained insufficient. Hence, this experiment aimed to evaluate the hepatoprotective effect and potential mechanisms of PD on ethanol-induced hepatotoxicity. Our results showed that PD pretreatment dramatically decreased the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in the serum, suppressed the malonaldehyde (MDA) and triglyceride (TG) content and the production of reactive oxygen species (ROS), and enhanced the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), andalcohol dehydrogenase (ADH), and aldehyde dehydrogenase (ALDH), paralleled by an improvement of histopathology alterations. The protective effect of PD against oxidative stress was probably associated with downregulation of cytochrome P450 2E1 (CYP2E1) and upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its target gene haem oxygenase-1 (HO-1). Moreover, PD inhibited the release of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) via downregulating toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) p65. To conclude, PD pretreatment protects against ethanol-induced liver injury via suppressing oxidative stress and inflammation.

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“…AST and ALT are known as being reliable markers for hepatocyte injury liver function leading to necrosis (Ozer et al, 2008). Damaged hepatocytes release their contents into the extracellular space, and so, increased levels of AST and ALT in serum indicate increased permeability and damage and/or necrosis of hepatocytes (Hsieh et al, 2015;Ozer et al, 2008). AST and ALT activities in serum have been previously found to be increased due to ischaemia-reperfusion injury (Gonzalez-Flecha et al, 1993).…”

Section: Enzymatic Activities Of Liver Injury Biomarkers In Serummentioning

confidence: 99%

Therapeutic activity of superoxide dismutase-containing enzymosomes on rat liver ischaemia-reperfusion injury followed by magnetic resonance microscopy

Marcelino

Marinho

Campos

et al. 2017

European Journal of Pharmaceutical Sciences

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Liver ischaemia-reperfusion injury (IRI) may occur during hepatic surgery and is unavoidable in liver transplantation. Superoxide dismutase enzymosomes (SOD-enzymosomes), liposomes where SOD is at the liposomal surface expressing enzymatic activity in intact form without the need of liposomal disruption, were developed with the aim of having a better insight into its antioxidant therapeutic outcome in IRI. We also aimed at validating magnetic resonance microscopy (MRM) at 7T as a tool to follow IRI. SOD-enzymosomes were characterized and tested in a rat ischaemia-reperfusion model and the therapeutic outcome was compared with conventional long circulating SOD liposomes and free SOD using biochemical liver injury biomarkers, histology and MRM. MRM results correlated with those obtained using classical biochemical biomarkers of liver injury and liver histology. Moreover, MRM images suggested that the therapeutic efficacy of both SOD liposomal formulations used was related to prevention of peripheral biliary ductular damage and disrupted vascular architecture. Therefore, MRM at 7T is a useful technique to follow IRI. SOD-enzymosomes were more effective than conventional liposomes in reducing liver ischaemia-reperfusion injury and this may be due to a short therapeutic window.

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Protective effects of Cholestin on ethanol induced oxidative stress in rats

Cited by 12 publications

References 35 publications

The hepato-protective effect of eupatilin on an alcoholic liver disease model of rats

The hepato-protective effect of eupatilin on an alcoholic liver disease model of rats

Polydatin Protects Rat Liver against Ethanol‐Induced Injury: Involvement of CYP2E1/ROS/Nrf2 and TLR4/NF‐κB p65 Pathway

Therapeutic activity of superoxide dismutase-containing enzymosomes on rat liver ischaemia-reperfusion injury followed by magnetic resonance microscopy

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