• Journal of Nutrition and Health
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• v.49 no.6
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• pp.420-428
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• 2016

Purpose: In this study, we investigated the effects of Cirsium setidens ethanolic extract (CS) on the development of alcoholic fatty liver and associated injury. Methods: Sprague-Dawley male rats were fed either Lieber-DeCarli control (C) or ethanol (35.5% of total calories) liquid diet with 0 (E), 100 mg/kgBW CS (E+LCS), or 500 mg/kgBW CS (E+HCS) for 8 weeks. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities as well as TG and cholesterol concentrations in the serum and liver tissues were measured by colorimetric assays. Liver histopathology was examined by Hematoxylin-eosin staining of the fixed liver tissues. Protein levels of phosphorylated-AMP activated protein kinase (p-AMPK), phosphorylated-acetyl CoA carboxylase (p-ACC), phosphorylated-nuclear factor kappa B (p-$NF{\kappa}B$), and $TNF{\alpha}$ were measured by Western blot analyses. Results: Both doses of CS markedly suppressed alcohol-induced lipid droplets accumulation in the liver tissues and significantly inhibited alcohol-induced increases in activities of serum ALT and serum AST. Similarly, CS significantly reduced hepatic and serum TG concentrations. Compared to groups fed alcohol only, CS supplementation strongly increased hepatic levels of p-AMPK and p-ACC. Further, CS significantly inhibited alcohol-induced phosphorylation of $NF{\kappa}B$, which was associated with reduced hepatic protein levels of $TNF{\alpha}$. Conclusion: Our data demonstrated that CS has a protective effect against alcoholic liver injury, which was associated with activation of AMPK and inhibition of $NF{\kappa}B$.

• YAKHAK HOEJI
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• v.40 no.5
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• pp.563-573
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• 1996

The system most likely responsible for the accelerated metabolism of alcohol with chronic ingestion or at high blood ethanol levels, is the microsomal ethanol-oxidizing system(M EOS). While the increase in the MEOS with chronic ethanol ingestion is thought to be adaptive, it may also have serious adverse effects on the liver. The rates of the NADPH-dependent oxygen consumption by the liver microsomes from the prolonged ethanol fed rats were 2 times higher than the rates from the non-treated rats. With the alcohol ingestion, the total SH and nonprotein SH contents showed the significant decrease and at the same time, MDA in liver and GOT and GPT levels in blood showed the significant increase, which suggests the occurrence of liver damage due to the oxidative stress caused by chronic alcohol consumption. The mitochondrial aldehyde dehydrogenase(ALDH) activity was decreased by chronic ethanol ingestion, whereas the alcohol dehydrogenase activity and the cytosolic ALDH activity were not altered. These results suggest that the induction of cytochrome P450 by the chronic alcohol ingestion increases the oxidative stress which seems to result in the altered the physiological states of the liver including the ALDH activity, which may in turn to lead to the liver disease.

• Journal of Korean Medicine for Obesity Research
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• v.9 no.1
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• pp.79-86
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• 2009

Objectives The purpose of this study was to investigate the clinical effect of oriental obesity therapy on obese patient with non-alcoholic fatty liver disease(NAFLD). Methods The patient was treated from November 17, 2008 to May 15, 2009 for obesity treatment. And the patient had intensive care through admission treatment from November 17, 2008 to November 29, 2008. Electrolipolysis, auricular acupuncture, herbal medicine, low calorie diet and aerobic exercise were done during the treatment period. Results His body Weight decreased from 102.8kg to 82.7kg. The BMI decreased from 35.2kg/m$^2$ to 28.9kg/m$^2$. NAFLD effectively improved on sonography form grade II${\sim}$III to grade I${\sim}$II after oriental obesity therapy, AST decreased from 65 to 19. ALT decreased from 152 to 18. Oriental obesity therapy could be effective to treat obese patient with NAFLD. Conclusions The obese patient with NAFLD improved on sonography by oriental obesity therapy.

• The Korea Journal of Herbology
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• v.33 no.6
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• pp.61-70
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• 2018

Objectives : Non-alcoholic fatty liver disease (NAFLD) is characterized by the accumulation of hepatic triglycerides (TG) that leads to inflammation and fibrosis. Crataegi Fructus ethanol extract (CE) is a korean traditional herb that used for digestive diseases. It has been investigated that CE has the effect that prevent hepatotoxicity caused by CCl4 or GaIN and regulate the inflammatory in several organs. However, a hypolipidemic effect of CF has not been reported. Methods : The purpose of this study is that examine the lipid accumulation inhibitory effect of CE on NAFLD. We checked the body and liver weight change of MCD-diet induced mice with/without administration of CE. The blood lipid levels of C57BL/6J mice were checked by biochemistry. Also we observed the liver histology of MCD-diet induced mice and investigate the molecular mechanisms in MCD-diet-induced NAFLD in C57BL/6J mice. Results : CE improved MCD-diet-induced lipid accumulation and TG and TC levels. Also, CE decreased hepatic lipogenesis such as SREBP-1, $C/EBP{\alpha}$, $PPAR{\gamma}$, ACC and FAS. Besides, we also found out that CE increased AMPK phosphorylation. These results indicated that CE has the same ability to activate AMPK and then reduce SREBP-1, and FAS expression, finally leading to inhibit hepatic lipogenesis and hepatic antioxidative ability. Conclusions : In this report, we found CE exerted a regulatory effect on lipid accumulation by decreasing lipogenesis in MCD-diet induced NAFLD model. Therefore, CE extract may be active in the prevention of fatty liver.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.25 no.3
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• pp.240-250
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• 2022

Purpose: This study aimed to examine the advantages and usefulness of transient elastography (Fibroscan^®) in diagnosing non-alcoholic steatohepatitis in children and adolescents compared to those of abdominal computed tomography and liver ultrasonography. Methods: Forty-six children and adolescent participants aged between 6 and 16 years who underwent transient elastography (Fibroscan^®) as well as liver ultrasonography or abdominal computed tomography were included. Thirty-nine participants underwent liver ultrasonography and 11 underwent computed tomography. The physical measurements, blood test results, presence of metabolic syndrome, and the degree of liver steatosis and liver fibrosis were analyzed, and their correlations with transient elastography (Fibroscan^®), abdominal computed tomography, and liver ultrasonography, as well as the correlations between examinations, were analyzed. Results: Thirty-six participants (78.3%) were boys, and the mean age was 12.29±2.57 years, with a mean body mass index of 27.88±4.28. In the 46 participants, the mean values for aspartate aminotransferase, alanine aminotransferase, and total bilirubin were 89.87±118.69 IU/L, 138.54±141.79 IU/L, and 0.77±0.61 mg/dL, respectively. Although transient elastography (Fibroscan^®) and abdominal computed tomography grading had a statistically significant positive correlation with aspartate aminotransferase and alanine aminotransferase values, the correlations between the results of grading performed by transient elastography (Fibroscan^®), abdominal computed tomography, and liver ultrasonography were not statistically. Conclusion: We confirmed that each examination was correlated with the results of some blood tests, suggesting the usefulness and possibility of diagnosis and treatment of steatohepatitis mediated by transient elastography (Fibroscan^®) in the department of pediatrics.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.2
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• pp.169-176
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• 2017

Non-alcoholic fatty liver disease (NAFLD) is caused by chronic lipid accumulation due to dysregulation of lipid metabolism in the liver, and it is associated with various human diseases such as obesity, dyslipidemia, hypertension, and diabetes. Histone acetylation is a representative epigenetic mechanism regulated by histone acetyltransferases (HATs) and deacetylases. We observed that tartary buckwheat sprout (TBS) suppressed lipid accumulation in HepG2 cells through its anti-HAT activity. We showed that TBS was a novel HAT inhibitor with specificity for the major HAT enzyme p300. Importantly, TBS reduced acetylation of total and histone proteins, H3K9, H3K36, and H4K8, resulting in decreased transcriptional activities of sterol regulatory element-binding protein 1c, ATP citrate lyase, and fatty acid synthase. These results suggest that TBS inhibits the NAFLD transcription-modulating activity of lipogenesis-related genes through modification of histone acetylation.

• Journal of Nutrition and Health
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• v.56 no.2
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• pp.123-139
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• 2023

Purpose: This study was conducted to establish whether an ethanol extract of Lycium barbarum leaves (LLE) and an ethanol extract of Lycium barbarum leaves from which chlorophyll has been removed, denoted as LLE(Ch^-), have a protective effect against hepatic fat accumulation. Methods: The inhibitory effects of LLE and LLE(Ch^-) on liver fat accumulation were examined in C57BL/6 mice with non-alcoholic fatty liver disease (NAFLD) induced by an methionine and choline deficient diet and in HepG2 cells with palmitic acid-induced fat accumulation. Results: The plasma triglyceride, aspartate aminotransferase, and alanine aminotransferase levels were lower in the LLE(Ch^-) group, whereas the plasma ALT activity decreased significantly in the LLE group. In both the LLE and the LLE(Ch^-) groups, the triglyceride and cholesterol contents in the hepatic tissue were significantly reduced. A greater inhibitory effect on tissue fat accumulation was observed in the LLE(Ch^-) group than in the LLE group. In HepG2 cells, LLE and LLE(Ch^-) were non-toxic up to a concentration of 1,000 ㎍/mL. Compared to the control group, intracellular fat accumulation in the LLE and LLE(Ch^-) groups were significantly reduced at concentrations of 200 ㎍/mL and 500 ㎍/mL, respectively. The expression of phosphorylated adenosine monophosphate-activated protein kinase and phosphorylated acetyl-CoA carboxylase in both LLE groups increased at the concentrations of 100 ㎍/mL and 500 ㎍/mL. The fatty acid synthase expression was suppressed in a concentration-dependent manner at 10 ㎍/mL. Conclusion: The examined two ethanol extracts of LLE inhibit hepatic fat accumulation in NAFLD. This effect was more pronounced in the LLE(Ch^-) group. Therefore, these 2 extracts have an anti-steatosis effect and can be used for NAFLD treatment.

• The Journal of Internal Korean Medicine
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• v.41 no.3
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• pp.542-551
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• 2020

Objectives: The purpose of this study was to retrospectively assess the effectiveness of Chunggan plus extract (CGX) in improving liver function in a Korean medical clinic. Methods: We collected the data of inpatients who received CGX to improve abnormal liver function test (LFT) results from March 2016 to February 2020. We analyzed the changes in LFT and adverse events based on subjective symptom changes and creatinine results. Results: The data of eight patients, three male and five female, were selected by inclusion criteria (patients who did LFT before and after the prescription of CGX and who prescribed CGX more than 6 days) and exclusion criteria (patients who administered other herbal medicine for improving liver function except CGX and who are diagnosed with terminal stage of hepatobiliary cancer). As a cause of abnormal LFT, one case was diagnosed with alcoholic liver disease, two cases with non-alcoholic fatty hepatitis, and one case with cholecystitis. Three of the other four were suspected to have drug-induced hepatitis, and one case was determined to have an unknown cause. Most patients showed a decrease in LFT results (Aspartate transaminase 87.5%, Alanine transaminase 87.5%, and Alkaline Phosphatase 100%) without any critical adverse events. Conclusions: CGX may be an efficient and convenient herbal medicine for improving liver function regardless of the chief impression. Further study should be conducted to evaluate the effectiveness of CGX.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.5
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• pp.611-616
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• 2013

Alcoholic liver disease (ALD) is a major cause of morbidity and mortality around the world. Although much progress has been made in understanding the pathogenesis of ALD, there remains no effective therapy for it. Accumulated evidence indicates that oxidative stress is the main pathological factors in the development of ALD. Ethanol administration causes accumulation of reactive oxygen species (ROS), including superoxide, hydroxyl radical, and hydrogen peroxide. ROS, in turn, cause lipid peroxidation of cellular membranes, and protein and DNA oxidation, which results in hepatocyte injury. In addition to pro-oxidants formation, antioxidants depletion caused by ethanol administration also results in oxidative stress. The objective of this study is to investigate the effects of Shiryung-tang extract on the chronic alcoholic liver injury induced by EtOH. Male Sprague Dawley rats were used in this study. All rats were maintained under standard laboratory conditions ($23{\pm}1^{\circ}C$, 12h light/12h dark cycles). All animals (n=30) were randomly divided into following groups: (1) Normal group, treated with distilled water (n=10); (2) Control group, treated with ethanol (n=10); (3) Sample group, treated with ethanol + pharmacopuncture (n=10). For oral administration of ethanol in Control and Sample group, the ethanol was dissolved in distilled water in concentrations of 25%(v/v). Throughout the experiment of 8 week, the rats were allowed free access to water and standard chow. Sample group were administrated by Shiryung-tang extract daily for 8 weeks. Control group were given normal saline for same weeks. As a results, the oral administration of ethanol for 8 weeks leads to hepatotoxicity. The levels of hepatic marker such as HDL-cholesterol, triglyceride, aspartate aminotransferase and alanine aminotransferase were altered. The ethanol also increased lipid peroxidation and depletion of antioxidant enzyme activities as well as hepatic tissue injury. However, the treatment of Shiryung-tang extract prevented all the alterations induced by ethanol and returned their levels to near normal. These data suggest that Shiryung-tang extract could have a beneficial effect in inhibiting the oxidative damage induced by chronic ethanol administration. Therefore, Shiryung-tang extract can be a candidate to protect against EtOH-induced liver injury.

• Nutritional Sciences
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• v.9 no.2
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• pp.106-111
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• 2006

Chronic alcohol consumption is associated with perturbation of hepatic metabolism of sulphur-containing amino acid. The goal of present study was to evaluate the influence of dietary supplementation of methionine or folate to chronically ethanol-fed mts on the metabolism of sulfur-containing amino acids and one-carbon metabolism. Sprague-Dawley male mts were fed Lieber-Decarli liquid diet with 0% ethanol (control), 36% ethanol (E), 36% ethanol combined with methionine supplement (EM) or folate supplement (EF) for 8 weeks. Hepatic S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), plasma folate and homocysteine (Hcy), urinary excretion of folate and formiminoglutamate were investigated after feeding experimental diets. Growth was retarded by 36% ethanol consupmtion (E, EM and EF) (p<0.01). Liver total fat (p<0.05) and plasma ALT (P<0.01) were increased by methionine supplementation (EM), implicating fatty liver and liver injury. Liver folate was increased slightly by folate supplementation (EF) (p=0.077). Urinary folate loss was increased 2.3 fold by ethanol consumption (E) and 17.2 fold by folate supplementation (EF), while decreased by methionine supplementation (EM) (p<0.000l). Plasma Hcy was increased 1.9 fold by methionine supplementation (EM) in ethanol-fed mts (p<0.05), which was related with decreased methionine synthase activity (p<0.05). Hepatic SAM/SAH ratio was depressed by methionine supplementation in ethanol-fed mts (EM) (p<0.05). Urinary formininoglutamate (Figlu) excretion after histidine loading was increased by ethanol ingestion and reduced by methionine supplementation (p<0.00l). Based on these data, methionine supplementation appears to accelerate histidine oxidation. In conclusion, dietary supplementation of methionine to ethanol-fed mts exacerbates alcoholic liver injury possibly by complicating sulphur-containing amino acid metabolism, as while it may have beneficial effects on folate and histidine metabolism.