The effect of ginseng methanol extract on hepatic drug metabolizing enzyme in rat was investigated. The ginseng methanol extract (100mg/kg) was administered orally to Sprague Dawley rats for 7days and the contents of cytochrome $P_{450}$ and NADPH cytochrome c reductase in liver were measured by the method of Stanton et al. and Mazel respectively. The content of liver cytochrome $P_{450}$ and NADPH cytochrome c reductase in the rats treated with ginseng methanol extract (100mg/kg) were increased by 21.9% and l6.6% respectively and their increases were statistically significant. Single i.p. injection of phenobarbital (100mg/kg) to the rats produced approximately 25% increase in cytochrome $P_{450}$ content in this investigation and further stimulation was produced in the rats pretreated with ginseng methanol extract (100mg/kg). On the other hand, single i.p. injection of 95% $CCl_{4}$ (0.5ml/kg) showed 29% decrease in cytochrome $P_{450}$ content and 10.5% decrease in NADPH cytochrome c reductase activity. The degree of inhibition of cytochrome $P_{450}$ content in the rats pretreated with ginseng methanol extract (100mg/kg) was similar to that observed in the $CCl_{4}$ alone treated group, but NADPH cytochrome c reductase activity was increased by 65% in the rats pretreated with ginseng methanol extract (100mg/kg). These results suggest that ginseng is the hepatic drug metabolizing enzyme inducing agent in the rat and the effect is similar to phenobarbital.
Lee, Da Young;Lee, Seung Yun;Kang, Hea Jin;Park, Yeonhwa;Hur, Sun Jin
Journal of Animal Science and Technology
/
v.62
no.6
/
pp.933-947
/
2020
This study was conducted to develop an effective heparin extraction method by using low-cost and highly effective enzymes from six pig by-products (liver, lung, heart, stomach, small intestine, and large intestine), and analyze their bioavailability. Low-cost and highly effective enzymes (alkaline-AK and papain) and a common enzyme (trypsin) were used for the heparin extraction. The angiotensin I- converting enzyme (ACE) inhibitory activity and the antimicrobial activity of extracted heparin were analyzed to verify their bioavailability. The average amount of heparin extracted per kilogram of pig by-products was 439 mg from the liver, 127 mg from the lung, 398 mg from the heart, 261 mg from the stomach, 197 mg from the small intestine, and 239 mg from the large intestine. Various enzymes were used to extract heparin, and the amount of extracted heparin was similar. Based on 1 g of pig by-product, the enzymes trypsin, papain, and alkaline-AK could extract 1,718 mg, 1,697 mg, and 1,905 mg of heparin, respectively. Heparin extracted from pig by-products showed antihypertensive activity and antimicrobial activity against Staphylococcus aureus at low populations. These results indicated that heparin can be obtained from pig by-products at a low cost.
Seung Bae Rho;Hyun Jung Byun;Boh-Ram Kim;Chang Hoon Lee
Biomolecules & Therapeutics
/
v.31
no.3
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pp.330-339
/
2023
Liver kinase B1 (LKB1) is a crucial tumor suppressor involved in various cellular processes, including embryonic development, tumor initiation and progression, cell adhesion, apoptosis, and metabolism. However, the precise mechanisms underlying its functions remain elusive. In this study, we demonstrate that LKB1 interacts directly with malic enzyme 3 (ME3) through the N-terminus of the enzyme and identified the binding regions necessary for this interaction. The binding activity was confirmed to promote the expression of ME3 in an LKB1-dependent manner and was also shown to induce apoptosis activity. Furthermore, LKB1 and ME3 overexpression upregulated the expression of tumour suppressor proteins (p53 and p21) and downregulated the expression of antiapoptotic proteins (nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and B-cell lymphoma 2 (Bcl-2)). Additionally, LKB1 and ME3 enhanced the transcription of p21 and p53 and inhibited the transcription of NF-κB. Moreover, LKB1 and ME3 suppressed the phosphorylation of various components of the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B signaling pathway. Overall, these results suggest that LKB1 promotes pro-apoptotic activities by inducing ME3 expression.
Objectives : This study was done to investigate the protective effects of Gagaminjakdowha-Tang on liver injury of rats induced by $CCl_4$ and d-galactosamine. Methods : All animals were divided into 5 groups, those were normal group(untreated), control group(treated with 0.9% Saline solution), sample I group(200mg/kg administrated), sample II group(400mg/kg administrated), Silymarin(200mg/kg administrated) group. Liver injury of rats were induced by $CCl_4$ and d-galactosamine, and then the serumtransaminase(ALT & AST) alkaline phosphatase(ALP), lactic dehydrogenase(LDH) for enzyme activities, Liver cytosol malondialdehyde(MDA), catalase, superoxide dismutase(SOD), glutathione S-transferase(GST) and glutathione-peroxidase(GPX) for enzyme activities were measured. Results : The inhibitory effects on the serum ALT activities were noted in both sample I and sample II group. The inhibitory effects on the serum AST activities were noted in only sample II group. The inhibitory effects on the serum ALP activities were noted in both sample I and sample II group. The inhibitory effects on the serum LDH activities were noted in only sample II group. The inhibitory effects on the liver cytosol malondialdehyde were noted in only sample II group. The decresed effects on the liver cytosol catalase activities were inhibited in only sample II group. The decresed effects on the liver cytosol superoxide dismutase activities were inhibited in only sample II group. The decresed effects on the liver cytosol GST activities were inhibited in only sample II group. The decresed effects on the liver cytosol GPX activities were inhibited in only sample II group. The inhibitory effects of the serum ALT activities were noted in both sample I and sample II. The inhibitory effects of the serum AST activities were noted in only sample II group. The inhibitory effects of the serum ALP activities were noted in only sample II group. The inhibitory effects of the serum LDH activities were noted in both sample I and sample II group. Conclusions : Gagaminjakdowha-Tang has protective effects against liver injury in rats induced by $CCl_4$ and d-galactosamine.
This study was conducted to investigate the effects of effects of enprostil, a prostaglandin $E_2$, analogue, on liver triacylglycerol content and factors that regulate liver lipid metabolism in mice. Mice received vehicle or $10{\mu}g$ enprostil/kg body weight intraperitoneally every 6 h, and were killed at 0, 6, 12, 18 and 24 h after the first injection. Enprostil significantly lowered liver triacylglycerol content after 12 h of the first injection. However, the peroxisomal ${\beta}$-oxidation activity was inconsistent with the result of liver triacylglycerol content, because its activity was lovered by enprosil. In another experiment, the effect of enprostil on lipid metabolism in mice was investigated in a short period. Mice received $10{\mu}g$ enprostil/kg body weight intraperitoneally, and were killed after 0, 5, 10, 30 and 60 min. After 30 min, malic enzyme activity was significantly increased by the administration of enprostil compared with the activity at 5 min after. No significant changes in liver carnitine palmitoyltransferase and peroxisomal ${\beta}$-oxidation activities were observed. Plasma free fatty acid concentrations were markedly reduced from 5 through 60 min after the administration of enprostil. Consequently, enprostil suppressive effect on liver triacylglycerol concentration might result from the decreased entry of free fatty acid into liver.
Apium graveolens Linn. (Apiaceae) is an indigenous plant of the North and South Americas, Southern Europe, and Asia and has been widely used as a food or a traditional medicine for treatment of inflammation and arthritis. The purpose of this study was to investigate the antioxidant effects of a methanolic extract of A. graveolens (AGE) against liver oxidative stress in an adjuvant-induced arthritic rat model. The AGE (250, 500, and 1,000 mg/kg) was given orally for 24 consecutive days after induction by injecting complete Freund's adjuvant. Liver and spleen weights were recorded. The superoxide anion level, total peroxide (TP), glutathione peroxidase (GPx) activity, superoxide dismutase (SOD) activity, total antioxidant status, and oxidative stress index (OSI) were also measured. AGE treatment significantly decreased the levels of the superoxide anion, TP, and OSI whereas the GPx and SOD activities significantly increased in the liver of the arthritic rats. These results indicated that AGE showed an ameliorative effect against liver oxidative stress in adjuvant-induced arthritic rats by reducing the generation of liver free radicals and increasing the liver antioxidant enzyme activity.
This study was performed to investigate the effect of dietary $\beta$-carotene supplementation on lipid metabolism and antioxidant enzyme activities in hyperlipidemic rats. Fifty Sprague-Dawley male rats aging 7 weeks were fed the control diet (CD,5% corn oil) and the high fat diet (HFD,15% beef tallow +1% cholesterol) for 4 weeks and then 0.02% $\beta$-carotene was supplemented to CD and HFD group for 8 more weeks. Serum lipid compositions, lipid peroxides and antioxidative enzymes in liver were analyzed at 4, 8 and 12week of the experiment. Serum levels of total lipid, total cholesterol, triglyceride, LDL-cholesterol, VLDL-cholesterol were higher in HFD groups than in CD groups (p < 0.001), Serum levels of HDL-cholesterol were higher in CD groups than in HFD groups (p < 0.01) . The effect of $\beta$-carotene supplementation was not significant in all groups but tended to be lower in total lipid, total cholesterol and Triglyceride. Thiobarbituric acid reactive substances (TBARS) levels in plasma and liver were showed significantly higher in HFD groups (p < 0.001, p < 0.05). The effects of $\beta$-carotene supplementation on the level of plasma and liver TBARS were not found except HFD groups at 12 week. Liver conjugated diene levels in HFD groups were higher than in CD groups (p < 0.01), but the effect of $\beta$-carotene supplementation did not show any differences. Liver lipofuscin levels were not significantly different among all groups. The activities of superoxide dismutase (SOD) and catalase were significantly lower in HFD groups at 8 week (p < 0.001) but were not significantly different at 4 and 12week. The activity of SOD in $\beta$-carotene supplemented HFD group was significantly higher at 8 week (p < 0.01). Glutathione peroxidase (GSH-Px) activity was significantly lower in HFD groups (p < 0.01) and was significantly increased in groups supplemented $\beta$-carotene (p < 0.05). It is suggested that $\beta$-carotene supplementation partly decreases the serum lipid and lipid peroxide levels and increases the activities of antioxidant enzymes in hyperlipidemic rats.
There has been increasing interest in the value of using soybean to delay or reduce the tumor incidence. This study was undertaken to investigate the possible protective effects of soybean against hepatocarcinogenesis induced by DL-ethionine. Accordingly, we measured biochemical changes occurring in serum and liver of rats treated with DL-ethionine in the presence or absence of soybean. Male albino rats were fed a control diet containing the hepatocarcinogen, DL-ethionine, or the control diet plus soybean 30%, or the control diet plus soybean plus DL-ethionine 0.25% for three months and then returned to a control diet for up to nine months. Rats fed a control diet plus DL-ethionine showed a gradual decrease in liver DNA, RNA, total protein, and liver weight and enzyme activites of liver transaminases (GOT and GPT) and alkaline phosphatase over the 7-month study period. This was followed by a large increase in the liver parameters at the end of the $9^{th}$ month, except for 5'-nucleotidase and glucose-6-phosphatase that showed a large decrease. On the other hand, a gradual increase in the serum enzyme activities of GOT, GPT, 5-nucleotidase, alkaline phosphatase, and in the albumin/globulin (A/G) ratio is observed in the group of rats fed a control diet plus DL-ethionine compared to the control group over 8 months, and this was followed by a large increase in all serum parameters studied at nine-months. The administration of 30% soybean to the rat diet in addition to DL-ethionine maintained all parameters studied at near control values until the end of the $9^{th}$ month. This study suggests that soybean has a protective effect against the hepatocarcinogenesis induced by DL-ethionine.
Albio rats right after weaning, weighing $50{\sim}55g$, were divided into the control, high-carbohydrate-, high-lipid-, and high-protein-fed groups. and were fed for 12 weeks with the respective diets to observe the increase in body weights as well as changes in the chemical constituentes and enzyme activities in the liver tissue, with the following results. (1) There was little difference in the rate of increase in the body weights among the groups, showing normal growth, except the high-protein-fed group which showed decrease in rate of body weight increase from the 7th week after feeding. (2) The liver weight was either increased after 12 weeks of feeding with the high-carbohydrate and high-Lipid diets, or showed no difference with the high-protein diet, as compared to the control weight. (3) The liver cytosol protein content was increased when fed with the high-protein diet, but decreased when fed with the high-carbohydrate and high lipid diets, as compared to the control content. (4) The triglyceride and cholesterol contents in the liver were decreased in the high-protein-fed group, but increased markedly in the high-carbohydrate- and high-lipid-fed groups as compared to the control values. (5) The hepatic glucokinase, G6PD, LDH, and fatty acid synthetase activities were increased in the high-carbohydrate and high-lipid-fed groups, and GOT and CPT activities were increased in the high-protein-fed group. From the above results. it was known that the high-carbohydrate and high-lipid diets stimulated the hepatic lipid metabolism, giving rise to lipogenesis, but the high- protein diet could prevent the lipogeuesis leading to the body weight increase.
Objectives: Alcohol abuse is a public issue and one of the major causes of liver disease worldwide. This study was aimed at investigating the protective effect of Ganoderma lucidum pharmacopuncture (GLP) against hepatotoxicity induced by acute ethanol (EtOH) intoxication in rats. Methods: Sprague-Dawley (SD) rats were divided into 4 groups of 8 animals each: normal, control, normal saline pharmacopuncture (NP) and GLP groups. The control, NP and GLP groups received ethanol orally. The NP and the GLP groups were treated daily with injections of normal saline and Ganoderma lucidum extract, respectively. The control group received no treatment. The rats in all groups, except the normal group, were intoxicated for 6 hours by oral administration of EtOH (6 g/kg BW). The same volume of distilled water was administered to the rats in the normal group. Two local acupoints were used: Qimen (LR14) and Taechung (LR3). A histopathological analysis was performed, and the liver function and the activities of antioxidant enzymes were assessed. Results: GLP treatment reduced the histological changes due to acute liver injury induced by EtOH and significantly reduced the increase in the alanine aminotransferase (ALT) enzyme; however, it had an insignificant effect in reducing the increase in aspartate aminotransferase (AST) enzyme. It also significantly ameliorated the superoxide dismutase (SOD) and the catalase (CAT) activities. Conclusion: The present study suggests that GLP treatment is effective in protecting against ethanol-induced acute hepatic injury in SD rats by modulating the activities of ethanol-metabolizing enzymes and by attenuating oxidative stress.
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