• Title/Summary/Keyword: DHEA-S

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Effect of DHEA on Recovery of Muscle Atrophy Induced by Parkinson' s Disease

  • Choe, Myoung-Ae;An, Gyeong-Ju;Koo, Byung-Soo;Jeon, Song-Hee
    • Journal of Korean Academy of Nursing
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    • v.41 no.6
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    • pp.834-842
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    • 2011
  • Purpose: The purpose of this study was to determine the effect of dehydroepiandrosterone (DHEA) on recovery of muscle atrophy induced by Parkinson's disease. Methods: The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 20 ${\mu}g$) into the left striatum using stereotaxic surgery. Rats were divided into two groups; the Parkinson's disease group with vehicle treatment (Vehicle; n=12) or DHEA treatment group (DHEA; n=22). DHEA or vehicle was administrated intraperitoneally daily at a dose of 0.34 mmol/kg for 21 days. At 22-days after DHEA treatment, soleus, plantaris, and striatum were dissected. Results: The DHEA group showed significant increase (p<.01) in the number of tyrosine hydroxylase (TH) positive neurons in the lesioned side substantia nigra compared to the vehicle group. Weights and Type I fiber cross-sectional areas of the contralateral soleus of the DHEA group were significantly greater than those of the vehicle group (p=.02, p=.00). Moreover, extracellular signal-regulated kinase (ERK) phosphorylation significantly decreased in the lesioned striatum, but was recovered with DHEA and also in the contralateral soleus muscle, Akt and ERK phosphorylation recovered significantly and the expression level of myosin heavy chain also recovered by DHEA treatment. Conclusion: Our results suggest that DHEA treatment recovers Parkinson's disease induced contralateral soleus muscle atrophy through Akt and ERK phosphorylation.

Effect of DHEA Administration Alone or Exercise combined with DHEA before Steroid Treatment on Rat Hindlimb Muscles (스테로이드 치료 전 DHEA 단독투여와 DHEA 투여와 운동의 동시적용이 스테로이드에 의해 유발되는 쥐 뒷다리근의 위축 예방에 미치는 효과)

  • Choe, Myoung-Ae;An, Gyeong-Ju
    • Journal of Korean Academy of Nursing
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    • v.39 no.3
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    • pp.321-328
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    • 2009
  • Purpose: The purpose of this study was to determine the effect of Dehydroepiandrosterone(DHEA) administration alone or exercise combined with DHEA before steroid treatment on rat hindlimb muscles. Methods: Male Sprague-Dawley rats were assigned to one of three groups: a steroid group(S, n=10) that had no treatment for 7 days before steroid treatment; a DHEA-steroid group(DS, n=8) that had 0.34 mmol/kg/day DHEA injection once a day for 7 days before steroid treatment and an exercise+DHEA-steroid group(EDS, n=9) that ran on the treadmill combined with 0.34 mmol/kg/day DHEA injection for 7 days before steroid treatment. At 15 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles were dissected. Body weight, food intake, muscle weight, myofibillar protein content and cross-sectional area of the dissected muscles were determined. Results: The DS group showed significant increases(p<.05) as compared to the steroid group in body weight, and muscle weight of gastrocnemius muscles. The EDS group showed significant increases(p<.05) as compared to the S group in body weight, muscle weight, myofibrillar protein content, and Type II fiber cross-sectional area of soleus, plantaris and gastrocnemius muscles. Conclusion: Exercise combined with DHEA administration before steroid treatment prevents steroid induced muscle atrophy, with exercise combined with DHEA administration being more effective than DHEA administration alone in preventing muscle atrophy.

Dehydroepiandrosterone supplement increases malate dehydrogenase activity and decreases NADPH-dependent antioxidant enzyme activity in rat hepatocellular carcinogenesis

  • Kim, Jee-Won;Kim, Sook-Hee;Choi, Hay-Mie
    • Nutrition Research and Practice
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    • v.2 no.2
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    • pp.80-84
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    • 2008
  • Beneficial effects of dehydroepiandrosterone (DHEA) supplement on age-associated chronic diseases such as cancer, cardiovascular disease, insulin resistance and diabetes, have been reported. However, its mechanism of action in hepatocellular carcinoma in vivo has not been investigated in detail. We have previously shown that during hepatocellular carcinogenesis, DHEA treatment decreases formation of preneoplastic glutathione S-transferase placental form-positive foci in the liver and has antioxidant effects. Here we aimed to determine the mechanism of actions of DHEA, in comparison to vitamin E, in a chemically-induced hepatocellular carcinoma model in rats. Sprague-Dawley rats were administered with control diet without a carcinogen, diets with 1.5% vitamin E, 0.5% DHEA and both of the compounds with a carcinogen for 6 weeks. The doses were previously reported to have anti-cancer effects in animals without known toxicities. With DHEA treatment, cytosolic malate dehydrogenase activities were significantly increased by ${\sim}5$ fold and glucose 6-phosphate dehydrogenase activities were decreased by ${\sim}25%$ compared to carcinogen treated group. Activities of Se-glutathione peroxidase in the cytotol was decreased siguificantly with DHEA treatment, confirming its antioxidative effect. However, liver microsomal cytochrome P-450 content and NADPH-dependent cytochrome P-450 reductase activities were not altered with DHEA treatment. Vitamin E treatment decreased cytosolic Se-glutathione peroxidase activities in accordance with our previous reports. However, vitamin E did not alter glucose 6-phosphate dehydrogenase or malate dehydrogenase activities. Our results suggest that DHEA may have decreased tumor nodule formation and reduced lipid peroxidation as previously reported, possibly by increasing the production of NADPH, a reducing equivalent for NADPH-dependent antioxidant enzymes. DHEA treatment tended to reduce glucose 6-phosphate dehydrogenase activities, which may have resulted in limited supply for de novo synthesis of DNA via inhibiting the hexose monophophaste pathway. Although both DHEA and vitamin E effectively reduced preneoplastic foci in this model, they seemed to fimction in different mechanisms. In conclusion, DHEA may be used to reduce hepatocellular carcinoma growth by targeting NADPH synthesis, cell proliferation and anti-oxidant enzyme activities during tumor growth.

Effect of DHEA Administration on PUFA/SFA Ratio and Lipid Peroxide in Rat Liver Microsome (DHEA 투여로 인한 쥐 간 소포체분획에서의 PUFA/SFA 비율과 지질과산화의 감소 효과)

  • Kwak Chune Shil;Kim Mee Yeon
    • Journal of Nutrition and Health
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    • v.38 no.4
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    • pp.297-306
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    • 2005
  • It is known that dehydroepiandrosterone (DHEA) shows a dual effect, prooxidant or antioxidant, depending on the do-sage or physiological status of animals. The purpose of this study was to determine the effects of DHEA administration at low dose on lipid peroxidation, protein carbonylation and fatty acid composition in liver. Sprague Dawley male rats were fed either com oil diet containing $15\%$ com oil or fish oil diet containing $2\%$ corn oil + $13\%$ sardine oil, with or without $0.2\%$ DHEA for 9 weeks. Atherogenic index and hepatic triglyceride and cholesterol levels were significantly reduced by DHEA administration in rats fed with fish oil diet. Hepatic lipid peroxide product (TBARS) and protein carbonyl levels were significantly higher in rats fed with fish oil diet than in rats fed with corn oil diet. However, DHEA administration significantly reduced the hepatic thiobarbituric acid-reactive substance (TBARS) and conjugated diene levels in rats fed with fish oil diet. Contents of C16 : 0, C16 : 1, C20 : 5 and C22 : 6 in hepatic microsome were higher in rats fed with fish oil diet than in rats fed with corn oil diet, and contents of C18 : 2 and C20 : 4 were lower than in rats fed with com oil diet. DHEA administration significantly increased C16 : 0 and C18 : 3 contents and reduced C18 : 2 content in rats fed with com oil diet, while it increased C16 : 0 and C18 : 1 and reduced C20 : 5 and C22 : 6 in rats fed with fish oil diet. On overall, DHEA administration increased saturated fatty acid (SFA) and reduced polyunsaturated fatty acid (PUFA) in hepatic microsome, thereby PUFA/SFA ratio was significantly (p < 0.0001) reduced without the change of n-3/n-6 ratio. Taken together, low dose of DHEA administration lowered PUFA/SFA ratio in hepatic microsomal membranes and also showed antioxidative effect especially in fish oil-induced highly oxidative stress condition through blocking increases of C20 : 5 and C22 : 6 contents.

Correlation of Occupational Stress Index with 24-hour Urine Cortisol and Serum DHEA Sulfate among City Bus Drivers: A Cross-sectional Study

  • Du, Chung-Li;Lin, Mia Chihya;Lu, Luo;Tai, John Jen
    • Safety and Health at Work
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    • v.2 no.2
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    • pp.169-175
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    • 2011
  • Objectives: The questionnaire of occupational stress index (OSI) has been popular in the workplace, and it has been tailored for bus drivers in Taiwan. Nevertheless, its outcomes for participants are based on self-evaluations, thus validation by their physiological stress biomarker is warranted and this is the main goal of this study. Methods: A cross-sectional study of sixty-three city bus drivers and fifty-four supporting staffs for comparison was conducted. Questionnaire surveys, 24-hour urine cortisol testing, and blood draws for dehydroepiandrosterone-sulfate (DHEA-S) testing were performed. The measured concentrations of these biological measures were logarithmically transformed before the statistical analysis where various scores of stressor factors, moderators, and stress effects of each OSI domain were analyzed by applying multiple linear regression models. Results: For drivers, the elevated 24-hour urine cortisol level was associated with a worker's relationship with their supervisor and any life change events in the most recent 3 months. The DHEA-S level was higher in drivers of younger age as well as drivers with more concerns relating to their salary and bonuses. Non-drivers showed no association between any stressor or satisfaction and urine cortisol and blood DHEA-S levels. Conclusion: Measurements of biomarkers may offer additional stress evaluations with OSI questionnaires for bus drivers. Increased DHEA-S and cortisol levels may result from stressors like income security. Prevention efforts towards occupational stress and life events and health promotional efforts for aged driver were important anti-stress remedies.

Effects of Vitamin E and Dehydroepiandrosterone on the Formation of Preneoplastic Lesions in Rat Hepatocellular Carcinogenesis (비타민 E와 Dehydroepiandrosterone이 화학적 발암원으로 유도한 쥐간의 전암성 병변에 미치는 영향)

  • Kim, Sook-Hee;Choi, Hay-Mie
    • Journal of Nutrition and Health
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    • v.38 no.5
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    • pp.364-372
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    • 2005
  • This study is designed to examine the effects of dietary supplementation with vitamin E and dehydroepiandrosterone (DHEA) on the formation of preneoplastic lesions in diethylnitrosamine (DEN) induced rat hepatocarcinogenesis. All Weaning male Sprague-Dawley rats were initiated by a single dose of DEN (200mg/kg body weight), subjected to two­thirds partial hepatectomy 3 weeks later and were sacrificed 8 weeks after DEN initiation. Two weeks after initiation, rats were fed Purina purified rodent diet 5053 (Ralston Purina Rat chow, USA) with $1.5\%$ (15,000 IU/kg diet) vitamin E, $0.5\%$ DHEA and both of those supplemented diet for 6 weeks. Placental glutathione S-transferase (GST-P) positive foci, the activities of catalase, total-glutathione peroxidase (GPx) , glutathione reductase (GR), glutathione S-transferase (GST) and thiobarbituric acid reactive substances (TBARS) contents were decreased significantly by vitaimin E supplement. On the other hand GST-P positive foci number, Cu/Zn-superoxide dismutase (SOD) and glucose 6-phosphatase (G6Pase) activities weren't changed by vitamin E supplement. It might suggest that protective effect of vitamin E against hepatocarcinogens is not involved in the formation of the GST-P positive foci but related to the expansion of that. It seemed that vitamin E supplement helped endogenous defense system in carcinogenesis by decreasing TBARS contents, $H_2O_2$, organic peroxides. Therefore, vitamin E seemed to protect cell from free radical damage in carcinogenesis. By DHEA supplement liver weight and liver/body ratio were increased, the area and number of GST-P positive foci, the activities of catalase, GR, total GPx, GST and the TBARS contents were decreased significantly. On the other hand Cu/Zn-SOD and G6Pase activities weren't changed by DHEA supplement. In hepatocarcinogenesis the activities of antioxidant enzymes weren't increased by DHEA supplement. DHEA did not increase the oxidative stress, while DHEA seems to have anticarcinogenic effect in rats hepatocarcinogenesis.

Effects of combined exercise on the blood inflammatory factors, DHEA-s and arterial stiffness of elderly women (복합운동이 고령여성의 혈중 염증인자, DHEA-s 및 동맥경직도에 미치는 영향)

  • Ha, Soo-Min;Kim, Jung-Sook;Kim, Ji-Hyeon;Kim, Do-Yeon
    • Journal of the Korean Applied Science and Technology
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    • v.35 no.4
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    • pp.1096-1107
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    • 2018
  • The purpose of this study was to investigate the effects of combined exercise on blood inflammatory factors, DHEA-s and arterial stiffness in elderly women. The subjects were 42 elderly females volunteers, aged 70 to 85 years, composed of the combined exercise group (n=21) and control group (n=21). The 60 minute combined exercise program(aquarobics 1 time/week, strength exercise 2 times/week) was performed 3 times per week for 12 weeks, and the intensity was progressively increased every 4 weeks(1-4 weeks: RPE 12 to 13, 5-8 weeks: RPE 13 to 14, 9-12weeks: RPE 14 to 15). The test data were analyzed by two-way repeated measures ANOVA, paired t-test, independent t-test and the alpha level of .05 was set for all tests of significance. As a result, the combined exercise for 12 weeks reduced the inflammatory response of elderly women, and DHEA-s was found to have a positive effect on aging hormone. The arterial stiffness decreased the central arterial blood pressure (systolic and diastolic), prevented the increase of the pulse pressure and the wave increase index, and decreased the pulse wave velocity. These results suggest that regular and continuous combined exercise may be recommended for the healthy aging and longevity of elderly women by inducing anti-inflammation effect and improving the aging hormonal function and the vascular health.

Effect of Electrical Vagus Nerve Stimulation to Control Systemic Inflammation and Anti-Aging Hormone on Elder (미주신경 전기 자극이 노인의 항노화 호르몬과 전신적 염증에 미치는 효과)

  • Moon, Hyunju;Goo, Bongoh
    • Journal of The Korean Society of Integrative Medicine
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    • v.6 no.4
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    • pp.183-189
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    • 2018
  • Purpose : As age increases, a low-level systemic inflammatory state develops and the levels of anti-aging hormones decrease. The vagus nerve activates parasympathetic nerves and promotes sulfation and secretion of neurotransmitter in the brain. Therefore, the purpose of this study was to investigate the effects of electrical vagus nerve stimulation on systemic inflammation (CRP) and anti-aging hormone (DHEA-S) levels in elder people. Methods : A total of 30 healthy elder people participated in this study, randomly divided into two groups of 15 subjects. Electrical vagus nerve stimulation was applied to the experimental group for 4 weeks. CRP and DHEA-S levels were compared with those of the control group. Results : The CRP level was significantly lower in the experimental group than in the control group. In the experimental group, there was a significant decrease in CRP before and after the intervention. However, the DHEA-S level was not significantly different between groups. Conclusion : Electrical vagus nerve stimulation may alleviate the low-level systemic inflammatory state found in elderly people. These results suggest that it may have the effect of reducing the degenerative inflammatory diseases of the elderly and delaying aging.

The Effect of Dehydroepiandrosterone on Isoproterenol-induced Cardiomyopathy in Rats

  • Jeong, Ji-Hoon;Kim, Chan-Woong;Yim, Sung-Hyuk;Shin, Yong-Kyoo;Park, Kyung-Wha;Park, Eon-Sub
    • The Korean Journal of Physiology and Pharmacology
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    • v.10 no.2
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    • pp.79-83
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    • 2006
  • We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.

Promotion of Liver Lesion Development in the Syrian Hamster by Deitary fat Following Multi-Organ Initiation is Inhibited by Dhea-S Administration

  • Park, Cheol-Beom;Kim, Sun-Hee;Shim, Young-Hee;Kim, Dae-Joong;Lee, Jong-Sung;Park, Jong-Il;Kang, Jong-Koo;Moore, Malcome.A.;Iroyuki, Tsuda.H.
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2003.10b
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    • pp.118-118
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    • 2003
  • The influence of dietary supplementation with dehydroepiandrosterone-sulphate (DHEA-S) at 0.6% was investigated in male Syrian golden hamsters initiated by treatments with azoxymethane(AOM), and dihydroxy-di-n-propyl nitrosamine (DHPN), timed after transfer from a choline-deficient to a normal diet.(omitted)

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