Objectives: The purpose of this study was to evaluate the anti-climacterium effects of Jibaekjihwang-tang (JBJHT), especially on estrogenic, anti-obesity, hypolipidemic, hepatoprotective against fatty liver and anti-osteoporotic effects by Ovariectomy (OVX) mice. Methods: In order to evaluate anti-climacterium effects of JBJHT, we used bilateral OVX female ddY mice. In this study, six groups were used; sham control, OVX control, estradiol, JBJHT 500, 250 and 125 mg/kg treated groups. Since 28 days after OVX surgery, JBJHT extracts were orally treated, and $17{\beta}$-estradiol $0.03{\mu}g/head$ were subcutaneously injected for 84 days, once a day. And then, we observed anti-climacterium effects classified into five categories; estrogenic, anti-obesity, hypolipidemic, hepatoprotective against fatty liver and anti-osteoporotic effects. The results were compared with $17{\beta}$-estradiol $0.03{\mu}g/head$/day subcutaneous treated OVX mice. Results: OVX control mice showed noticeable hypertrophic changes of adipocytes in abdominal fat pads, fatty liver, uterine atrophic changes, decreases of bone strength were also observed in OVX control. However, these estrogen-deficient climacterium symptoms were significantly and dose-dependently inhibited by JBJHT 500, 250 and 125 mg/kg treatment. Moreover, JBJHT 500 mg/kg showed comparable inhibitory effects as compared to those of estradiol $0.03{\mu}g/head$/day subcutaneous treatment. Conclusions: The results suggest that oral administration of JBJHT 500, 250 and 125 mg/kg has clear dose-dependent anti-climacterium effects in OVX mice.
Proceedings of the Plant Resources Society of Korea Conference
/
v.18
no.1
/
pp.52-60
/
2005
The objectives of present study were to investigate the hepatoprotective and antioxidative effects of onion extracts. Primary cultures of rat hepatocytes were incubated with 1.5 mM tert-butyl hydroperoxide(t-BHP), potent oxidizing agent for liver injury for 1 hr in the presence or absence of various concentrations (0, 0.01, 0.05, 0.1 or 0.3 mg/ml) of onion extract. Cytotoxicity and cell viability were determined by measuring glutamic oxaloacetic transaminase(GOT) activity, lactate dehydrogenase(LDH) activity and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) value. Lipid peroxidation was evaluated using thiobarbituric acid reactive substances(TBARS) assay. Effects on antioxidant system were determined by measuring catalase, glutathione peroxidase(GSH-Px), glutathione reductase(GSH-Rd) activities as well as DNA strand breaking assay. Incubation with t-BHP alone increased GOT and LDH activities and TBARS concentration but decreased MTT reduction. Onion extracts at the concentration of 0.05 mg/ml began to decrease GOT and LDH activities induced by 1.5 mM t-BHP. Decreased MTT reduction began to be increased by onion extract at the concentration of 0.01 mg/ml. Onion extracts at the concentration of 0.01 mg/ml began to decrease TBARS concentration induced by t-BHP. Taken together, onion extracts prevented t-BHP-induced hepatocyte injury and lipid peroxidation. Catalase, GSH-Px and GSH-Rd activities of hepatocytes were significantly decreased by 1.5 mM t-BHP for 1 hr incubation. Onion extracts, on the other hand, at the concentration of 0.1 mg/ml began to prevent t-BHP-induced decrease in catalase, GSH-Px and GSH-Rd activities. Onion extracts prevented hydroxyl radical-induced single-strand breakage in dose-dependent manner when plasmid DNA was incubated with various concentrations of onion extracts in the presence of Fenton regents producing hydroxyl radical. These results demonstrate that onion extracts suppressed t-BHP-induced cytoctoxicity, decreased viability and lipid peroxidation and increased GSH-Px, GSH-Rd and catalase activities. Thus hepatoprotective and antioxidant effects of onion extract seem to be due to, at least in part, the increase in antioxidant enzyme activities as well as prevention from hydroxyl radical-induced oxidation, followed by inhibition in lipid peroxidation.
Ryu, Ji Hyeon;Kim, Eun-Jin;Xie, Chengliang;Nyiramana, Marie Merci;Siregar, Adrian S.;Park, Si-Hyang;Cho, Soo Buem;Song, Dae Hyun;Kim, Nam-Gil;Choi, Yeung Joon;Kang, Sang Soo;Kang, Dawon
Journal of the Korean Society of Food Science and Nutrition
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v.46
no.6
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pp.659-670
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2017
Oxidative stress and inflammation are key factors responsible for progression of liver injury. A variety of functions of oyster hydrolysate (OH) are affected by their antioxidant and anti-inflammatory activities. However, little is known regarding the effects of OH on a liver injury model. This study was performed to evaluate the effects of OH on acute liver injury induced by lipopolysaccharide/D-galactosamine (LPS/D-GalN) in mice. Experimental groups were divided into six groups as follows (each group, n=10): control (saline), LPS/D-GalN, LPS/D-GalN+OH (100 mg/kg), LPS/D-GalN+OH (200 mg/kg), LPS/D-GalN+OH (400 mg/kg), and LPS/D-GalN+silymarin (25 mg/kg, positive control). The experimental acute liver injury model was induced with LPS ($1{\mu}g/kg$) and D-GalN (400 mg/kg). We first analyzed antioxidant and anti-inflammatory activities in OH. OH showed high DPPH and ABTS radical scavenging activities and reduced ROS generation in Chang cells in a dose-dependent manner. In addition, OH showed anti-inflammatory activities, such as inhibition of cyclooxygenase-2 and 5-lipooxygenase. Treatment with OH down-regulated tumor necrosis factor $(TNF)-{\alpha}$, interleukin (IL)-6, and $IL-1{\alpha}$ expression levels in LPS-stimulated RAW264.7 cells. OH significantly reduced LPS/D-GalN-induced increases in the concentrations of alanine transaminase and aspartate aminotransferase in serum. In the LPS/D-GalN group, liver tissues exhibited apoptosis of hepatocytes with hemorrhages. These pathological alterations were ameliorated by OH treatment. Consistently, hepatic catalase activity was low in the LPS/D-GalN group compared to the control group, and catalase activity was significantly restored by OH treatment (P<0.05). Furthermore, OH markedly reduced the LPS/D-GalN-induced increase in $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 levels in liver tissue. Taken together, these results show that OH has hepatoprotective effects on LPS/D-GalN-induced acute liver injury via inhibition of oxidative stress and inflammation, suggesting that OH could be used as a health functional food and potential therapeutic agent for acute liver injury.
Journal of the Korean Society of Food Science and Nutrition
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v.22
no.4
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pp.381-391
/
1993
To evaluate the antioxidizing effect of flavonoid on fish oil and peroxidized fish oil, rats were fed with diets containing 5% corn oil (CO), 5% corn oil and 15% fresh fish oil (FO) or peroxidixed fish oil (PFO) for 4weeks. An half of FO and PFO group rats were injected with 10mg flavonoid (+)-catechin (a day per kg body weight) (FO-C and PFO-C). FO and FO-C group rats showed higher increase in body weight as compared to PFO, PFO-C group rats. Whereas, the opposite result was obtained in case of liver weight increase. In addition, catechin apparently reduced liver weight by 12~17%. Phospholipid, cholesterol, triglyceride and lipid peroxide content in serum and cholesterol, lipid peroxide content in liver and adipose tissue of PFO, PFO-C group rats were significantly higher than those of FO, FO-C one. These results suggested that catechin reduced the synthesis of lipid and protected effectively against lipid peroxidation. In fatty acids profile of neutral lipid and phospholipid, the ratio of polyunsaturated fatty acids (PUFA) versus saturated fatty acids (SFA) in PFO, PFO-C were lower than that of FO or FO-C because of ruduced PUFA. Contrary to our expectation, the enzyme activities of superoxide dismutase(SOD), catalase and glutathione peroxidase (GSH-Px) in rat liver of FO and FO-C group were lower than those of PFO and PFO-C group. These results were quite interesting and might be explained in terms of homeostasis. In case of total lipid in liver, $C_{20:5}$, $C_{22:6}$ fatty acids were decreased in rat fed peroxidized fish oil. In conclusion, catechin was considered to be an antioxidative and hepatoprotective drug and hypolipidemic agent.
The objective of present study was to investigate the hepatoprotective and antioxidative effects of onion extracts. Primary cultures of rat hepatocytes were incubated with 1.5 mM tort-butyl hydroperoxide(t-BHP), potent oxidizing agent to liver, for 1 hr in the presence or absence of various concentrations (0, 0.01, 0.05, 0.1 or 0.3 mg/ml) of onion extract. Incubation with t-BHP increased glutamic oxaloacetic transaminase(GOT) and lactate dehydrogenase(LDH) acitivities and thiobarbituric acid reactive substances(TBARS) concentration but decreased 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) reduction. Onion extracts at the concentration of 0.05 mg/ml decreased t-BHP-induced GOT and LDH activities. Onion extract at the concentration of 0.1 mg/ml increased t-BHP-induced MTT reduction. Onion extract at the concentration of 0.01 mg/ml decreased t-BHP-induced TBARS concentration. Taken together, onion extracts prevented t-BHP-induced hepatocyte injury and lipid peroxidation. Catalase, glutathione peroxidase(GSH-Px) and glutathione reductase(GSH-Rd) activities of hepatocytes were significantly decreased by t-BHP. Onion extracts at the concentration of 0.1 mg/ml prevented t-BHP-induced decrease in catalase, GSH-Px and GSH-Rd activities. Onion extracts prevented hydroxyl radical-induced single-strand breakage in dose-dependent manner when plasmid DNA was incubated with various concentrations of onion extracts in the presence of Fenton reagents producing hydroxyl radical. These results demonstrate that onion extracts suppressed t-BHP-induced cytoctoxicity, decreased viability and lipid peroxidation and increased GSH-Px, GSH-Rd and catalase activities. Thus hepatoprotective and antioxidant effects of onion extract seem to be due to, at least in part, the increase in antioxidant enzyme activities as well as prevention from hydroxyl radical-induced oxidation, followed by inhibition of lipid peroxidation.
Kwon, Bong Seok;Park, Seon Kyeong;Kim, Jong Min;Kang, Jin Yong;Park, Sang Hyun;Kang, Jeong Eun;Lee, Chang Jun;Park, Su Bin;Yoo, Seul Ki;Lee, Uk;Heo, Ho Jin
Korean Journal of Food Science and Technology
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v.50
no.2
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pp.216-224
/
2018
To evaluate physiological effect of Aralia elata, in vitro antioxidant activity and hepatic protective effects were investigated. Ethyl acetate fraction from Aralia elata (EFAE) had higher total phenolic content than other fractions (n-hexane, chloroform, and distilled water layers). EFAE also showed significantly greater radical scavenging activity against 2,2'-azino-bis (3-ethylbenzthiazoline-6-sulfonic acid) diammonium salt (ABTS) and 1,1-diphenyl-2-picrylhydrazyl (DPPH), than other fractions. Moreover, EFAE showed dose-dependent inhibitory effect of malondialdehyde (MDA). Hepatoprotective effects of EFAE against ethanol- and $H_2O_2$-induced oxidative stress and cytotoxicity in H4IIE and HepG2 hepatic cells were examined using 2',7'-dichlorofluorescein diacetate (DCF-DA) and 3-[4,5-dimethythiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay. The results showed that EFAE reduced cellular oxidative stress, and increased hepatic cell viability. In addition, EFAE inhibited ethanol-induced lipid accumulation in HepG2 cells. Finally, physiological substances of EFAE were analyzed using high performance liquid chromatography (HPLC), and the major bioactive compounds identified were 3,5-dicaffeoylquinic acid and chlorogenic acid.
Park, Se-Ho;Lee, Jae-Yeul;Jhee, Kwang-Hwan;Yang, Seun-Ah
Journal of Life Science
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v.30
no.4
/
pp.370-378
/
2020
This study aimed to investigate the hepatoprotective effect of Dendropanax morbifera (D. morbifera) leaf hot-water extract on carbon tetrachloride (CCl4)-treated HepG2 cells. Treatment with D. morbifera leaf hot-water extract increased the cell viability of CCl4-treated HepG2 cells without inducing cytotoxicity. The levels of alanine transaminase (ALT) and aspartate transaminase (AST) released by CCl4-treated cells were 27.6 U/L and 52.4 U/L, respectively, and were significantly higher than those in untreated control cells (10.0 U/L and 15.2 U/L, respectively). Moreover, the level of γ-glutamyl transpeptidase (GGT) was 5.4 times higher, while that of glutathione was 44.0% lower in CCl4-treated cells than in control cells. However, treatment with D. morbifera leaf hot-water extract resulted in a dose-dependent decrease in the levels of ALT, AST, and GGT, and an increase in the level of glutathione. Moreover, the malondialdehyde (MDA) content in CCl4-treated HepG2 cells was effectively reduced after treatment with D. morbifera leaf hot-water extract. Additionally, overproduction of intracellular lipids induced by CCl4 treatment was effectively inhibited by D. morbifera leaf hot-water extract treatment. Furthermore, DCFDA staining showed that overproduction of reactive oxygen species (ROS) induced by CCl4 treatment was effectively reduced by treatment with D. morbifera leaf hot-water extract. Our results indicate that owing to its beneficial effects, D. morbifera leaf extract has considerable potential as a functional food material for liver protection.
Journal of the Korean Society of Food Science and Nutrition
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v.30
no.6
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pp.1260-1265
/
2001
This study was performed to investigate the protective effects of Hovenia dulcis Thunb on hepatotoxicity in carbon tetrachloride-intoxicated rats. Male Sprague-Dawley rats (220~240 g) were used as experimental groups, which were divided into 7 groups; Control group, $CCl_4$-treated group, hexane fraction pretreated and $CCl_4$-treated group, chloroform fraction pretreated and $CCl_4$-treated group, ethylacetate fraction pretreated and $CCl_4$-treated group, butanol fraction pretreated and $CCl_4$-treated group, $H_2O$ fraction pretreated and $CCl_4$-treated group. After 6 days, the activities of aminotransferase, contents of cholesterol, TG and hepatic lipid peroxide content in chloroform fraction pretreated and $CCl_4$-treated group were significantly decreased (p<0.05) compared to the only $CCl_4$-treated group. The content of glutathione and activities of GST in chloroform fraction pretreated and $CCl_4$-treated group were also significantly increased (p<0.05) compared to the only $CCl_4$-treated group. In addition, activities of SOD, catalase and GSH-Px in chloroform fraction pretreated and $CCl_4$-treated group were significantly decreased (p<0.05) compared to the only $CCl_4$-treated group. These results indicated that the chloroform fraction of Hovenia dulcis Thunb methanol extract showed hepatoprotective effect in carbon tetrachloride-intoxicated rats.
Song, Eun Jin;Cho, Kyoung Hwan;Choo, Ho Jin;Yang, Eun Young;Jung, Yoon Kyoung;Seo, Min Gyun;Kim, Jong Cheol;Kang, Eun Ju;Ryu, Gi Hyung;Park, Beom Yong;Hah, Young-Sool
Food Engineering Progress
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v.21
no.4
/
pp.318-325
/
2017
Alcoholic steatosis is a fundamental metabolic disorder and may precede the onset of more severe forms of alcoholic liver disease. In this study, we isolated enzymatichydrolysate from Semisulcospira libertine by alcalase hydrolysis and investigated the protective effect of Semisulcospira libertine hydrolysate on liver injury induced by alcohol in the mouse model of chronic and binge ethanol feeding (NIAAA). In an in vitro study, the hydrolysate protects HepG2 cells from ethanol toxicity. Liver damage was assessed by histopathological examination, as well as by quantitating activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). After the administration of S. libertina hydrolysate, fat accumulation and infiltration of inflammatory cells in liver tissues were significantly decreased in the NIAAA mouse model. The elevated levels of serum AST, ALT, and ALP activities, along with the lipid contents of a damaged liver, were recovered in experimental mice administrated with S. libertina hydrolysate, suggesting its role in blood enzyme activation and lipid content restoration within damaged liver tissues. Moreover, treatment with S. libertine hydrolysate reduced the expression rate of cyclooxygenase (COX-2), interleukin $(IL)-1{\beta}$, and IL-6, which accelerate inflammation and induces tissue damage. All data showed that S. libertine hydrolysate has a preventive role against alcohol-induced liver damages by improving the activities of blood enzymes and modulating the expression of inflammation factor, suggesting S. libertine hydrolysate could be a commercially potential material for the restoration of hepatotoxicity.
The biological activities of non-edible extracts of asparagus stems and roots were investigated using hot water and ethanol. The highest contents of rutin and total polyphenol were 31.74 mg/g and 20.14 mg GAE/g, respectively, in the stem hot water extract. ABTS and DPPH radical scavenging activities were 541.1±21.0 and 649.5±6.6 ㎍/mL, respectively, in stem hot water extract. All extracts were non-cytotoxic in HepG2 cells, but 200 ㎍/mL stem extracts tended to decrease the viability of RAW 264.7 cells. The highest xanthine oxidase inhibitory activity was 43.68% in the root hot water extract at 200 ㎍/mL. The expression level of MMP-9 was significantly decreased in the asparagus extracts. The highest GGT, AST, and LDH activities showed a concentration-dependent decrease in the stem ethanol extract. In conclusion, the presence of bioactive substances in the non-edible extracts of asparagus was confirmed for the development of extracts with antioxidant, hepatoprotective and anti-gout activities.
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