Excessive alcohol consumption is the cause of several diseases and thus is of a major concern for society. Worldwide alcohol consumption has increased by many folds over the past decades. This urgently calls for intervention and relapse counteract measures. Modern pharmacological solutions induce complete alcohol self-restraint and prevent relapse, but they have many side effects. Natural products are most promising as they cause fewer adverse effects. Here we discuss in detail the medicinal plants used in various traditional/folklore medicine systems for targeting alcohol abuse. We also comprehensively describe preclinical and clinical studies done on some of these plants along with the possible mechanisms of action.

Many studies reported that Korean medicine (KM) is effective for treating liver disease, including hepatitis A. However, KM, specifically with herbal medicine (Chungganplus, CGP) has not been reported yet. We aimed to report a patient with hepatitis A who was treated with KM including CGP, acupuncture, and moxibustion for 12 days.

A 39-year-old man with hepatitis A who was hospitalized for 12 days after being admitted to our hospital with abdominal pain, diarrhea and vomiting. We prescribed CGP three times a day, with acupuncture performed twice daily and moxibustion at conception vessel (CV)-12 once a day. Follow-up blood tests have been done 4 times during the admission in order to access the effect of the treatment.

In 12 days the symptoms had disappeared and the blood test results improved steadily. His AST level have declined from 1,189 IU/L to 44 IU/L, ALT from 2,423 IU/L to 127 IU/L, r-GTP from 1,347 IU/L to 339 IU/L, ALP from 384 IU/L to 205 IU/L, and total bilirubin from 3.6 mg/dL to 0.89 mg/dL.

This case suggests that KM-based treatment using CGP may be effective for hepatitis A with no adverse effect. Further research and clinical trial on CGP would be needed to make the basis more valid.

To evaluate protective effects of Chunggan extract (CGX), a traditional herbal formula, under 4 wk of alcohol consumption-induced liver injury.

Male Sprague-Dawley Rats were orally administered 30% ethanol daily for 4 wk with or without CGX. The pharmaceutical properties were assessed through liver enzymes, histopathology, fibrogenic cytokines, and alcohol metabolism in hepatic tissues as well as by in vitro experiment using HSC-T6 cells.

Four weeks of alcohol consumption notably increased liver enzymes and malondialdehyde levels in serum and hepatic tissue. CGX not only prevented the collagen deposition determined by histopathology and hydroxyproline content, but also normalized transforming growth factor-beta, platelet-derived growth factor-beta and connective tissue growth factor at the gene expression and protein levels in liver tissue. Moreover, CGX treatment also significantly normalized the abnormal changes in gene expression profiles of extracellular matrix proteins, matrix metalloproteinase and their inhibitors, alcohol metabolism, and inflammatory reactions. In the acetaldehyde-stimulated HSC-T6 cells, CGX considerably inhibited collagen production and normalized fibrogenic cytokines in both gene expression and protein levels.

The present study evidenced that CGX has hepatoprotective properties via modulation of fibrogenic cytokines and alcohol metabolism in alcoholic liver injury.

CGX is a modification of a traditional herbal medicine that has been used for various liver disorders as a meaning of "cleaning the liver". The cholestatic liver disorders become prevalent. BACK GROUND AND AIM: This study aimed to investigate the anti-hepatic fibrosis effects of CGX and its underlying mechanisms in a rat model of bile duct ligation (BDL).

BDL was conducted in SD rats except shame operation group. The rats were orally administrated with distilled water, CGX (25 or 50 mg/kg) or ursodeoxycholic acid (UDCA, 25 mg/kg) for two weeks. The pharmaceutical effects and mechanisms were analyzed in histopathology, biochemistry, oxidative stress/antioxidant biomarkers and hepatic fibrogenic cytokines levels.

BDL markedly elevated white blood cell (WBC) counts as well as changed subset proportions such as increased neutrophils and decreased lymphocytes in peripheral blood. BDL drastically elevated the serum levels of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), total bilirubin, and hepatic tissue levels of hydroxyproline and malondialdehyde (MDA), while it reduced the total glutathione (GSH) content and the activities of GSH-redox system enzymes such as GSH-peroxidase, GSH-reductase and GSH-S-transferase. These alterations were significantly attenuated by CGX treatment (mainly 50 mg/kg). CGX treatment normalized both the accumulation of collagen in hepatic tissue and the increased levels of profibrogenic cytokine including transforming growth factor-β1 (TGF-β1) and platelet-derived growth factor-BB (PDGF-BB). Moreover, CGX treatment enhanced interferon-gamma (IFN-γ) expression compare to the BDL group at the protein and gene level.

These results suggest that CGX exerts anti-hepatofibrotic effect in rat BDL model, and the responsible mechanisms involve the inhibition of hepatic fibrogenic cytokines and oxidative stress.

Chunggan extract (CGX) is a hepatotherapeutic herbal formula which has been traditionally used for patients suffering from various hepatic disorders. This study aimed to elucidate antifibrotic effect and mechanisms of CGX in thioacetamide (TAA) model. Hepatic fibrosis was induced in 45 Sprague-Dawley rats by TAA (200 mg kg(-1), intraperitoneally [ip]) on twice per week for 12 weeks. CGX (100 or 200 mg kg(-1), per oral [po]) was administrated once a day throughout the experiment. CGX treatment ameliorated serum biomarkers. CGX administration significantly attenuated distortion of histopathologic finding, and accumulation of hydroxyproline and malondialdehyde (MDA). CGX treatment significantly decreased transforming growth factor-beta (TGF-β) concentrations and inactivated hepatic stellate cells (HSCs). CGX treatment drastically restored glutathione (GSH) system, while inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-α) significantly down-regulated in liver tissue. CGX showed antifibrotic effect in thioacetamide-induced chronic liver injury model. Its corresponding mechanisms may be mediated via anti-oxidative stress property sustaining GSH system and inhibition of ROS production.

CGX is a traditional Korean herbal medicine used to treat chronic liver diseases.

The purpose of this study was to evaluate the pharmaceutical safety of hepatoprotective herbal medicine, CGX via systemic 6-month repeated dose toxicity study in SD rats.

Male and female SD rats were administered CGX for 6 months (0, 100, 200, or 400 mg kg(-1), respectively). The rats were visually inspected for changes in behavior, body weight, food and water consumption, and appearance during the experiment period. At the end of the experiment, urine, hematological, biochemical analysis, and histopathological examination were carried out.

No drug-induced abnormalities were found as clinical signs or in the histopathology, hematology, blood biochemistry, and urinalysis results for any administered doses of CGX.

The results suggest that CGX is safe and could be considered as an effective and prospective herbal formulation in clinical applications with a wide therapeutic index.

CGX is a modification of a traditional herbal medicine for "liver cleaning," which is used to treat various chronic liver disorders in oriental clinics. This study investigated the antifibrotic effects and associated mechanisms of CGX.

Liver fibrosis was induced in rats by dimethylnitrosamine (DMN; 10 mg kg(-1), ip) injection on 3 consecutive days per week for 4 weeks. CGX (100 or 200 mg kg(-1), po) was administrated once a day for 4 weeks. Three cell lines (HepG2, RAW 264.7, and HSC-T6) were used to examine its mechanisms.

CGX treatment dramatically ameliorated the change in liver and spleen weight and serum albumin (p<0.01), aspartate transaminase (p<0.01), alanine transaminase (p<0.01), alkaline phosphatase (p<0.01), and total bilirubin (p<0.01) levels. Histopathologically, CGX administration decreased necrosis, inflammatory cell infiltration, and collagen accumulation. The antifibrotic effects of CGX were confirmed from hydroxyproline determination and the reduction in the numbers of activated hepatic stellate cells. In addition, antioxidant proteins, glutathione content, and glutathione peroxidase, catalase, and superoxide dismutase activities were maintained in the CGX-treated groups compared with the DMN group. CGX downregulated fibrosis-related genes (inducible nitric oxide synthase, tumor necrosis factor-alpha, transforming growth factor-beta, connective tissue growth factor, and platelet-derived growth factor-beta) and decreased the protein levels of profibrotic cytokines (transforming growth factor-beta and platelet-derived growth factor-beta) in liver tissues. In the cell line-based studies, CGX showed supportive effects, such as the protection of hepatocytes from CCl(4)-toxicity, inhibition of NO production in RAW 264.7 cells, and inactivation of hepatic stellate cells.

These results demonstrated the antifibrotic effects of CGX and the corresponding mechanisms associated with sustaining the antioxidative system and inhibiting hepatic stellate cell activation via the downregulation of fibrogenic cytokines.

CGX is a potential hepatoprotective herbal medicine used to treat various chronic liver disorders. The purpose of the study was to evaluate the pharmaceutical safety of CGX via a systemic 13-week repeated dose toxicity test in beagle dogs. Male and female beagle dogs were divided into four groups and two animals each from the control and high-dose group (400 mg/kg) were allocated into recovery groups. The dogs were administered with CGX (0, 100, 200, 400 mg/kg) for 13 weeks. During the experimental period, the dogs were observed for signs of gross toxicity and for behavioral changes; body weight and food consumption were measured. An ophthalmologic examination and urinalysis were performed at 0 and 13th week and blood biochemistry and hematological parameters analyses were performed at 0, 6th, and 13th week. A histopathological examination was also performed at the end of the experiment. There were no CGX-induced abnormalities in clinical signs, organ weights, food consumption, hematological, urine, and blood biochemical parameters, or histopathological findings in any of the groups during or after the 13 weeks. We demonstrated the safety of CGX for 13-week repeated dose and considered that it is safe for chronic clinical use.

CGX, a modified traditional Chinese herbal drug whose name means "liver cleaning," is used to treat various liver disorders. This study investigated the protective effects of CGX and its mechanisms.

After pretreating ICR mice twice daily with CGX (po, 50 or 100mg/kg) or distilled water for three consecutive days, acute liver injury was induced by a single injection of CCl(4) (ip, 10mL/kg of 0.2% in olive oil) (n=8 per group).

Pretreatment with CGX significantly attenuated the elevation in biochemical parameters, such as alanine transaminase (ALT), aspartate transaminase (AST), and lactate dehydrogenase (LDH) in serum, and the malondialdehyde concentrations in liver tissue. Pretreatment with CGX significantly restored the reduction of catalase activity and glutathione (GSH) content, but not superoxide dismutase (SOD) activity, and it inhibited the CCl(4)-induced high expression of iNOS and TNF-alpha in hepatic tissue.

This study showed that CGX has hepatoprotective effects against free radical-induced acute injury via primarily antioxidative properties.