• Journal of Physiology & Pathology in Korean Medicine
• /
• v.30 no.4
• /
• pp.279-288
• /
• 2016

To observe the potential hepatoprotective effects of Gongjin-dan on the acute ethanol (EtOH)-induced liver damages in C57BL/6 mice with its possible action mechanisms. EtOH-mediated acute hepatic damages were induced by oral administration of EtOH total 3 doses. The changes on the body weight, liver weight, albumin, TG, AST, ALP, ALT, hepatic TG contents, hepatic antioxidant defense system, TNF-α, CYP 2E1 activity and mRNA expressions of hepatic lipogenic genes - SREBP-1c, SCD1, ACC1, FAS, PPARγ and DGAT2 or genes involved in fatty acid oxidation - PPARα, ACO and CPT1 were observed with final liver histopathological inspections after 15 days of continuous administration of silymarin 200 mg/kg, Gongjin-dan (GJD) 400, 200 and 100 mg/kg. The results were compared with silymarin 200 mg/kg treated mice. Marked decreases of body and liver weights, increases of serum AST, ALT, Albumin and TG levels, hepatic TG contents, TNF-α level, CYP 2E1 activity and mRNA expressions of hepatic lipogenic genes or decreases mRNA expressions of genes involved in fatty acid oxidation were observed with histopathological changes related hepatosteatosis increases of immunolabelled hepatocytes, as the results of a binge drinking of EtOH in the present study. Also destroys of hepatic antioxidant defense systems were demonstrated in EtOH control mice as compared with intact vehicle control mice, respectively. The results suggest that oral administration of 400, 200 and 100 mg/kg of GJD favorably protected the liver damages from acute mouse EtOH intoxications.

• Food Science and Biotechnology
• /
• v.15 no.4
• /
• pp.612-616
• /
• 2006

The protective effect of water extract of ash tree leaves (ALE) against oxidative damages was investigated in paracetamol-induced BALB/c mice. Biochemical analysis of anti-oxidative enzymes, immunoblot analyses of hepatic cytochrome P450 2El (CYP2E1), and the gene expression of tumor necrosis factor (TNF-${\alpha}$) were examined to determine the extract's protective effect and its possible mechanisms. BALB/c mice were divided into three groups: normal, paracetamol-administered, and ALE-pretreated groups. A single dose of paracetamol led to a marked increase in lipid peroxidation as measured by malondialdehyde (MDA). This was associated with a significant reduction in the hepatic antioxidant system, e.g., glutathione (GSH). Paracetamol administration also significantly elevated the expression of CYP2E1, according to immunoblot analysis, and of TNF-${\alpha}$ mRNA in liver. However, ALE pretreatment prior to the administration of paracetamol significantly decreased hepatic MDA levels. ALE restored hepatic glutathione and catalase levels and suppressed the expression of CYP2E1 and TNF-${\alpha}$ observed in inflammatory tissues. Moreover, ALE restored mitochondrial ATP content depleted by the drug administration. These results show that the extract of ash tree leaves protects against paracetamol-induced oxidative damages by blocking oxidative stress and CYP2E1-mediated paracetamol bioactivation.

• BMB Reports
• /
• v.55 no.4
• /
• pp.166-174
• /
• 2022

Hepatic macrophages are key immune cells associated with the broad ranges of liver diseases including steatosis, inflammation and fibrosis. Hepatic macrophages interact with other immune cells and orchestrate hepatic immune circumstances. Recently, the heterogenous populations of hepatic macrophages have been discovered termed residential Kupffer cells and monocyte-derived macrophages, and identified their distinct population dynamics during the progression of various liver diseases. Liver injury lead to Kupffer cells activation with induction of inflammatory cytokines and chemokines, which triggers recruitment of inflammatory monocyte-derived macrophages. To understand liver pathology, the functions of different subtypes of liver macrophages should be regarded with different perspectives. In this review, we summarize recent advances in the roles of hepatic macrophages under liver damages and suggest hepatic macrophages as promising therapeutic targets for treating liver diseases.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.29 no.5
• /
• pp.394-402
• /
• 2015

To evaluate the benefits of Hyangsayangyi-tang aqueous extracts (HSYYT) on the propylthiouracil (PTU)-induced Rat hypothyroidism. 6 groups, each consisting 8 Rats were used in the present study - Intact vehicle control, PTU control, LT₄, HSYYT 500, 250 and 125 ㎎/㎏ treated groups. HSYYT was given, once day for 42 days from 2 weeks before start of PTU treatment as an oral dose of 500, 250 and 125 ㎎/㎏(body weight), and for 28 days while the PTU 10 ㎎/㎏ by daily subcutaneous treatment induced hypothyroidism. Compared the results with LT₄ 0.5 ㎎/㎏ intraperitoneally treated rats in this experiment. Results of the PTU treatment included; decreases of body weight, increase in thyroid weight, decrease in liver weight, in serum T₃, and T₄ level decrease with increase of serum TSH levels, in serum HDL increase and in TG content decrease, decrease in liver antioxidants defense system, increase of serum AST levels were observed. However, these PTU induced hypothyroidism and related hepatic damages were dose-dependently inhibited by treatment of HSYYT 500 and 250 ㎎/㎏, and they also effectively regulated the PTU-induced abnormal antioxidant defense system changes in liver. Therefore, in comparison with the PTU control group, it was effective and advantageous changes were not observed in HSYYT 125 ㎎/㎏ treated rats on the PTU induced hypothyroidism and related hepatic damages. In this experiment, HSYYT 500 and 250 ㎎/㎏ dose-dependently inhibited PTU-induced hypothyroidism and related liver damage in rats but not in HSYYT 125 ㎎/㎏.

• Biomolecules & Therapeutics
• /
• v.5 no.2
• /
• pp.194-201
• /
• 1997

The hepatoprotective activity of six extracts (BE, EE, HH, PS-1, PS-2, KP) from Artimisia iwayomogi was investigated against experimentally produced hepatic damages. Silymarin, DDB and UDCA were used as reference compounds. Treatment with PS-1 extract reduced hepatic demages induced by $CCl_4$, acetaminophen and ANIT but it did not alter ethionine-induced hepatotoxicity In addition, PS-1 extract showed a protective effect against chronic $CCl_4$-induced hepatotoxicity as well as liver regeneration. PS-2 and KP extracts exhibited significant antihepatotoxic effects on D-galactosamine-induced hepatitis. Treatment with EE extract inhibited ethionine-induced fatty liver. These data indicate that the PS-1 extract is the roost hepato-protective constituent and rationalize the traditional use of this plant in hepatobiliary disorders.

• The Journal of Korean Medicine
• /
• v.20 no.3 s.39
• /
• pp.18-26
• /
• 1999

This paper aims to determine the effect of CBW on the liver of mice treated with PQ (paraquat) examined by light and transmission electron microscope. Under light microscopic observations, the 2 days control showed mild congestion and necrosis of liver while those were manifest in the 7 days control. When electron microscopy was used, mitochondria and rough endoplasmic reticulum were dilated or destructed in the 2 days control and 7 days control, respectively. Under light microscopic observations, the 2 days experimental group did not show any hepatic damages while accumulation of glycogen granules in the cytoplasm was conspicuous in the 7 days experimental group. When electron microscopy was used, mitochondria and rough endoplasmic reticulum were less dilated in the 2 days experirrlental group. On the other hand, denaturation of cell organelles was not observed in the 7 days experimental group. These results suggest that CBW seems related with recovery from the PQ cytotoxity.

• Journal of Sasang Constitutional Medicine
• /
• v.28 no.2
• /
• pp.132-146
• /
• 2016

Objectives This study's object was to observe the comparative effects of Yangkyuksanhwa-tang, Palmulgunja-tang and Cheongpyesagan-tang on the chronic LT4(levothyroxine) induced hyperthyroidism in rats.Methods Six groups, each of 8 rats in group, were used in this study. Saline and distilled water treated rats are intact control group. Hyperthyroidism was induced by daily subcutaneous LT4 300 μg/kg treatment for 27 days(LT4 control). Since 12th LT4 treatment PTU(propylthiouracil) 10 mg/kg was intraperitoneal injected(PTU group) and aqueous extracts of Yangkyuksanhwa-tang, Palmulgunja-tang and Cheongpyesagan-tang(YS, PG and CS) 500 mg/kg were orally administrated(YS, PG, CS group), once a day for 15 days. The differences in the body, thyroid gland and epididymal fat pad weights, serum T3(tri-iodothyronine), T4(thyroxine), TSH(thyroid-stimulating hormone), thyroid gland and epididymal fat pad histopathology, liver weight, AST(asparte aminotransferase), ALT(alanine aminotransferase) concentrations, hepatic lipid peroxidation, GSH(glutathione), SOD(superoxide dismutase), CAT(catalase) activities, liver histopathology were observed to evaluate effects on hyperthyroidism, liver damages and antioxidant effects.Results As results of LT4 treatment, hyperthyroidism and related liver damages such as lower body, thyroid weights, higher serum T3, T4, AST, ALT levels, thinner follicular lining epithelium in thyroid glands were observed. However, these symptoms were inhibited by oral treatment of YS, PG and CS. As compared with PTU treatment, these herbal prescriptions showed lower overall efficacy on the hyperthyroidism, but YS showed more favorable effects on the hepatic antioxidant defense systems.Conclusions This results suggest that YS, PG and CS favorably control the LT4 induced hyperthyroidism and related liver damages in rats through modulation of the hepatic antioxidative defense systems.

• Journal of Veterinary Clinics
• /
• v.25 no.6
• /
• pp.510-513
• /
• 2008

Two dogs were referred due to vomiting, depression and anorexia after ingestion of xylitol gum. Both dogs were presented with hepatic failure and one dog had concurrent renal failure. Aggressive supportive treatment was performed, but these dogs died. Necropsy of one dog revealed acute hepatic necrosis, severe renal damages, and hemoperitoneum. This case report demonstrates potential hazard of xylitol toxicity for dogs with clinicopathological and pathological findings.

• YAKHAK HOEJI
• /
• v.29 no.1
• /
• pp.43-49
• /
• 1985

Polysaccharides obtained from Sappan Lignum, Mori Radicis Cortex and Olibanum were examined for their liver protective effects against carbon tetrachloride-and D-galactosamine intoxication in ICR-mice. Hexobarbital sleeping time and serum transaminases (S-GOT and S-GPT) were measured as parameters for the evaluation of liver protective effects. All polysaccharides tested in this experiment showed remarkable positive effects on the prevention of hepatic intoxication with carbon tetrachloride-and D-galactosamine. Much better liver protective effects of polysaccharides were observed in D-galactosamine-liver injuries than in carbon tetrachloride-injuries.

• BMB Reports
• /
• v.40 no.6
• /
• pp.1039-1049
• /
• 2007

Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.