• Title/Summary/Keyword: liver disorder

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Review on the Kampo Treatment and Education Program for Children with Developmental Disabilities in Japan (일본에서 발달장애아를 대상으로 Kampo치료 및 교육프로그램의 제공에 대한 연구동향)

  • Kim, Mi-Suk;Ko, Byoung Seob
    • The Journal of Pediatrics of Korean Medicine
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    • v.33 no.4
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    • pp.60-73
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    • 2019
  • Objectives This study reviewed the effects of a combined treatment with Kampo and Western medicine for Developmental disability in Japan, and the provision of education programs in clinical care. Methods The search database includes J-STAGE. To narrow the search, the following key words were used: 'pervasive developmental disorders, Attention-Deficit/Hyperactivity Disorder, Learning Disorders or Learning Disabilities, Intellectual Disability, and Kampo'. The search was limited to the publication date from 2001 to 2019. Results 1. Japan analyzed five sections: The usage of the Kampo medicine ranges from 25.2% to 71.6%, and the Kampo medicine was highly used in large cities. 2. In Japan, the educational programs were provided for the caregiver and special educational programs were available for children with disabilities. 3. In Japan, there were 9 studies regarding developmental disability treating with herbal remedies. There were seven clinical trial reports, and two were published in a review or report form. 4. The results showed benefits of using Kampo for patients with lack of Yin in blood in treatment of developmental disorder. It is also important to control the liver qi and Yin in blood. 5. Seven papers reported no side effects or abnormal findings. They have reduced the use of antipsychotics. Conclusions These review studies in regards to the combined treatment of Kampo and Western medicines can be helpful to improve long term side effects of the antipsychotics used in developmental disorders.

Hypersensitive Large Intestine Syndrome in Hyungsang Medicine (과민성대장증후군의 형상의학적 고찰 -동의보감(東醫寶鑑)을 중심으로-)

  • Choi Byung-Tae;Choi Yung-Hyun;Han Jin-Soo;Lee Yong-Tae
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.5
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    • pp.1129-1136
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    • 2005
  • The writer reports the conclusions gained from study about the cause of the hypersensitive large intestine syndrome with Dongeuibogam as the central figure through researching the disharmony among Body Essence, Vital Energy, Mentality, and Blood, mutual action of five viscera and six bowels, and external shapes. The hypersensitive large intestine syndrome is generally chronic and recurred in many cases, so it is more efficacious than symptomatic to treat according to find the contradictions of individual shapes. The shapes and cases suffering frequently the hypersensitive large intestine syndrome are Gi-kwa and Sin-kwa, having a long nose, having a bruised spot on Triple warmer, man with inclined mouth, Taeeum type, man with congested fluids, man with colic symptoms. The hypersensitive large intestine syndrome in Oriental medicine is recognized of diarrhea, constipation, abdominal pain, abdominal distention and fullness caused by seven emotions. In Dongeuibogam it can be found out the similarity in depressive symptoms due to disorder of Gi, stagnation of Gi, dysphasia due to disorder of Gi, diarrhea due to disorder of Gi, fullness of due to Gi, diarrhea due to phlegm-retention, retention of undigested food, immoderate drinking, hypo-function of the spleen, or deficiency, abdominal pain from colic symptom, and difficulty in defecation and urination, internal injury, diarrhea due to weakness and fatigue. If the Jung, Gi, Sin, and Hyul composed the human body is broken harmony, the function of large intestinal transmission would be fallen, so similar symptoms like the hypersensitive large intestine syndrome are gotten. Especially Gi-kwa suffers diarrhea, constipation abdominal pain, and abdominal distention and fullness due to depressive symptoms from disorder of Seven emotions or Seven Gi. And Sin-kwa suffers from the hypersensitive large intestine syndrome due to emotional restlessness having an influence on rhythmic movement of abdomen. Examining between five viscera and six bowels and the hypersensitive large intestine syndrome, Liver cannot disperse well having influence on mutual relation of Liver-Large intestine, Heart reduces the function of defecation and urination not to control the seven emotions, Lung having exterior and interior relation with intestine has an influence on primordial energy and let the main symptoms occur, Spleen circulating the body fluid let the main symptoms occur due to malfunction of circulation, Kidney locating in lower part of the body has deep connection with intestine, so let the disorder. Urinary bladder is connected with intestine in moisture metabolism, Stomach is connected in receive and transmission, Small intestine is connected in absorption and excretion, from small intestine pain disturbing the abdominal movement, Samcho managing the catharsis of lower heater if declined its function causes the hypersensitive large intestine syndrome. The colic symptoms of Front private parts which disorder in lower abdomen give rise to abdominal pains, difficulty in defecation and urination due to Cold are similar to the hypersensitive large intestine syndrome. The treatments of applying the shapes of colic syndrome advocated by Master Park can be efficacious cure in clinic. Researching after the clinical cases of Master Park advocating Hyungsang medicine, we came to know that plenty of prescriptions of internal injury are applied and take good effects.

Protective Effect of a 43 kD Protein from the Leaves of the Herb, Cajanus indicus L on Chloroform Induced Hepatic-disorder

  • Ghosh, Ayantika;Sarkar, Kasturi;Sil, Parames C.
    • BMB Reports
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    • v.39 no.2
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    • pp.197-207
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    • 2006
  • Cajanus indicus is a herb with medicinal properties and is traditionally used to treat various forms of liver disorders. Present study aimed to evaluate the effect of a 43 kD protein isolated from the leaves of this herb against chloroform induced hepatotoxicity. Male albino mice were intraperitoneally treated with 2mg/kg body weight of the protein for 5 days followed by oral application of chloroform (0.75ml/kg body weight) for 2 days. Different biochemical parameters related to physiology and pathophysiology of liver, such as, serum glutamate pyruvate transaminase and alkaline phosphatase were determined in the murine sera under various experimental conditions. Direct antioxidant role of the protein was also determined from its reaction with Diphenyl picryl hydraxyl radical, superoxide radical and hydrogen peroxide. To find out the mode of action of this protein against chloroform induced liver damage, levels of antioxidant enzymes catalase, superoxide dismutase and glutathione-S-transferase were measured from liver homogenates. Peroxidation of membrane lipids both in vivo and in vitro were also measured as malonaldialdehyde. Finally, histopathological analyses were done from liver sections of control, toxin treated and protein pre- and post-treated (along with the toxin) mice. Levels of serum glutamate pyruvate transaminase and alkaline phosphatase, which showed an elevation in chloroform induced hepatic damage, were brought down near to the normal levels with the protein pretreatment. On the contrary, the levels of anti-oxidant enzymes such as catalase, superoxide dismutase and glutathione-S-transferase that had gone down in mice orally fed with chloroform were significantly elevated in protein pretreated ones. Besides, chloroform induced lipid peroxidation was effectively reduced by protein treatment both in vivo and in vitro. In cell free system the protein effectively quenched diphenyl picryl hydrazyl radical and superoxide radical, though it could not catalyse the breakdown of hydrogen peroxide. Post treatment with the protein for 3 days after 2 days of chloroform administration showed similar results. Histopathological studies indicated that chloroform induced extensive tissue damage was less severe in the mice livers treated with the 43 kD protein prior and post to the toxin administration. Results from all these data suggest that the protein possesses both preventive and curative role against chloroform induced hepatotoxicity and probably acts by an anti-oxidative defense mechanism.

Protective Effect of Astragalus polysaccharides on Liver Injury Induced by Several Different Chemotherapeutics in Mice

  • Liu, Wen;Gao, Fang-Fang;Li, Qun;Lv, Jia-Wei;Wang, Ying;Hu, Peng-Chao;Xiang, Qing-Ming;Wei, Lei
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.23
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    • pp.10413-10420
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    • 2015
  • Side effects are an unavoidable consequence of chemotherapy drugs, during which liver injury often takes place. The current study was designed to investigate the protective effect of Astragalus polysaccharides (APS) against the hepatotoxicity induced by frequently-used chemical therapy agents, cyclophosphamide (CTX), docetaxel (DTX) and epirubicin (EPI)) in mice. Mice were divided into five groups, controls, low or high dose groups ($DTX_L$, $CTX_L$, $EPI_L$ or $DTX_H$, $CTX_H$, $EPI_H$), and low or high dose chemotherapeutics+APS groups ($DTX_L$+APS, $CTX_L$+APS, $EPI_L$+APS or $DTX_H$+APS, $CTX_H$+APS, $EPI_H$+APS). Controls were treated with equivalent normal saline for 28 days every other day; low or high dose group were intraperitoneal (i.p) injected with low or high doses of CTX, DTX and EPI for 28 days every other day; low or high dose chemotherapeutics+APS group were separately intraperitoneal (i.p) injected with chemotherapeutics for 28 days every other day and i.p with APS (100 mg/kg) for 7 days continually from the 22th to the 28th days. The body weight, serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), histopathological features, and ultrastructure morphological change of liver tissues, protein expression level of caspase-3 were estimated at different time points. With high dose treatment of DTX, CTX and EPI, weight gain was inhibited and serum levels of ALT and AST were significantly increased. Sections of liver tissue showed massive hepatotoxicity in $CTX_H$ group compared to the control group, including hepatic lobule disorder, granular and vacuolar degeneration and necrosis in hepatic cells. These changes were confirmed at ultrastructural level, including obvious pyknosis, heterochromatin aggregation, nuclear membrane resolution, and chondrosome crystal decrease. Western blotting revealed that the protein levels of caspase-3 increased in $CTX_H$ group. The low dose groups exhibited trivial hepatotoxicity. More interestingly, after 100 mg/kg APS, liver injury was redecued not only regarding serum transaminase activities (low or high dose chemotherapeutics+APS group), but also from pathological and ultrastructural changes and the protein levels of caspase-3 ($CTX_H$+APS group). In conclusion, DTX, CTX and EPI induce liver damage in a dose dependent manner, whereas APS exerted protective effects.

Standardized rice bran extract improves hepatic steatosis in HepG2 cells and ovariectomized rats

  • Lim, Dong Wook;Jeon, Hyejin;Kim, Minji;Yoon, Minseok;Jung, Jonghoon;Kwon, Sangoh;Cho, Suengmok;Um, Min Young
    • Nutrition Research and Practice
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    • v.14 no.6
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    • pp.568-579
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    • 2020
  • BACKGROUD/OBJECTIVES: Hepatic steatosis is the most common liver disorder, particularly in postmenopausal women. This study investigated the protective effects of standardized rice bran extract (RBS) on ovariectomized (OVX)-induced hepatic steatosis in rats. MATERIALS/METHODS: HepG2 cells were incubated with 200 µM oleic acid to induce lipid accumulation with or without RBS and γ-oryzanol. OVX rats were separated into three groups and fed a normal diet (ND) or the ND containing 17β-estradiol (E2; 10 ㎍/kg) and RBS (500 mg/kg) for 16 weeks. RESULTS: RBS supplementation improved serum triglyceride and free fatty acid levels in OVX rats. Histological analysis showed that RBS significantly attenuated hepatic fat accumulation and decreased hepatic lipid, total cholesterol, and triglyceride levels. Additionally, RBS suppressed the estrogen deficiency-induced upregulation of lipogenic genes, such as sterol regulatory element-binding protein 1 (SREBP1), acetyl-CoA carboxylase 1, fatty acid synthase, glycerol-3-phosphate acyltransferase, and stearoyl-CoA desaturase 1. CONCLUSIONS: RBS and γ-oryzanol effectively reduced lipid accumulation in a HepG2 cell hepatic steatosis model. RBS improves OVX-induced hepatic steatosis by regulating the SREBP1-mediated activation of lipogenic genes, suggesting the benefits of RBS in preventing fatty liver in postmenopausal women.

Hepatoprotective Effect of Fermented Artemisia princeps PAMPANINI by Lactic Acid Bacteria (발효강화쑥의 간장해 보호효과)

  • Choi, Hyuck-Jae;Kim, Eun-Jin;Han, Myung-Joo;Baek, Nam-In;Kim, Dong-Hyun;Jung, Hae-Gon;Kim, Nam-Jae
    • Korean Journal of Pharmacognosy
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    • v.38 no.3 s.150
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    • pp.245-253
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    • 2007
  • Artemisia princeps PAMPANINI has been used in traditional medicine of the treatment of inflammatory, liver dysfunction and order disorder in the far east countries including Korea. The present study was carried out to investigate the hepatoprotective effects of ethanol extract of Artemisia princeps (AP) and its fermented agents (AP-F) by lactic acid bacteria derived from human intestinal bacteria on liver injured rat induced by $CCl_4$ and d-galactosamine. Hepatoprotective activity was monitored by estimating serum ALT, AST, ALP, LDH, superoxide dismutase (SOD), glutathione redeuctase (GR) and glutathione peroxidase (Gpx) activities in the liver injured by hepatotoxin. Pretreating rats with AP or AP-F at the same dosage regimen significantly suppressed the acute elevation of serum transaminase, ALP, LDH and GR activities, and significantly increased the lowering of blood SOD and GR activites induced by hepatoxin. Based on these findings, it is presumed that AP and APF may have the hepatoprotective effect on $CCl_4$ and d-galactosamine-induced hepatotoxicity rat.

Effect of Hfe Deficiency on Memory Capacity and Motor Coordination after Manganese Exposure by Drinking Water in Mice

  • Alsulimani, Helal Hussain;Ye, Qi;Kim, Jonghan
    • Toxicological Research
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    • v.31 no.4
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    • pp.347-354
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    • 2015
  • Excess manganese (Mn) is neurotoxic. Increased manganese stores in the brain are associated with a number of behavioral problems, including motor dysfunction, memory loss and psychiatric disorders. We previously showed that the transport and neurotoxicity of manganese after intranasal instillation of the metal are altered in Hfe-deficient mice, a mouse model of the iron overload disorder hereditary hemochromatosis (HH). However, it is not fully understood whether loss of Hfe function modifies Mn neurotoxicity after ingestion. To investigate the role of Hfe in oral Mn toxicity, we exposed Hfe-knockout ($Hfe^{-/-}$) and their control wild-type ($Hfe^{+/+}$) mice to $MnCl_2$ in drinking water (5 mg/mL) for 5 weeks. Motor coordination and spatial memory capacity were determined by the rotarod test and the Barnes maze test, respectively. Brain and liver metal levels were analyzed by inductively coupled plasma mass spectrometry. Compared with the water-drinking group, mice drinking Mn significantly increased Mn concentrations in the liver and brain of both genotypes. Mn exposure decreased iron levels in the liver, but not in the brain. Neither Mn nor Hfe deficiency altered tissue concentrations of copper or zinc. The rotarod test showed that Mn exposure decreased motor skills in $Hfe^{+/+}$ mice, but not in $Hfe^{-/-}$ mice (p = 0.023). In the Barns maze test, latency to find the target hole was not altered in Mn-exposed $Hfe^{+/+}$ compared with water-drinking $Hfe^{+/+}$ mice. However, Mn-exposed $Hfe^{-/-}$ mice spent more time to find the target hole than Mn-drinking $Hfe^{+/+}$ mice (p = 0.028). These data indicate that loss of Hfe function impairs spatial memory upon Mn exposure in drinking water. Our results suggest that individuals with hemochromatosis could be more vulnerable to memory deficits induced by Mn ingestion from our environment. The pathophysiological role of HFE in manganese neurotoxicity should be carefully examined in patients with HFE-associated hemochromatosis and other iron overload disorders.

A case of Menkes disease with unusual hepatomegaly (멘케스병에서 간비대를 보인 1례)

  • Jeong, Go Un;Cho, Anna;Hwang, Hee;Hwang, Yong Seung;Kim, Ki Joong;Chae, Jong Hee;Seo, Jeong Kee
    • Clinical and Experimental Pediatrics
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    • v.51 no.5
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    • pp.538-541
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    • 2008
  • Menkes disease is an X-linked recessive copper transport disorder characterized by neurological deterioration, connective-tissue damage, and abnormal hair growth. It is caused by the mutation of the ATP7A gene. This report describes a four-month-old boy with neurological symptoms typical of Menkes disease plus unusual liver involvement. He developed seizures at three months of age and exhibited hypotonia, cephalhematoma, a sagging face, redundant and hypopigmented skin, and abnormal hair growth. In addition, he had unexplained hepatomegaly and high hepatic transaminase. We confirmed the diagnosis of Menkes disease by mutation analysis of the ATP7A gene. To exclude other possible causes for the hepatic abnormalities, a liver biopsy was performed, revealing intracytoplasmic cholestasis, focal spotty necrosis, and minimal lobular activity. The patient's liver involvement may be an underestimated complication of Menkes disease.

Recurrent Hepatic Alveolar Echinococcosis: Report of The First Case in Korea with Unproven Infection Route

  • Kim, Su-Jin;Kim, Jong-Han;Han, Sang-Young;Kim, Young-Hoon;Cho, Jin-Han;Chai, Jong-Yil;Jeong, Jin-Sook
    • Parasites, Hosts and Diseases
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    • v.49 no.4
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    • pp.413-418
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    • 2011
  • Human alveolar echinococcosis (AE), a hepatic disorder that resembles liver cancer, is a highly aggressive and lethal zoonotic infection caused by the larval stage of the fox tapeworm, Echinococcus multilocularis. E. multilocularis is widely distributed in the northern hemisphere; the disease-endemic area stretches from north America through Europe to central and east Asia, including northern parts of Japan, but it has not been reported in Korea. Herein, we represent a first case of AE in Korea. A 41-year-old woman was found to have a large liver mass on routine medical examination. The excised mass showed multinodular, necrotic, and spongiform appearance with small irregular pseudocystic spaces. Microscopically, the mass was composed of chronic granulomatous inflammation with extensive coagulation necrosis and parasite-like structure, which was revealed as parasitic vesicles and laminated layer delineated by periodic acid-Schiff (PAS) stain. Clinical and histologic features were consistent with AE. After 8 years, a new liver mass and multiple metastatic pulmonary nodules were found and the recurred mass showed similar histologic features to the initial mass. She had never visited endemic areas of AE, and thus the exact infection route is unclear.

Clinical Study on the efficacy of Panax ginseng C. A. Meyer on Acute viral(B) Hepatitis- (1) (고려인삼이 비루스성 급성간염의 치료효과에 미치는 임상학적 연구(1))

  • 구국회;주충노
    • Journal of Ginseng Research
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    • v.7 no.2
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    • pp.115-124
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    • 1983
  • The effect of ginseng administration on the patients of acute viral (B type) hepatitis has been oberved and the results were as follows. The albumin/globulin ratio of the ginseng administered group has significantly improved 4 weeks after admission while that of control group has not been improved suggesting that the ginseng might be effective in improving the protein metabolism. The thymol turbidity test again gave a similar result. Recovery of the disorder of bilirubin metabolism was also accelerated in the ginseng administered group compared with control group. The raised bilirubin value of the former returnedto the normal value 2 week after admission while that of the latter reached to normal 4-5 weeks after admission. However no significant difference of the bilirubin level between ginseng treated and non-treated groups could be observed. Cholesterol metabolism is also stimulated in ginseng administered group. The lowered cholesterol level of the ginseng group returned to normal 3-4 weeks after admission while that of latter reached to normal 5-6 weeks after admission. The raised S-GOT and S-GPT levels of the ginseng treated group returned to the normal value 3-4 weeks after admission while those of control group rehimed to normal in 5 weeks after admission suggesting that the ginseng improved impaired liver function. The improvement of the raised transaminase level seemed to be accelerate6 by the ginseng administration, however, no significant difference of the transaminase level between the ginseng treated and non-treated group could be observed. A significant effect of ginseng on the raised alkaline phosphatase level was observed. From the above results, it seemed that ginseng might stimulate the improvement of the disturbance of liver function, particularly at the early phase of its development of acute liver disease suggesting that panax ginseng might play a significant role in preventing the disease developing to be chronic.

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