• Title/Summary/Keyword: Immature rat

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Effects of Spermine on Quisqualate-induced Excitotoxicity in Rat Immature Cortical Neurons (흰쥐 미숙 대뇌피질 신경세포에서 Quisqualate로 유발된 흥분성 세포독성에 대한 spermine의 영향)

  • 조정숙
    • YAKHAK HOEJI
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    • v.43 no.4
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    • pp.535-540
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    • 1999
  • Glutamate (Glu) receptor-mediated excitoxicity has been implicated in many acute and chronic types of neurological disorders. Exposure of mature rat cortical neurons (15-18 days in culture) to the various concentrations of Glu resulted in a marked neuronal death, whereas immature rat cortical neurons (4∼5 days in culture) were resistant to the Glu-induced toxicity. Glu receptor subtype-specific agonists showed differential extent of toxicity in the immature neurons. The neurons treated with NMDA or kainate (KA) did not exhibit damage. However, quisqualate (QA) treatment induced a considerable cell death (36.1%) in immature enurons. The non-NMDA antagonist DNQX did not reduce this response. Interestingly, the QA-induced toxicity was potentiated by spermine in a concentration-dependent manner. Again, the spermine-enhanced damage was not altered by the polyamine antagonist ifenprodil. Taken together, unlike NMDA or KA, QA can induce neurotoxicity in immature rat cortical neurons and the QA-induced toxicity was potentiated by spermine. The lack of antagonizing effects of DNQX and ifenprodil on QA-induced toxicity and the potentiated toxicity by spermine, respectively, implies that both QA receptor and the polyamine site of NMDA receptor may not mediate the neurotoxicity observed in this study, and that a distinct mechanism(s) may be involved in excitotoxicity in immature neurons.

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Expression of steroidogenic acute regulatory protein mRNA in immature and adult rat testes (미성숙과 성숙한 흰쥐 고환에서의 Steroidogenic acute regulatory protein mRNA의 발현)

  • Koh, Phil-ok;Kwak, Soo-dong
    • Korean Journal of Veterinary Research
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    • v.40 no.2
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    • pp.229-236
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    • 2000
  • The synthesis of steroid hormone starts from cholesterol. Steroidogenic acute regulatory protein (StAR) acutely transfers cholesterol from the outer mitochondrial membrane to the inner in the early step of steroidogenesis. Many kinds of steroid hormone are mainly synthesized in adrenal grand, ovary, and testis. Among the steroid hormone, testosterone is synthesized in Leydig cells of the testis, the production of testosterone significantly increases in adult testis after puberty onset. Therefore, we think that the expression of StAR mRNA in testis will change according to the testicular development. The aim of this study is to determine the distribution of StAR mRNA in immature and adult rat testes and to confirm the functions of StAR in these testes. Thus, in situ hybridization was used in rat testes of the 2, 4, and 10 weeks of age. StAR mRNA was expressed in Leydig cells. Positive signals of StAR mRNA were weakly detected in Leydig cells of the 2 weeks of age. But, StAR mRNA was strongly expressed in Leydig cells of the 4 and 10 weeks of age, where steroidogenesis actively occur. In our results, the pattern of StAR mRNA expression was similar to the pattern of testosterone production in immature and adult rat testes. In conclusion, we can suggest that StAR acts as an important factor to regulate the synthesis of testosterone in Leydig cells of the rat testis.

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Experimental Studies on Oxygen Tolerance and Poisoning under Hyperbaric Oxygen Environment (고압산소환경(高壓酸素環境)에서의 산소중독(酸素中毒) 및 내성(耐性)에 관(關)한 실험적(實驗的) 연구(硏究))

  • Lee, Won-Chang
    • Korean Journal of Veterinary Research
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    • v.9 no.1
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    • pp.11-22
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    • 1969
  • Experimental studies were performed to observe the difference in tolerance of small animals to oxygen poisoning, and also to examine the effects of certain drug for it. The three experimental groups consisted of mature rat group, immature rat group and mouse group. The animals were exposed to 5 atm. of 100% oxygen using hyperbaric chamber, and they were observed for oxygen poisoning by pulmonary and central nervous system manifestation. The tolerance to oxygen poisoning was represented by half fatality time in each experimental group. The drug applied was ammonium chloride $NH_4Cl$ and it was administered intraperitoneally in various dosages for particular attribution of its prophylactic effect. The following conclusions were made; 1. The immature rat group showed the higher degree of tolerance to oxygen poisoning, as evidenced by a more prolonged half fatality time in the group. No significant difference in the half fatality time between the mature rat and the mouse group was observed. 2. The fact that the immature group showed the higher degree of tolerance as compared with the mature rat group represented by delayed onset of convulsion. 3. There was a remarkable difference in the Lung Weight/Body Weight ratio between the experimental and control group. 4. The animals with a shorter half fatality time uniformally displayed an earlier onset of convulsive seizure as the sign of oxygen poisoning and a significant elevated Lung Weight/Body Weight ratio. 5. Ammonium chloride at the dosage of 450mg per kg body weight had the most pronounced prophylactic effect on oxygen poisoning.

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Pyometra in the PMSG-treated Immature Female Rats (PMSG를 투여한 미성숙랫드에 발생한 자궁축농증 발생례)

  • 김영홍;이근우
    • Journal of Veterinary Clinics
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    • v.17 no.1
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    • pp.285-288
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    • 2000
  • Nine immature 30-day-old female rats were injected sc at 0800 hr with pregnant mare serum gonadotrophin(PMSG) to induce ovulation and mating. Fifty-six hours later the animals were placed with mature male rats overnight (one female and one male). Five of 9 immature female rats treated with PMSG were pregnant and allowed to maintain the pregnancy to term. Three of 5 pregnant rats were failed to maintain pregnancy to term. Two of 5 pregnant rats seemed to be developed normally and increased abdominal enlargement as pregnancy progresses, but did not occurred parturition on day of 43 or 48 of pregnancy, respectively. On day 44 or 49, pregnant rats were killed and examined uterus and ovaries. There was no fetus but approximately 50∼60ml. of mucopurulent fluids were accumulated in the uterine cavity and 40 or 42 corpora lutea persisted in the ovaries. Pyometra was developed after coitus in PMSG-treated immature female rat.

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INVESTIGATION OF IN VITRO AND IN VIVO ESTROGENIC OR ANTIESTROGENIC ACTIVITY OF CYPERMETHRIN

  • Kim, Soon-Sun;Rhee, Gyu-Seek;Kwack, Seung-Jun;Sohn, Kyung-Hee;Kim, So-Hee;Lee, Rhee-Da;An, Sang-Mi;Ki-Eun. Jeong;Sheen, Yhun-Yhong
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2002.11b
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    • pp.166-166
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    • 2002
  • In the present study, estrogenic or antiestrogenic activity of cypermethrin, a pyrethroid insecticide was investigated. We used immature rat uterotrophic assay, estrogen-responsive calbindin-D9k (CaBP-9k) gene expression assay and luciferase reporter gene assay for measure of estrogenic potential of cypermethrin.(omitted)

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Expression of peroxiredoxin I regulated by gonadotropins in the rat ovary

  • Lee, Yu-Il;Kang, Woo-Dae;Kim, Mi-Young;Cho, Moon-Kyoung;Chun, Sang-Young
    • Clinical and Experimental Reproductive Medicine
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    • v.38 no.1
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    • pp.18-23
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    • 2011
  • Objective: Peroxiredoxins (Prxs) play an important role in regulating cellular differentiation and proliferation in several types of mammalian cells. This report examined the expression of Prx isotype I in the rat ovary after hormone treatment. Methods: Immature rats were injected with 10 IU of pregnant mare's serum gonadotropin (PMSG) to induce the growth of multiple preovulatory follicles and 10 IU of human chorionic gonadotropin (hCG) to induce ovulation. Immature rats were also treated with diethylstilbestrol (DES), an estrogen analogue, to induce the growth of multiple immature follicles. Northern blot analysis was performed to detect gene expression. Cell-type specific localization of Prx I mRNA were detected by in situ hybridization analysis. Results: During follicle development, ovarian Prx I gene expression was detected in 3-day-old rats and had increased in 21-day-old rats. The levels of Prx I mRNA slightly declined one to two days following treatment with DES. A gradual increase in Prx I gene expression was observed in ovaries obtained from PMSG-treated immature rats. Furthermore, hCG treatment of PMSG-primed rats resulted in a gradual stimulation of Prx I mRNA levels by 24 hours (2.1-fold increase) following treatment, which remained high until 72 hours following treatment. In situ hybridization analysis revealed the expression of the Prx I gene in the granulosa cells of PMSG-primed ovaries and in the corpora lutea of ovaries stimulated with hCG for 72 hours. Conclusion: These results demonstrate the gonadotropin and granulosa cell-specific stimulation of Prx I gene expression, suggesting its role as a local regulator of follicle development.

The effect of Jackyakgamcho-tang on Follicular Maturation and Estrogen Production in the Immature Rat (작약감초탕이 미성숙 흰쥐에서 난포성숙 및 Estrogen생성에 미치는 효과)

  • Jung, Ki-Kyung;Kang, Seog-Youn;Kim, Tae-Gyun;Kim, Chang-Ok;Moon, A-Ree;Ryu, Kyung-Za;Lee, Song-Deuk;Ryeu, Hang-Mook;Kim, Seung-Hee
    • Korean Journal of Pharmacognosy
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    • v.28 no.3
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    • pp.104-111
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    • 1997
  • The traditional herbal medicine, Jackyakgamcho-tang(JGT), was reported to decrease serum testosterone levels and make pregnancy possibel in anovulatory woman and rat. JGT contains Paeoniae Radix(PR) and Glycyrrhizae Radix(GR) in equal amount. This study was designed to investigate the effect of JGT and its components(PR, GR, paeoniflorin and glycyrrhizin) on uterine and ovarian responses, follicular development, and estrogen secretion in the immature rat. The samples(water extracts of JGT, PR, GR; pure compound of paeoniflorin and glycyrrhizin) were administered orally to rats from the 21th day of age to the 28th or 30th days of age for 7 or 9 days. JGT(400mg/kg) and PR(100mg/kg, 200mg/kg) treatments significantly increased serum estradiol above levels in control rats, but both GR and glycyrrhizin had no effect on this parameter. Gross observation and histological analysis revealed that an increased number of growing follicules was observed in the ovaries of JGT and PR treated rat. However the lutenized follicles and ova present in the oviducts were not observed in all rats except one treated with estrogen as a positive control. These results indicate that JGT stimulates the estrogen production and follicular maturation in the immature rat and PR is the main component to induce such reaction.

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Effect of 3-Methylcholanthrene on Rat Uterus: Uterine Growth and Mechanism of Action of 3-Methylcholanthrene

  • Sheen, Yhun-Y.;Kim, Sun-S.;Yun, Hea-C.
    • Archives of Pharmacal Research
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    • v.16 no.4
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    • pp.276-282
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    • 1993
  • This study has been undertaken to examine the effect of 3-methylcholanthrene (3MC) on rat uterine growth and to understand the mechanism of action of 3MC in rat uterus. After diethylstilbesterol(DES) or tamoxifen(TAM) or 3MC or DES plus TAM or DES plus 3MC was administered into immature female rats, uterine weight over corn oil-treated uteri. 3MC treatment had no effect on uterine weight but, DES stimulated uterine weight was inhibited by 3MC concomitant tratment. While TAM alone treatment showed slight increase in uterine wieght, inhibited uterine growth simulated by DES when it was adiministrated with DES condirect binding assay with $[^3H]$ estradiol and the relative binding affinities of 3MC and TAM were estimated by competetion assy. Estradiol tumed out to have high affinity for rat uterine estrogen receptor (kd = 0.4 nM). The relative binding affinities of TAM and 3MC were 1% and 4.7% that of DES for rat uterine estrogen receptor, respectively. 3MC was shown to have similar affinity for eat uterine estrogen receptor to that of TAM. Effects of DES 3MC and TAM administration in vivo on rat uterine estrogen recptor level were examined. It was confirmed that the estrogen, DES and antiestrogen, TAM decreased estrogen receptor levels from rat ulterus and also 3MC decreased rat uterine estrogen receptor level when rats were treated with DES, TAM and 3MC in vivo. Data indicates that 3MC acts as an antiestrogen mediated through estrogen receptor system.

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