• Journal of Korean Academy of Nursing
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• v.34 no.1
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• pp.150-159
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• 2004

Purpose: The purpose of this study was to determine the effect of DHEA on hindlimb muscles(soleus, plantaris and gastrocnemius) in a focal brain ischemia model rat. Method: Twenty-seven male Sprague-Dawley rats were randomly divided into three groups: CINS(cerebral ischemia + normal saline), CIDH(cerebral ischemia + DHEA), or SHNS(sham + normal saline). Both the CINS and CIDH groups underwent a transient right middle cerebral artery occlusion operation. In the SHNS group, a sham operation was done. 0.34mmol/kg DHEA was administered daily by an intraperitoneal injection for 7days. Results: The muscle weight, muscle fiber cross-sectional area of the Type I muscle fiber of soleus and Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of gastrocnemius, and muscle strength in the CINS group decreased compared with the SHNS group. The muscle weight, muscle fiber cross-sectional area of the Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of soleus, and muscle strength in the CIDH group increased compared with the CINS group. Conclusion: It was identified that muscle atrophy could be induced during 7 days after a cerebral infarction, and DHEA administration during the early stages of a cerebral infarction might attenuate muscle atrophy.

• Journal of Korean Biological Nursing Science
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• v.3 no.1
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• pp.63-74
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• 2001

The purpose of this study was to determine the effect of DHEA with dexamethasone on body weight and wet weight and relative weight of atrophied hindlimb muscles induced by dexamethasone treatment. $200{\sim}225g$ Wistar rats were divided into control(C), dexamethasone(D), dexamethasone and DHEA(DDH) groups. Dexamethasone was injected daily at a dose of 5mg/kg. DHEA was administered daily at a dose of 5mg/kg by oral ingestion during 7days. The data were analyzed by Kruskal-Wallis test and Mann-Whitney U test using the SPSSWIN 9.0 program. Body weight and muscle weight of plantaris and gastrocnemius of dexamethasone group decreased significantly compared with that of control group. Muscle weight of plantaris of DDH group increased significantly compared with dexamethasone group. Body weight of DDH group decreased significantly compared to control group, but relative weight of plantaris and gastrocnemius of DDH group increased significantly compared to control group. Based on these results, it can be suggested that DHEA administration during dexamethasone treatment can be suggested that DHEA administration during dexamethasone treatment can increase weight of atrophied plantaris muscle induced by dexamethasone treatment.

• Korean Journal of Exercise Nutrition
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• v.24 no.4
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• pp.24-27
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• 2020

[Purpose] Dehydroepiandrosterone (DHEA) administration reportedly recovers osteoporosis, a bone disorder associated with bone deficiency in postmenopausal women. However, the physiological mechanism of DHEA in osteoporosis remains elusive, especially in terms of intestinal calcium absorption. Therefore, we investigated the effect of DHEA administration on calcium absorption in ovariectomized (OVX) female rats using an estrogen receptor antagonist. [Methods] Female Sprague-Dawley rats (n=23, 6 weeks old) were randomized into three groups: OVX control group (OC, n=7), OVX with DHEA treatment group (OD, n=8), and OVX with DHEA inhibitor group (ODI, n=8) for 8 weeks. [Results] Intestinal calcium accumulation, as well as the rate of absorption, demonstrated no significant differences during the experimental period among investigated groups. The bone mineral density (BMD) of the tibia at the proximal metaphysis was higher in the OD group than that in the OC group (p<0.05); however, BMD of the ODI group showed no significant difference from investigated groups. Furthermore, the BMD of the tibia at the diaphysis did not significantly differ among these groups. [Conclusion] We revealed that DHEA administration does not involve intestinal Ca absorption, although this treatment improves BMD levels in OVX rats. These observations indicate that the effect of DHEA on the bone in postmenopausal women is solely due to its influence on bone metabolism and not intestinal calcium absorption.

• 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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.2
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• pp.311-317
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• 2011

The goal of this study was to clarify effects of sleep restriction on a diurnal rhythm of salivary cortisol and DHEA levels in Korean adolescents.83 middle school students were recruited to participate in restricted sleep period group (less than 4h/day) or unrestricted sleep period group (from 6h/day to 7h/day). Both were 14 to 17 years old. They were instructed to keep the sleep-awakening schedule and sampling protocol. Saliva samples of cortisol and DHEA were collected at 8h, 12h, 16h and 20h. Salivary hormones were analysed with salivary cortisol(or DHEA) EIA kit according to a fixed assay protocol. Cortisol levels of restricted sleep period group and unrestricted sleep period group significantly decreased according to the sampling times. Cortisol levels of sleep restricted group was significantly higher than those of usual sleep group at all sampling times. At 8h, DHEA levels of both groups were significantly higher than those at 12h, 16h and 20h. However, DHEA levels of restricted sleep period group did not differ from those of unrestricted sleep period group at all sampling times.Cortisol and DHEA levels of both group showed the typical diurnal rhythm regardless of sleep status. Restricted sleep may increased cortisol release, not DHEA release, which indicated a changed HPA axis.

• Archives of Pharmacal Research
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• v.22 no.5
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• pp.474-478
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• 1999

Modulation of unscheduled DNA synthesis by dehydroepiandrosterone (DHEA) after exposure to various chemical carcinogens was investigated in the primary rat hepatocytes. Unscheduled DNA synthesis was induced by treatment of such direct acting carcinogens as methly methanesulfonate (MMS) and ethyl methanesulfonate (EMS) or procarcinogens including benzo(a)pyrene (BaP) and 7, 12-dimethylbenz(a)anthracene (DMBA). Unscheduled DNA synthesis was determined by measuring [methyl-3H]thymidine radioactivity incorporated into nuclear DNA of hepatocytes treated with carcinogens in the presence or absence of DHEA. Hydroxyurea $(5{\times}10^{-3} M)$was added to growth medium to selectively suppress normal replication. DHEA at concentrations ranging from $(1{\times}10^{-6} M)$ to$(5{\times}10^{-4} M)$ did not significantly inhibit unscheduled DNA synthesis induced by either MMS $(1{\times}10^{-4} M)$ or EMS $(1{\times}10^{-2} M)$. In contrast, DHEA-significantly inhibited unscheduled DNA synthesis induced by BaP $(6.5{\times}10^{-5} M)$ and DMBA.$(2{\times}10^{-5} M)$. DHEA-induced hepatotoxicity in rats was examined using lactate dehydrogenase (LDH) release as an indicator of cytotoxicity. DHEA exhibit no significant increase in LDH release compared with the control at 18 h. These data suggest that nontoxic concentration of DHEA does not affect the DNA excision repair process, but it probably influence the enzymatic system responsible for the metabolic activation of procarcinogens and thereby decreases the amount of the effective DNA adducts formed by the ultimate reactive carcinogenic species.

• The Science & Technology
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• v.30 no.6 s.337
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• pp.86-87
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• 1997

DHEA는 현대인의 불로초인가. 한국인 관광객그룹이 미국에서 싹쓸이 해간다는 DHEA를 왜 미국인들은 외면하고 있는 것인가. 임상되어 있지 않기 때문이다. 현대인의 고민을 모두 풀어준다는 과장 선전도 문제이지만 건강과 정력에 좋은 약이라면 물불을 못가리는 우리 국민들의 생활습성이 안타깝다.

• The Korean Journal of Pharmacology
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• v.26 no.1
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• pp.67-76
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• 1990

Hydrocortisone 50 mg/kg (HC), dehydroepiandrosterone 250 mg/kg (DHEA), ${\beta}-estradiol$ 5 mg/kg (E2), and testosterone 20 mg/kg (TS) were subcutaneously injected into the castrated ICR mice at noon for four days, and the animals were sacrificed at 10-12 A.M. of the fifth day. The intestinal DAO activity was significantly decreased by HC, but it was rather increased by E2 and TS, respectively. And DHEA did not change the DAO activity. But the hepatic MAO activity was not affected by anyone of HC, DHEA, E2, and TS. Aminoguanidine 25 mg/kg produced the marked decrease of the intestinal DAO activity and the significant increases of the intestinal PT and SD contents, but it did not change the hepatic polyamine contents. HC and DHEA induced the significant increase of the intestinal PT content. E2 induced the marked increase of the hepatic PT content and the moderate increase of the intestinal PT content. TS little affected the polyamine contents of the liver and intestine. These results suggest that the E2-induced increase of the hepatic PT content is rather ascribed to the greater enhancement of PT synthesis than the inhibition of polyamine catabolism, and that the HC-induced increase of the intestinal PT content is due partly to the inhibition of polyamine catabolism via DAO.

• Journal of Korean Academy of Nursing
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• v.39 no.5
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• pp.632-640
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• 2009

Purpose: The purpose of this study was to examine the effect of DHEA (Dehydroepiandrosterone) on muscle weight and Type I and II fiber cross-sectional area of affected and unaffected hindlimb muscles in rats with neuropathic pain induced by unilateral peripheral nerve injury. Methods: Neuropathic pain was induced by ligation and cutting of the left L5 spinal nerve. Adult male Sprague-Dawley rats were randomly assigned to one of two groups: The DHEA group (n=10) had DHEA injections daily for 14 days, and the Vehicle group (n=10) had vehicle injections daily for 14 days. Withdrawal threshold, body weight, food intake and activity were measured every day. At 15 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles were dissected from the both hindlimbs. Body weight, food intake, activity, muscle weight and Type I, II fiber cross-sectional area of the dissected muscles were measured. Results: The DHEA group showed significant increases (p<.05), as compared to the vehicle group for muscle weight of the unaffected plantaris, and in Type II fiber cross-sectional area of the gastrocnemius muscle. The DHEA group demonstrated a higher pain threshold than the vehicle group whereas total diet intake and activity score were not significantly different between the two groups. Conclusion: DHEA administration for 14 days attenuates unaffected plantaris and gastrocnemius muscle atrophy.

• 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.