• Advances in Traditional Medicine
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• 제10권2호
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• pp.111-115
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• 2010

The flowers of Nyctanthes arbor-tristis Linn. of Oleaceae widely used in Ayurvedic system of medicine for the treatment of diuresis, liver disorder, spleen enlargement sciatica, bitter, stomachic, carminative and tonic to hair. The aim of the present study was to evaluate the alcoholic and aqueous extracts of the flowers of Nyctanthes arbor-tristis for hepatoprotective effect against carbontetrachloride induced liver damage in rats. Administration of alcoholic and aqueous extracts of the leaves of Nyctanthes arbor-tristis protect the liver from toxic effects of carbontetrachloride by reducing the elevated levels of Serum glutamate pyruvate transaminase, Serum glutamate oxaloacetate transaminase, Alkaline phosphatase and serum bilirubin. Results revealed that both the alcoholic and aqueous extracts showed significant hepatoprotective activity by reducing the elevated levels of biochemical parameters at a dose of 200 mg/kg body weight. The results were supported by histopathological studies of liver samples which showed regeneration of hepatocytes by the extracts.

• IMMUNE NETWORK
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• 제10권6호
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• pp.181-187
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• 2010

Excessive alcohol consumption is one of the critical causative factors leading to alcoholic liver disease (ALD). ALD is characterized by a wide spectrum of liver damage, ranging from simple uncomplicated liver steatosis (fatty liver) to steatohepatitis and liver fibrosis/cirrhosis. It has been believed that the obvious underlying cause for ALD is due to hepatocyte death induced by alcohol itself. However, recent sparkling studies have shown that diverse immune responses contribute to ALD because liver is enriched with numerous immune cells. Especially, a line of evidence has suggested that innate immune cells such as Kupffer cells and natural killer (NK)/NKT cells are significantly involved in the pathogenesis of ALD via production of pro-inflammatory cytokines and other mediators. Indeed, more interestingly, hepatic stellate cells (HSCs), known as a major cell inducing liver steatosis and fibrosis, can be killed by liver NK cells, which could be suppressed by chronic alcohol consumption. In this review, with the view of liver as predominant innate immune organ, we describe the pathogenesis of ALD in which what roles of innate immune cells are and how they are interacting with HSCs.

• 대한융합한의학회지
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• 제5권1호
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• pp.45-54
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• 2023

Objectives : Alcohol-induced liver disease advances as to reactive oxygen species (ROS) and cellular lipid peroxidation increase. We examined the hepatoprotective effects of Zingiber officinale Roscoe rhizome extract (ZR), Pueraria lobata Ohwi flower extracts (PF), and a newly developed herbal juice (HJ), which was a combination of ZR and PF extracts, against ethanol-induced hepatotoxicity. Methods: The study utilized the human hepatoma cell line HepG2 cells to validate the hepatoprotective effect of HJ (50~200 ㎍/mL) against ethanol (EtOH, 700 mM)-induced liver damage. Results: HJ effectively reduced the protein expression of sterol regulatory element-binding transcription factor 1, adiponectin, and AMP-activated protein kinase in EtOH-induced HepG2 cells. The levels of ROS, total cholesterol, and triglycerides, which are the result of various synthesis and lipogenesis processes induced by EtOH in the liver, were reduced by HJ. Furthermore, the activities of alcohol dehydrogenase and aldehyde dehydrogenase, enzymes linked to alcohol degradation, were more effectively downregulated by HJ treatment compared to treatment with ZR and PF alone, all without causing cytotoxic effects. Conclusions: HJ protects the liver by inhibiting EtOH-induced lipogenesis, lowering ROS generation, and improving alcohol degradation, which is more effective than ZR and PF alone. Further, in vivo experiments can offer additional evidence regarding the effectiveness, safety, and underlying mechanism of action of HJ.

• Toxicological Research
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• 제24권2호
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• pp.113-117
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• 2008

Chronic exposure to ethanol induces cumulative damage to the liver starting from fatty infiltration to cirrhosis depending on the dose and duration of exposure. The whole process leading to the development of alcoholic liver disease is very complex and the mechanisms involved are not fully understood. Among many experimental animal models, Lieber-DeCarli liquid diet provides moderate to severe pathophysiological outcome depending on the compositional changes. In the present study, we investigated the temporal changes in the early phase hepatic disease in rats fed with standard Lieber-DeCarli diet. Male Wistar rats were fed with Lieber-Decarli ethanol diet for 6 weeks and the liver samples were obtained after 2, 4 and 6 weeks. Mild fatty infiltration was observed in 2 weeks of feeding and it became evident in 4 and 6 week samples. The level of hepatic triglyceride showed a good agreement with the data obtained in the pathological analysis. Feeding mice with ethanol diet resulted in the maturation and translocation of SREBP-1 to nucleus in the liver. Western blot analysis of the pooled liver sample of control and ethanol fed animals showed a clear-cut time-dependent increase in the expression of nSREBP-1. These data provide important information for selecting proper time point in experimental intervention study in the field of drug development for alcoholic liver disease.

• The Korean Journal of Physiology and Pharmacology
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• 제24권5호
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• pp.385-394
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• 2020

Eupatilin is known to possess anti-apoptotic, anti-oxidative, and anti-inflammatory 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)-α and interleukin (IL)-1β 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-α, and IL-1β, 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.

• Advances in Traditional Medicine
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• 제7권3호
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• pp.311-320
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• 2007

The present study was designed to estimate the protective effect of (-) epigallocatechin gallate (EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day ${\times}$ 60 days) caused liver damage that was manifested by the elevation of markers of liver dysfunction - aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin and ${\gamma}$-glutamyl transferase in plasma and reduction in liver glycogen. The activities of alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase were found to be altered in alcohol-treated group. Ethanol administration resulted in the induction of cytochrome p450 and cytochrome-$b_{5}$ activities and reduction of cytochrome-c reductase and glutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced the viability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and induced hepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats with EGCG restored the levels of markers of liver injury and mitigated the alterations in alcohol metabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viability and reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findings suggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.

• 한국축산식품학회지
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• 제37권6호
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• pp.931-939
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• 2017

Alcoholic liver disease (ALD) is a complex multifaceted disease that involves oxidative stress and inflammation as the key mediators. Despite decades of intensive research, there are no FDA-approved therapies, and/or no effective cure is yet available. Probiotics have received increasing attention in the past few years due to their well-documented gastrointestinal health-promoting effects. Interestingly, emerging studies have suggested that certain probiotics may offer benefits beyond the gut. Lactobacillus fermentum LA12 has been previously demonstrated to play a role in inflammatory-related disease. However, the possible protective effect of L. fermentum LA12 on ALD still remain to be explored. Thus, the aim of this study was to evaluate the possible protective effect of L. fermentum LA12 on alcohol-induced gut barrier dysfunction and liver damage in a rat model of alcoholic steatohepatitis (ASH). Daily oral administration of L. fermentum LA12 in rat model of ASH for four weeks was shown to significantly reduced intestinal nitric oxide production and hyperpermeability. Moreover, small intestinal histological- and qRT-PCR analysis further revealed that L. fermentum LA12 treatment was capable of up-regulating the mRNA expression levels of tight junction proteins, thereby stimulating the restitution of barrier structure and function. Serum and hepatic analyses also revealed that the restoration of epithelial barrier function may prevent the leakage of endotoxin into the blood, subsequently improve liver function and hepatic steatosis in the L. fermentum LA12-treated rats. Altogether, results in this study suggest that L. fermentum LA12 may be used as a dietary adjunct for the prevention and treatment of ASH.

• Natural Product Sciences
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• 제13권2호
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• pp.105-109
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• 2007

Alcoholic extract of Terminalia arjuna [TA] was evaluated far its hepatoprotective activity against carbon tetrachloride (CCl$_4$)-induced hepatic damage in rats. The hepatoprotective activity of TA was evaluated by measuring levels of serum marker enzymes like serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase (SALP). The serum levels of total proteins(TP), total albumins (TAL) and bilirubin (BILN) were also estimated. The histological studies were also carried out to support the above parameters. Silymarin (SM) was used as standard drug. Administration of TA (250 and 500 mg/kg/po) markedly prevented CCl$_4$-induced elevation of levels of SGOT, SGPT, SALP, TP, TAL and BILN. These biochemical observations were supplemented by histopathological examination of liver sections. Alcoholic extract of TA also shown significant in-vitro free radical scavenging activity against 1, 1-diphenyl-2-picryl hydrazyl (DPPH) and nitric oxide (NO) radicals. Thus, the present study provides a scientific rationale for the traditional use of this plant in the management of liver diseases.

• Journal of Nutrition and Health
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• 제48권5호
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• pp.390-397
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• 2015

본 연구에서는 Sprague-Dawley 종 랫트 수컷을 대조군, EtOH군, Fe군, EtOH + Fe군으로 나누어, 알코올과 철분을 액상 사료로 8주간 공급한 후, 간 조직과 간 세포 mtDNA의 손상 정도를 알아보았다. EtOH + Fe군은 대조군, EtOH군, Fe군의 다른 세 군에 비해 혈청 ALT와 혈청 AST 수치가 가장 유의적으로 높았으며, 간 조직 검사의 결과에서도 다수의 지방구, 염증성 세포 침입 및 조직의 괴사가 관찰되는 등 가장 심한 간 손상이 확인되었다. DNA 손상 여부를 긴 영역 PCR을 사용하여 분석한 결과, 만성적인 알코올과 철분에 의한 노출은 간 세포의 mtDNA 손상을 유발하는 것으로 나타났으며, 핵 DNA에는 영향을 미치지 않았다. 또한 미토콘드리아의 호흡에 관여하는 Cox1과 Nd4 유전자 발현 정도를 real-time PCR으로 분석한 결과, 알코올 또는 철분은 간 세포의 Cox1 mRNA와 Nd4 mRNA 수준을 유의적으로 낮추는 것으로 나타났다. 이상의 결과는 만성 알코올 또는 과잉의 철분에 의한 간 손상에 mtDNA 손상 및 미토콘드리아 기능 저하가 관여함을 제시한다.

• Toxicological Research
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• 제30권1호
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• pp.49-54
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• 2014

In this study, we investigated the hepatoprotective effects of aged black garlic (ABG) in rodent models of liver injury. ABG inhibited carbon tetrachloride-induced elevation of aspartate transaminase (AST) and alanine transaminase (ALT), which are markers of hepatocellular damage, in SD rats. D-galactosamine-induced hepatocellular damage was also suppressed by ABG treatment. However, ABG does not affect the elevation of alkaline phosphatase (ALP), a marker of hepatobilliary damage, in rats treated with carbon tetrachloride or D-galactosamine. We also examined the effect of ABG on high-fat diet (HFD)-induced fatty liver and subsequent liver damage. ABG had no significant effect on body weight increase and plasma lipid profile in HFD-fed mice. However, HFD-induced increase in AST and ALT, but not ALP, was significantly suppressed by ABG treatment. These results demonstrate that ABG has hepatoprotective effects and suggest that ABG supplementation might be a good adjuvant therapy for the management of liver injury.