The object of this study was to examine whether the germanium fortified yeast administered to SD rat is accumulated in the liver and kidney. The administration doses were within 2,000 mg/kg which is the level of NOAEL (no observed adverse effect level) proved through the previous study of single/consecutive oral toxicity test. There were no significant clinical symptoms and mortality following the administration of organic germanium-fortified yeast (0, 500, 1,000, 2,000 mg/kg) during the whole test period, and also no difference in the consumed amount of feed and water for each group. No significant abnormalities of hematology and blood chemistry parameters were found in all groups of organic germanium-fortified yeast (0, 500, 1,000, 2,000 mg/kg). The amount of germanium accumulated in liver and kidney was 0 g/kg by ICP-AES method in the group of organic germanium-fortified yeast. In the positive control group of $GeO_2$ (150 mg/kg), the amount of accumulation was shown to 3135.0 and 4277.2 g/kg in each female and male kidney and 1044.3 and 2135.8 g/kg in each female and male liver, respectively. Organic germanium-fortified yeast, a biosynthetic product resulting from putting germanium into yeast, did not show any clinical symptoms, blood chemical significance, and residues in kidney and liver. It could be inferred that the non-toxic amount of organic germanium-fortified yeast was up to 2,000 mg/kg.
Acetaminophen (N-acety1-p-aminophenol, paracetamol) is widely used as an over-the-counter analgesic and antipyretic drug. Intake of a over dose of acetaminophen may result in severe hepatic necrosis. In this study, we investigated the liver damage in mice using single dose (300 mg/kg) of acetaminophen and the possible protective effects of administration (50-200 mg/kg body weight) of SB-Ex on acetaminophen-induced liver damage in mice. The alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activities were determined in the plasma of mice. The effect of SB-Ex on lipid peroxidation product thiobarbituric reacting substances (TBARS) and some antioxidant enzymes superoxide dismutase (SOD), catalase, d-aminolevulinate dehydratase (${\sigma}$-ALA-D) activities, and gluthathione peroxidase (GPx), were also evaluated in the mouse liver homogenate. Acetaminophen caused liver damage as evident by statistically significant increased in plasma activities of AST and ALT. There were general statistically significant losses in the activities of SOD, catalase, ${\sigma}$-ALA-D, and GPx and an increase in TBARS in the liver of acetaminophen-treated group compared with the control group. However, SB-Ex was able to counteract these effects. These results suggest that SB-Ex can act as hepatoprotectives against acetaminophen toxicity and is a good candidate for further evaluation as an effective chemotherapeutic agent.
This study was designed to determine the effects of larval extracts from Protaetia brevitarsis seulensis shade dried larva from Korea and China on liver tissues of hepatic injury groups. The experimental groups are divided into five groups; Normal, carbon tetrachloride single injection ($CCl_4$), Pb-CHI ($CCl_4$ + P. brevitarsis shade dried larva from China), Pb-KOR ($CCl_4$ + P. brevitarsis shade dried larva from Korea) and SIL ($CCl_4$ + 0.35% silymarin) groups. Sprague Dawley rats were oral injected with $CCl_4$ at a dose l mg/kg (20% in corn oil) for induction of liver damage for 4 weeks. Each experimental group was fed with a dose 50 mg/kg of larval extracts based on medicinal preparations from 3 weeks to 4 weeks after $CCl_4$ treatment. At the end of 4 weeks, we evaluated the serum levels of glutamate-oxaloacetate transaminase (GOT), glutamate-pyruvate transferase (GPT), alkaline phosphatase (ALP) and blood urea nitrogen (BUN) in serum and the cytokine levels of tumor necrosis factor-${\alpha}$) (TNF-${\alpha}$) and transforming growth factor-${\beta}$ (TGF-${\beta}$) in the cells isolated from spleen and liver. The histological analysis was also conducted. The $CCl_4$ injection reduced body weight, induced congestion of middle lobe and hepatocytic degeneration, resulting in disintegration of hepatic cords, and increased biochemical markers of blood related to hepatic injury. On the other hand, the Pb-CHI and Pb-KOR group decreased the levels of biochemical markers in blood and cytokine levels in spleen and liver. Especially, the Pb-KOR group facilitated the recovery of biochemical values of blood related to hepatic injury, hepatic lesions and fibrosis. Taken together, larval extract from P. brevitarsis might prevent acute hepatotoxicity and enhance the recovery of liver fibrosis and cirrhosis induced by $CCl_4$, and the ingredients could be a promising candidate for the prevention and treatment of hepatic disorders.
Nam, Yoonjin;Bae, Jinhyung;Jeong, Ji Hoon;Ko, Sung Kwon;Sohn, Uy Dong
Journal of Ginseng Research
/
v.42
no.4
/
pp.540-548
/
2018
Background: Acute hepatic failure is a life-threatening critical condition associated with rapid deterioration of liver function and liver transplantation. Several studies have shown that Panax ginseng Mayer has antidiabetic and hepatoprotective effects. However, the hepatoprotective effect of ginseng berry is still unveiled. In this study, we evaluated the hepatoprotective effects of ultrasonication-processed ginseng berry extract (UGBE) on acute hepatic failure model in rats. Methods: Ginseng berry extract (GBE) was ultrasonically processed. The GBE, silymarin, and UGBE were orally administered to male Sprague-Dawley rats for 4 wk. Twenty-four h after the last administration, rats were challenged with D-galactosamine (D-GalN)/lipopolysaccharide (LPS). Results: After ultrasonication, the component ratio of ginsenosides Rg2, Rg3, Rh1, Rh4, Rk1, Rk3, and F4 in GBE had been elevated. Administration of UGBE significantly increased the survival rate of D-GalN/LPS-challenged rats. Pretreatment with UGBE significantly decreased serum alanine aminotransferase, aspartate aminotransferase, and total bilirubin levels in D-GalN/LPS-challenged rats in a dose-dependent manner. The levels of enzymatic markers for oxidative stress (superoxide dismutase, glutathione peroxidase, catalase, and glutathione) were increased by UGBE treatment in a dose-dependent manner. Tumor necrosis factor alphalevel, inducible nitric oxide synthase activities, and nitric oxide productions were reduced by UGBE treatment. In addition, hemeoxygenase-1 levels in liver were also significantly increased in the UGBE-treated group. The protein expression of toll-like receptor 4 was decreased by UGBE administration. Hematoxylin and eosin staining results also supported the results of this study showing normal appearance of liver histopathology in the UGBE-treated group. Conclusion: UGBE showed a great hepatoprotective effect on D-GalN/LPS-challenged rats via the toll-like receptor 4 signaling pathway.
Khotimchenko, Yuri S.;Kolenchenko, Elena A.;Khotimchenko, Maxim Y.;Kovalev, Valeri V.
Advances in Traditional Medicine
/
v.4
no.1
/
pp.28-36
/
2004
The purpose of this study was to investigate the pharmacological effects of low-esterified pectin on carbon tetrachloride $(CCL_4)-induced$ hepatotoxicity in rats. The study included two experiments. In the first experiment the animals were given daily $CCL_4$ through gavage for 7 days and then 10, 50, or 250 mg/kg b.w. of pectin for 21 days. At the end of experiment rats were killed within 24 hours. The increased bilirubin level, enhanced alanine aminotransferase and aspartate aminotransferase activity in plasma induced by $CCL_4$ were partly normalized by pectin administration in a dose-dependent manner. The pectin treatment also resulted in significant recovery of $CCL_4-induced$ decrease of the liver glycogen content. In addition, pectin significantly improved $CCL_4-induced$ alterations of pro-oxidant and antioxidant biochemical parameters in liver and plasma compared to those of rats administered $CCL_4$. In the second experiment the animals were given daily 10, 50 or 250 mg/ kg b.w. of pectin for 21 days before a 7-day administration of $CCL_4$. Rats were killed 24 hours after the end of experiment. Pretreatment with pectin before $CCL_4$ administration resulted in significantly inhibited increase of the blood enzymatic activities of alanine and aspartate aminotransferases and bilirubin level in a dose-dependent manner. Also, preliminary administration of pectin prevented elevation of malondialdehyde and conjugated diene levels in liver and plasma as well as a reduction of glutathione content in liver of rats given $CCL_4$. These results suggest that low-esterified pectin exert healing and preventive effects on $CCL_4-induced$ hepatotoxicity in rats.
Objectives: This study was performed to investigate the effect of TJGB on the liver of high-fat diet (HFD)-fed mice and the cell viability of HepG2 cells. Methods: After a week adaptation, 8-week-old C57BL/6N mice were fed with a 45% HFD or normal diet for 3 weeks. For the next 9 weeks, the mice were divided into 6 groups: normal diet group; HFD group; HFD plus orlistat group; HFD plus Ephedra sinica Stapf (ES) group; HFD plus low dose of TJGB group; HFD plus high dose of TJGB group. To estimate the effect of TJGB in the liver of HFD-fed mice, the protein expressions of phospho-acetyl-CoA carboxylase (p-ACC) and liver X Receptor (LXR) were determined by Western blot assay. The cell viability of ES and TJG was also evaluated in HepG2 cells. Results: The administration of TJGB had little effect on the protein expressions of p-ACC and LXR in the liver of HFD-fed mice. And the cytotoxicity was showed above 7.8 ㎍/mL in HepG2 cells. Conclusion: Further research is needed to evaluate the mechanism of TJGB on hepatic steatosis and cytotoxicity in HepG2 cells.
Jeong Won, Choi;Jin Young, Kim;Mi-Rae, Shin;Hae-Jin, Park
The Korea Journal of Herbology
/
v.38
no.1
/
pp.31-43
/
2023
Objective : Alcoholic liver disease (ALD) is caused by excess alcohol intake. In the liver, alcohol breakdown results formation of toxic byproducts that lead to damage to tissue. This study is to investigate the therapeutic effects of Paeoniae Radix Alba and Puerariae Radix combination (PP) on ALD. Methods : PP was analyzed for polyphenolic compounds and free radical scavenging activity. ALD mouse model was induced by feeding ethanol and water (Control), silymarin (50 mg/kg), low-dose (PP: 100 mg/kg) or high-dose (PP: 200 mg/kg) was orally administrated to ALD mice for 14 days. The serum was assessed with levels of AST, ALT, total bilirubin, total cholesterol, and triglyceride. Liver tissues were evaluated for ROS levels, degree of liver damage and protein expression. Results : The 3:1 (Paeoniae Radix Alba:Puerariae Radix) ratio showed the best antioxidant values for the experiment. In ALD model, levels of AST, ALT, total bilirubin, total cholesterol, and triglyceride were significantly increased in the Control and the levels were decreased by treatment of PP. In addition, increased ROS, ONOO- and MDA levels in the Control were reduced in the PP groups. Western blot analysis figured out that proteins related to ROS and cholesterol metabolism were higher in ALD than in PP-treated ALD. Antioxidant enzyme expression was low in the control group and increased by PP treatment. Conclusion : Our results suggest that PP has the potential to be a medicine in ALD in terms of regulating oxidative stress and adjusting lipid metabolism.
The present study, to evaluate the effect of vitamin E on the oxidative stress in STZ-treated rat and BB rat, was investigated the biochemical enzyme activity in the serum, and malondialdehyde and carbonyl group in the RBC membrane, liver and microsomal fraction after vitamin E and/ or insulin treatment. Results obtained through the experiments were summarized as follows; 1. Effect of vitamin E and/or insulin treatment in STZ-treated rat 1) Lipid peroxidation level in RBC membrane, liver and microsomal fraction was significantly decreased in vi. tamin E and/or insulin treatment group, and especially more significantly decreased in vitamin E with insulin treated group. 2) Protein oxidation level in RBC membrane, liver and microsomal fraction was significantly decreased in vitamin E and/or insulin treatment group. And it was especially more significantly decreased in RBC membrane and liver of vitamin E with insulin treated group. 3) In the enzyme activity in the serum, the activity of AST and ALT was not altered in all experimental group. The increased ALP activity in STZ-treated group was significantly decreased in insulin treated group and vitamin E with insulin treated group. 4) Decreased level of albumin and creatinine after STZ treatment was significantly increased in vitamin E and/or insulin treated group. 5) Level of glucose, cholesterol and triacylglycerol in serum: Glucose level was not significantly different in vitamin E treated group compared to STZ control group. But it was significantly different in the insulin treated group and vitamin E with insulin treated group compared to STZ control group. The cholesterol content in the serum was significantly increased in STZ control group compared to normal control group. And except low dose vitamin E treatment group, it was significantly decreased in vitamin E and/or insulin treated group compared to STZ control group. The triacylglycerol content in the serum was significantly decreased in STZ control group and increased in high dose vitamin E treated group and vitamin E with insulin treated group. But it was not significantly different in low dose vitamin E treated group and insulin treated group compared to STZ control group. 2. Effect of vitamin E and/or insulin treatment in BB rat 1) Lipid peroxidation level in liver was decreased by vitamin E with insulin treatment compared to insulin treatment. But it was not different in microsomal fractions. 2) Protein oxidation level in liver and microsomal fraction was decreased by vitamin E with insulin treatment compared to insulin treatment only in microsomal fractions. These results suggest that the combination treatment of vitamin E and insulin could prevent the oxidative change of lipid and protein of the RBC membrane, liver and microsomal fraction in STZ-treated rats and BB rats.
Chronical intake of alcohol can cause alcoholic fatty liver. Fatty liver is caused by fat infiltration: the state of high rate of fat in liver cells and by losing the balance between the synthesis and the secretion of fatty acid. It could be developed into liver necrosis and cirrhosis. Ka-Mi-Chung-Gan-Tang (KMCGT) is a decoction used for fatty liver as oriental medicines in China. The prescription is composed of Ginseng Radix, Bupleuri Radix, Scutellariae Radix, Pinelliae Tuber, Artemisiae capillaris Herba, Gardeniae Fructus, Zingiberis Rhizoma, Zizyphi Fructus and Glycyrrhizae Radix etc. We have induced alcoholic fatty liver by ethanol administration (6 g/kg, single dose/day, for a week) on rats and observed changes of triglyceride, cholesterol and lipid peroxidation in liver tissues of them. Also we checked the activities of GOT and GPT in blood of rats. KMCGT inhibited significantly the increase of triglyceride, cholesterol, lipid peroxidation level and effectively the increase of malondialdehyde (MDA).
In order to investigate radiation effects on the liver, functional changes of liver were analyzed after irradiation. Doses of 10 Gy, 15 Gy and 20 Gy were exposed partially to the liver of male rats(Sprague-Dawley) with X-ray(4MV linear accelerator) at room temperature. On 1, 2, 4 and 8 weeks after irradiation, liver tissues and sera of the animals were compared with those of unirradiated animal by liver function tests. Enzyme activities in sera such as alanine aminotransferase, aspartate aminotransferase, malondialdehyde. The content of malondialdehyde in the activities of many enzymes including alanine aminotransferase, aspartate aminotransferase in sera were increased slightly with increasing exposure dose in all experiments and the activities of these enzymes increased markedly in 20 Gy irradiated groups. From these above results, functional changes of the liver were induced in all irradiated groups. Damaged liver was recovered along with time collapse after irradiation to the doses of 10 Gy and 15 Gy while no recovery was deteced within 8 weeks after irradiation to 20 Gy. These results suggest that careful attention must be paid to liver not to be included in exposure field in radiation therapy.
본 웹사이트에 게시된 이메일 주소가 전자우편 수집 프로그램이나
그 밖의 기술적 장치를 이용하여 무단으로 수집되는 것을 거부하며,
이를 위반시 정보통신망법에 의해 형사 처벌됨을 유념하시기 바랍니다.
[게시일 2004년 10월 1일]
이용약관
제 1 장 총칙
제 1 조 (목적)
이 이용약관은 KoreaScience 홈페이지(이하 “당 사이트”)에서 제공하는 인터넷 서비스(이하 '서비스')의 가입조건 및 이용에 관한 제반 사항과 기타 필요한 사항을 구체적으로 규정함을 목적으로 합니다.
제 2 조 (용어의 정의)
① "이용자"라 함은 당 사이트에 접속하여 이 약관에 따라 당 사이트가 제공하는 서비스를 받는 회원 및 비회원을
말합니다.
② "회원"이라 함은 서비스를 이용하기 위하여 당 사이트에 개인정보를 제공하여 아이디(ID)와 비밀번호를 부여
받은 자를 말합니다.
③ "회원 아이디(ID)"라 함은 회원의 식별 및 서비스 이용을 위하여 자신이 선정한 문자 및 숫자의 조합을
말합니다.
④ "비밀번호(패스워드)"라 함은 회원이 자신의 비밀보호를 위하여 선정한 문자 및 숫자의 조합을 말합니다.
제 3 조 (이용약관의 효력 및 변경)
① 이 약관은 당 사이트에 게시하거나 기타의 방법으로 회원에게 공지함으로써 효력이 발생합니다.
② 당 사이트는 이 약관을 개정할 경우에 적용일자 및 개정사유를 명시하여 현행 약관과 함께 당 사이트의
초기화면에 그 적용일자 7일 이전부터 적용일자 전일까지 공지합니다. 다만, 회원에게 불리하게 약관내용을
변경하는 경우에는 최소한 30일 이상의 사전 유예기간을 두고 공지합니다. 이 경우 당 사이트는 개정 전
내용과 개정 후 내용을 명확하게 비교하여 이용자가 알기 쉽도록 표시합니다.
제 4 조(약관 외 준칙)
① 이 약관은 당 사이트가 제공하는 서비스에 관한 이용안내와 함께 적용됩니다.
② 이 약관에 명시되지 아니한 사항은 관계법령의 규정이 적용됩니다.
제 2 장 이용계약의 체결
제 5 조 (이용계약의 성립 등)
① 이용계약은 이용고객이 당 사이트가 정한 약관에 「동의합니다」를 선택하고, 당 사이트가 정한
온라인신청양식을 작성하여 서비스 이용을 신청한 후, 당 사이트가 이를 승낙함으로써 성립합니다.
② 제1항의 승낙은 당 사이트가 제공하는 과학기술정보검색, 맞춤정보, 서지정보 등 다른 서비스의 이용승낙을
포함합니다.
제 6 조 (회원가입)
서비스를 이용하고자 하는 고객은 당 사이트에서 정한 회원가입양식에 개인정보를 기재하여 가입을 하여야 합니다.
제 7 조 (개인정보의 보호 및 사용)
당 사이트는 관계법령이 정하는 바에 따라 회원 등록정보를 포함한 회원의 개인정보를 보호하기 위해 노력합니다. 회원 개인정보의 보호 및 사용에 대해서는 관련법령 및 당 사이트의 개인정보 보호정책이 적용됩니다.
제 8 조 (이용 신청의 승낙과 제한)
① 당 사이트는 제6조의 규정에 의한 이용신청고객에 대하여 서비스 이용을 승낙합니다.
② 당 사이트는 아래사항에 해당하는 경우에 대해서 승낙하지 아니 합니다.
- 이용계약 신청서의 내용을 허위로 기재한 경우
- 기타 규정한 제반사항을 위반하며 신청하는 경우
제 9 조 (회원 ID 부여 및 변경 등)
① 당 사이트는 이용고객에 대하여 약관에 정하는 바에 따라 자신이 선정한 회원 ID를 부여합니다.
② 회원 ID는 원칙적으로 변경이 불가하며 부득이한 사유로 인하여 변경 하고자 하는 경우에는 해당 ID를
해지하고 재가입해야 합니다.
③ 기타 회원 개인정보 관리 및 변경 등에 관한 사항은 서비스별 안내에 정하는 바에 의합니다.
제 3 장 계약 당사자의 의무
제 10 조 (KISTI의 의무)
① 당 사이트는 이용고객이 희망한 서비스 제공 개시일에 특별한 사정이 없는 한 서비스를 이용할 수 있도록
하여야 합니다.
② 당 사이트는 개인정보 보호를 위해 보안시스템을 구축하며 개인정보 보호정책을 공시하고 준수합니다.
③ 당 사이트는 회원으로부터 제기되는 의견이나 불만이 정당하다고 객관적으로 인정될 경우에는 적절한 절차를
거쳐 즉시 처리하여야 합니다. 다만, 즉시 처리가 곤란한 경우는 회원에게 그 사유와 처리일정을 통보하여야
합니다.
제 11 조 (회원의 의무)
① 이용자는 회원가입 신청 또는 회원정보 변경 시 실명으로 모든 사항을 사실에 근거하여 작성하여야 하며,
허위 또는 타인의 정보를 등록할 경우 일체의 권리를 주장할 수 없습니다.
② 당 사이트가 관계법령 및 개인정보 보호정책에 의거하여 그 책임을 지는 경우를 제외하고 회원에게 부여된
ID의 비밀번호 관리소홀, 부정사용에 의하여 발생하는 모든 결과에 대한 책임은 회원에게 있습니다.
③ 회원은 당 사이트 및 제 3자의 지적 재산권을 침해해서는 안 됩니다.
제 4 장 서비스의 이용
제 12 조 (서비스 이용 시간)
① 서비스 이용은 당 사이트의 업무상 또는 기술상 특별한 지장이 없는 한 연중무휴, 1일 24시간 운영을
원칙으로 합니다. 단, 당 사이트는 시스템 정기점검, 증설 및 교체를 위해 당 사이트가 정한 날이나 시간에
서비스를 일시 중단할 수 있으며, 예정되어 있는 작업으로 인한 서비스 일시중단은 당 사이트 홈페이지를
통해 사전에 공지합니다.
② 당 사이트는 서비스를 특정범위로 분할하여 각 범위별로 이용가능시간을 별도로 지정할 수 있습니다. 다만
이 경우 그 내용을 공지합니다.
제 13 조 (홈페이지 저작권)
① NDSL에서 제공하는 모든 저작물의 저작권은 원저작자에게 있으며, KISTI는 복제/배포/전송권을 확보하고
있습니다.
② NDSL에서 제공하는 콘텐츠를 상업적 및 기타 영리목적으로 복제/배포/전송할 경우 사전에 KISTI의 허락을
받아야 합니다.
③ NDSL에서 제공하는 콘텐츠를 보도, 비평, 교육, 연구 등을 위하여 정당한 범위 안에서 공정한 관행에
합치되게 인용할 수 있습니다.
④ NDSL에서 제공하는 콘텐츠를 무단 복제, 전송, 배포 기타 저작권법에 위반되는 방법으로 이용할 경우
저작권법 제136조에 따라 5년 이하의 징역 또는 5천만 원 이하의 벌금에 처해질 수 있습니다.
제 14 조 (유료서비스)
① 당 사이트 및 협력기관이 정한 유료서비스(원문복사 등)는 별도로 정해진 바에 따르며, 변경사항은 시행 전에
당 사이트 홈페이지를 통하여 회원에게 공지합니다.
② 유료서비스를 이용하려는 회원은 정해진 요금체계에 따라 요금을 납부해야 합니다.
제 5 장 계약 해지 및 이용 제한
제 15 조 (계약 해지)
회원이 이용계약을 해지하고자 하는 때에는 [가입해지] 메뉴를 이용해 직접 해지해야 합니다.
제 16 조 (서비스 이용제한)
① 당 사이트는 회원이 서비스 이용내용에 있어서 본 약관 제 11조 내용을 위반하거나, 다음 각 호에 해당하는
경우 서비스 이용을 제한할 수 있습니다.
- 2년 이상 서비스를 이용한 적이 없는 경우
- 기타 정상적인 서비스 운영에 방해가 될 경우
② 상기 이용제한 규정에 따라 서비스를 이용하는 회원에게 서비스 이용에 대하여 별도 공지 없이 서비스 이용의
일시정지, 이용계약 해지 할 수 있습니다.
제 17 조 (전자우편주소 수집 금지)
회원은 전자우편주소 추출기 등을 이용하여 전자우편주소를 수집 또는 제3자에게 제공할 수 없습니다.
제 6 장 손해배상 및 기타사항
제 18 조 (손해배상)
당 사이트는 무료로 제공되는 서비스와 관련하여 회원에게 어떠한 손해가 발생하더라도 당 사이트가 고의 또는 과실로 인한 손해발생을 제외하고는 이에 대하여 책임을 부담하지 아니합니다.
제 19 조 (관할 법원)
서비스 이용으로 발생한 분쟁에 대해 소송이 제기되는 경우 민사 소송법상의 관할 법원에 제기합니다.
[부 칙]
1. (시행일) 이 약관은 2016년 9월 5일부터 적용되며, 종전 약관은 본 약관으로 대체되며, 개정된 약관의 적용일 이전 가입자도 개정된 약관의 적용을 받습니다.