This study was to investigate the effects of Gibangganbang on the liver injury induced dimethylnitrosamine, CCl4, ethanol and partial hepatectomy. Hydroxyproline, hepatic fibrosis, hepatic inflammatory cell infiltration, fatty value, lipidoperoxide levels, glutathione levels, mitotic index, contents of protein in the serum and liver tissues were measured and observed. The results obtained were as follows. 1. The increasing level of hydroxyproline volume induced by dimethylnitrosamine in mice was decreased by the oral administration of Gibangganbang. 2. The degree of hitological fibrosis and hepatic inflammatory cell infiltration induced by $CCl_4$ was decreased by the oral administration of Gibangganbang. 3. The degree of fatty value and the increasing level of lipidoperoxide in liver tissues was decreased by the oral administration of Gibangganbang. 4. The level of glutathione in liver tissues was increasing by the oral administration of Gibangganbang. 5. The increasing level of microsomal lipidoperoxide in vitro assay was decreasing by the oral administration of Gibangganbang. 6. The increasing level of the mitotic index, weight of liver, contents of protein, RNA and DNA synthesis of the liver tissues after partial hepatectomy was activated by the oral administration of Gibangganbang. These results suggest that Gibangganbang not only inhibits liver cirrhotic change and ethanol-induced fatty change but also activates antioxidant enzymes and regeneration ability ocf liver.
Waly, Mostafa Ibrahim;Al Alawi, Ahmed Ali;Al Marhoobi, Insaaf Mohammad;Rahman, Mohammad Shafiur
Asian Pacific Journal of Cancer Prevention
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v.17
no.12
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pp.5071-5074
/
2016
Background: Azoxymethane (AOM) is a well-known colon cancer-inducing agent in experimental animals via mechanisms that include oxidative stress in rat colon and liver tissue. Few studies have investigated AOM-induced oxidative stress in rat liver tissue. Red seaweeds of the genera Hypnea Bryodies and Melanothamnus Somalensis are rich in polyphenolic compounds that may suppress cancer through antioxidant properties, yet limited research has been carried out to investigate their anti-carcinogenic and antioxidant influence against AOM-induced oxidative stress in rat liver. Objective: This study aims to determine protective effects of red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts against AOM-induced hepatotoxicity and oxidative stress. Materials and Methods: Sprague-Dawley rats received intraperitoneal injections of AOM, 15 mg/kg body weight, once a week for two consecutive weeks and then orally administered red seaweed (100 mg/kg body-weight) extracts for sixteen weeks. At the end of the experiment all animals were overnight fasted then sacrificed and blood and liver tissues were collected. Results: AOM treatment significantly decreased serum liver markers and induced hepatic oxidative stress as evidenced by increased liver tissue homogenate levels of nitric oxide and malondialdehyde, decreased total antioxidant capacity and glutathione, and inhibition of antioxidant enzymes (catalase, glutathione peroxidase, glutathione S-transferase, glutathione reductase and superoxide dismutase). Both red seaweed extracts abolished the AOM-associated oxidative stress and protected against liver injury as evidenced by increased serum levels of liver function markers. In addition, histological findings confirmed protective effects of the two red seaweed extracts against AOM-induced liver injury. Conclusion: Our findings indicate that red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts counteracted oxidative stress-induced hepatotoxicity in a rat model of colon cancer.
This study was performed to investigate the effect of dietary $\beta$-carotene supplementation on lipid peroxide levels and antioxidant enzyme activities in alcoholic fatty liver rats. Forty five Sprague-Dawley male rats aging 8 weeks were used as experimental animals, which were divided into the control diet (CD) and the ethanol diet (ED) and the ethanol + $0.02\%$$\beta$-carotene diet (EPD) groups and fed the experimental diet respectively for 5 weeks. After the feeding, rats were sacrificed to get blood and liver to analyze lipid and lipid peroxide levels and antioxidant enzyme activities. The mean body weight and food intake of the ethanol diet group was significantly lower than that of the control diet. The liver index (LI) of the ethanol diet group was significantly higher than those of the control diet and the $\beta$-carotene supplementation group. Serum levels of total lipid, triglyceride of the ethanol diet group were significantly higher than those of the control diet and the $\beta$-carotene supplementation group. Total cholesterol levels were not significantly different among all groups. HDL-cholesterol of the ethanol diet group was significantly lower than those of the control diet and the $\beta$-carotene supplementation group. Liver TBARS of the ethanol diet group was significantly higher than those of the control diet and the $\beta$-carotene supplementation group. Liver lipofuscin and conjugated diene levels were not significantly different among all groups. The superoxide dismutase activity of the ethanol diet group was significantly lower than those of the control diet and the $\beta$-carotene supplementation group. Catalase and glutathione peroxidase activities were not significantly different among all groups. Because v-carotene supplementation significantly decrease the serum total lipid, triglyceride, liver TBARS revels and increase the superoxide dismutase activity in alcoholic ratty liver rats, $\beta$-carotene supplementation seems to give beneficial effect for the alcoholics.
Liver sausage is flavorful and highly nutritious. However, liver has a relatively short shelf life due to acceleration of oxidation in the presence of endogenous enzymes and metals. Powders derived from natural sources, including plants or fruits, are applied to meat products for inhibiting oxidation without adverse effects on their quality. Hence, this study investigated the effects of natural powders derived from green tea leaf (GTL), lotus leaf (LL), and kimchi (KC) on the quality and change in lipid oxidation and freshness of chicken liver sausages during two weeks of storage. Chicken liver sausages were manufactured with chicken breast (70%) and liver (20%), pork back fat (5%), iced water (5%), various additives, and GTL, LL, and KC [0 (control) or 1%]. They were processed in three batches. For determination of the quality characteristics of chicken liver sausages with various plant powders, pH, color, and texture properties were assessed. In addition, lipid oxidation and freshness using thiobarbituric acid reactive substances (TBARS) and total volatile basic nitrogen (TVBN) were analyzed at day 0 and week 2 of refrigerated storage. Higher values were obtained for pH and cooking yield in sausage samples with LL and KC powders than in samples with the other treatments. For a* values, the sausage samples with KC showed similar (p > 0.05) values, whilst others had significantly lower values than the control. The addition of the three powders to sausage samples induced an increase (p < 0.05) in hardness, gumminess, and chewiness. The addition of plant powders did not influence TBARS and TVBN of sausage samples at the initial stage. However, after two weeks of storage, significantly lower TBARS and TVBN values were observed, and the sausage with KC (p < 0.05) showed the lowest values of both TBARS and TVBN. The results showed the potential ability of the three powders to improve the quality and inhibit lipid oxidation in liver sausages. Particularly, the addition of KC did not adversely affect the $a^*$ values of sausage samples. The effects on sensory properties and inhibition mechanisms of GTL, LL, and KC in meat products should be further studied.
Choi, Jeong Won;Shin, Mi-Rae;Lee, Ji Hye;Roh, Seong-Soo
Biomedical Science Letters
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v.27
no.3
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pp.142-153
/
2021
Liver fibrosis is a wound-healing response to chronic liver injury, which is caused by the continuous and excess deposition of extracellular matrix (ECM). The aim of this study is to investigate whether Uncaria rhynchophylla water extract (UR) can ameliorate thioacetamide (TAA)-induced liver fibrosis. The liver fibrosis model was induced on C57BL/6 mice by intraperitoneal injection with TAA three times a week for 8 weeks. UR (200 mg/kg) or silymarin (50 mg/kg) was administered orally daily for 8 weeks. Biochemical analyses including AST, ALT, MPO, and Ammonia levels were measured in serum. In the mice liver tissues, western blot and histological staining were analyzed. As a result, UR dramatically reduced the levels in serum AST, ALT, MPO, and Ammonia levels. UR treatment regulated NADPH oxidase factors expression, and antioxidant enzymes except for GPx-1/2 were significantly increased via Nrf2 activation. Furthermore, pro-inflammatory mediators, such as COX-2 and iNOS were markedly suppressed through the inhibition of NF-κB activation. Expressions of ECM-related protein including α-SMA and Collagen I were noticeably decreased. The additional histological evaluation confirmed that hepatocyte damage and collagenous fiber accumulation were attenuated. Taken together, these data suggest that UR possessed hepatoprotective effects in TAA-induced liver fibrosis via the NF-κB inactivation and Nrf2 activation. Therefore, UR may act as a potential therapeutic drug against liver fibrosis.
Purpose: The rising prevalence of childhood obesity in the past decades has caused non-alcoholic fatty liver disease (NAFLD) to become the most common cause of pediatric chronic liver disease worldwide. This study was aimed at determining the effect of vitamin D (Vit D) on ultrasonography and laboratory indices of NAFLD and some blood biochemical indicators in children. Methods: In this interventional study liver ultrasonography was performed in 200 children with overweight and obesity. A 108 had fatty liver among which 101 were randomly divided into two groups of study (n=51) and control (n=50). The study group was treated with Vit D, 50000 U once a week whereas the control group received placebo with the same dose and package, both for 12 weeks. At the end of the intervention lab tests and ultrasound study was performed once again to evaluate the response to treatment. Results: It was found out that Vit D supplementation improved the fatty liver grade in the study group. The mean changes in hemoglobin (Hb), uric acid, highdensity lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), insulin, albumin and alanine aminotransferase (ALT) was significantly higher in the study group compared to controls (p<0.05). After the intervention and means adjustment, a significant difference was obtained in HDL-C, insulin, LDL-C and homeostasis model assessment of insulin resistance (HOMA-IR) between the two groups. Conclusion: Vit D supplementation in addition to improving the fatty liver grade in ultrasonography and increasing the blood Vit D level, increases the HDL and Hb level besides decreasing uric acid, LDL, HOMA-IR, insulin and ALT levels.
The present study was designed to assess whether dietary inorganic and organic selenium (Se) could affect antioxidant enzymes, including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST), and the level of malondialdehyde (MDA), a marker of lipid peroxidation, in the intestine, serum, liver, and gastrocnemius muscle of Korean native goats. A total of eighteen Korean native goats was allotted into three dietary groups, consisting of basal diet (CON), or basal diet with either 0.25 ppm inorganic (IOSEL) or 0.25 ppm organic Se (ORSEL), and fed the corresponding diets for 5 wks. Growth performance, including body weight and total gain, and blood biochemical profiles, including GSH-Px, were not significantly different between the three dietary groups. Also, the specific activities of SOD, GSH-Px, and GST, and the level of MDA in the intestinal mucosa and liver from goats were not substantially affected by either inorganic Se or organic Se. However, goats fed the diet containing organic Se showed a significant increase in GSH-Px and GST activities in the gastrocnemius muscle compared with those fed the basal diet. In conclusion, increased muscle GSH-Px and GST activities suggest that dietary organic Se may affect, at least in part, the antioxidant defense system in muscle of Korean native goats under the conditions of our feeding regimen.
Aucubin, an iridoid glucoside which was previously reported to exhibit liver-protective activities against $CCl_4$ and ${\alpha}-amanitin$ induced liver damages, was subject to toxicological studies. To measure the lethal dose, the doses of 100mg/kg, 300mg/kg, 600mg/kg and 900mg/kg were administered intraperitoneally to experimental mice. No death was observed 24 hrs later, but serum GOT and alkaline phosphatase activities were deceased slightly at the doses of 300mg to 900mg/kg, and the triglyceride contents were slightly increased. To investigate acute toxicity of aucubin itself, multiple dosages(20 mg/kg, 40 mg/kg and 80 mg/kg for four times a week) were injected intraperitoneally into mice, then serum enzymes activities and chemistries were assayed; no significant change of the enzyme activities of alkaline phosphatase, GPT, GOT in the test groups were observed in comparison with those of the control group, and the contents of triglyceride, glucose, urea nitrogen and total proteins in the test group serums appeared to be almost same levels as those of the control group were. Histological examiation on liver biopsy samples indicated no gross changes between the control group and the test group were noted. Therefore, aucubin appears to be apparently low toxic substance and its minimum lethal dose in mouse seems to be more than 0.9 g.
Jo, Ji-Yeong;Kim, Tae-Hyung;Jeong, Hye-Young;Lim, Sung-Mee;Kim, Hyung-Sik;Im, Dong-Soon
Toxicological Research
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v.27
no.3
/
pp.185-190
/
2011
Di-(2-ethylhexyl)-phthalate (DEHP), the most widely utilized industrial plastizer and a ubiquitous environmental contaminant, can act on peroxisome proliferators-activated nuclear hormone receptor family (PPAR) isoforms. To understand the contribution of sphingolipid metabolism to DEHP-induced hepatotoxicity, effect of DEHP exposure on activities of sphingolipid metabolic enzymes in rat liver was investigated. DEHP (250, 500 or 750 mg/kg) was administered to the rats through oral gavage daily for 28 days. The activities of acidic and alkaline ceramidases were slightly increased in 250 mg/kg DEHP-administered rat livers and significantly elevated in 500 mg/kg DEHP-administered ones, although the level of 750 mg/kg DEHP-administered ones was not increased. Neutral ceramidase, acidic and neutral sphingomyelinases, sphingomyeline synthase and ceramide syhthase were not changed at all by DEHP exposure. Therefore, acidic and alkaline ceramidases might play important roles in DEHP-induced hepatotoxicity.
Razis, Ahmad Faizal Abdull;Konsue, Nattaya;Ioannides, Costas
Asian Pacific Journal of Cancer Prevention
/
v.16
no.7
/
pp.2679-2683
/
2015
Background: Phenethyl isothiocyanate (PEITC), the most comprehensively studied aromatic isothiocyanate, has been shown to act as an anti-cancer agent mainly through modulation of biotransformation enzymes responsible for metabolizing carcinogens in the human body. Humans are often exposed to carcinogenic factors, some of which through the diet, such as polycyclic aromatic hydrocarbon benzo[a]pyrene via the consumption of over-cooked meats. Inhibition of the enzymes responsible for the bioactivation of this carcinogen, for example CYP1A1, the major enzyme required for polycyclic aromatic hydrocarbons (PAHs) bioactivation, is recognized as a chemoprevention strategy. Objective: To evaluate the inhibitory effects of PEITC against benzo[a]pyrene-induced rise in rat liver CYP1A1 mRNA and apoprotein levels. Materials and Methods: Precision cut rat liver slices were treated with benzo[a]pyrene at 1 and $5{\mu}M$ in the presence of PEITC ($1-25{\mu}M$) for 24 hours, followed by determination of CYP1A1 mRNA and apoprotein levels using quantitative polymerase chain reaction and immunoblotting. Results: Findings revealed that PEITC inhibited benzo[a]pyrene-induced rise in rat liver CYP1A1 mRNA in a dose-dependent manner as well as the apoprotein levels of CYP1A. Conclusions: It was demonstrated that PEITC can directly inhibit the bioactivation of benzo[a]pyrene, indicating chemopreventive potential.
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