• Korean Journal of Veterinary Research
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• v.39 no.6
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• pp.1073-1080
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• 1999

Previous studies suggested that the inhibition of thyroxine ($T_4$) release by ${\alpha}_1$-adrenoceptor and muscarinic receptor stimulation results in activated protein kinase C (PKC) from mouse and guinea pig thyroids. In the present study, the effect of carbachol, methoxamine, phorbol myristate acetate (PMA), and R59022 on the release of $T_4$ from the mouse, rat, and guinea pig thyroids was compared to clarify the role of PKC in the regulation of the release of $T_4$. The thyroids were incubated in the medium containing the test agents, samples of the medium were assayed for $T_4$ by EIA kits. Forskolin, an adenylate cyclase activator, chlorophenylthio-cAMP sodium, a membrane permeable analog of cAMP, and isobutyl-methylxanthine, a phosphodiesterase inhibitor, like TSH (thyroid stimulating hormone), enhaced the release of $T_4$ from the mouse, rat, and guinea pig thyroids. Methoxamine, an ${\alpha}_1$-adrenoceptor agonist, inhibited the TSH-stimulated release of $T_4$ in mouse, but not rat and guinea pig thyroids. In contrast, carbachol, a muscarinic receptor agonist, inhibited the release of $T_4$ in guinea pig, but not mouse and rat thyroids. These inhibition were reversed by prazosin, an ${\alpha}_1$-adrenoceptor antagonist or atropine, a muscarinic antagonist or $M_1$- and $M_3$-muscarinic antagonists, in mouse or guinea pig thyroids. In addition, staurosporine, a PKC inhibitor, reversed methoxamine or carbachol inhibition of TSH stimulation. Furthermore, PMA, a PKC activator, and R59022, a diacylglycerol (DAG) kinase inhibitor, inhibited the TSH-stimulated release of $T_4$ in mouse, rat, and guinea pig thyroids. These inhibition were blocked by staurosporine. These findings suggest that the activation of receptor or DAG inhibits TSH-stimulated $T_4$ release through a PKC-dependent mechanism in thyroid gland.

• Journal of environmental and Sanitary engineering
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• v.21 no.2 s.60
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• pp.30-35
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• 2006

The purpose of this study finds out the effect of red ginseng extract (1.0g/kg) on TBTO (10, 20, and 40mg/kg) which poisons against some organs like thyroids gland, liver, kidney, testis, ovary, sex hormone activity of rats are examined by gastric tubing for 3 weeks. The weight of each organ in treated group were increased, especially liver in female and those of testis in males were significantly increased at 10, 20 and 40mg/kg (P<0.05, P<0.01). In case of sex hormone activity of each sex, the estradiol activity of female and testosterone activity of males were significantly decreased rather than the control group (P<0.05, P<0.01) According to between the TBTO treated group and 10+ rGe group of the testosterone activity each sex were significantly increased (P<0.01).

• Korean Journal of Veterinary Research
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• v.38 no.4
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• pp.712-719
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• 1998

Thyroid function is mainly regulated through cAMP and phophatidylinositol, and it is well known that TSH-stimulated thyroxine ($T_4$) release is inhibited by catecholamine from mouse thyroids via the ${\alpha}_1$-adrenoceptor stimulation. Previous study has established that the inhibition of $T_4$ release by ${\alpha}_1$-adrenoceptor stimulation results in activated protein kinase C (PKC). The purpose of this study was to determine if ion transport systems are involved in the inhibition of $T_4$ release elicited by ${\alpha}_1$-adrenergic agonist in mouse thyroids. TSH-, IBMX- and cAMP analogue-stimulated $T_4$ release were significantly inhibited by methoxamine, R59022 (diacylglycerol kinase inhibitor), and MDL (adenylate cyclase inhibitor). TSH-stimulated $T_4$ release could be inhibited by Bay K 8644 and cyclopiazoic acid, but not by verapamil and tetrodotoxin. The addition of nifedipine ($Ca^{2+}$ channel blocker), tetrodotoxin and lidocaine ($Na^+$ channel blockers), but not amiloride (EIPA) and ryanodine, completely blocked the inhibitory effects of methoxamine on $T_4$ release. TSH-stimulated $T_4$ release was also inhibited by benzamil ($Na^+-Ca^{2+}$ exchange inhibitor). TSH-, IBMX- and cAMP-stimulated $T_4$ release were inhibited by methoxamine or R59022, these effects were reversed by nifedipine. but not by verapamil. Furthermore, nifedipine reversed the inhibitory effects of benzamil and R59022 on TSH-stimulated $T_4$ release. These data suggest that the observed ${\alpha}_1$-adrenoceptor-mediated inhibition of $T_4$ release in mouse thyroids is the result of an increase in intracellular $Na^+$ or $Ca^{2+}$ effected via activation of fast $Na^+$ or nifedipine-sensitive $Ca^{2+}$ channels, and that $Na^+-Ca^{2+}$ exchange may play an important role in reducing thyroid hormone by increasing intracellular $Ca^{2+}$.

• Korean Journal of Oriental Medicine
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• v.1 no.1
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• pp.401-418
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• 1995

Aging process can be explained by many factors. In this study, we counted complete Blood Cells (CBC) such as WBC, Lymphocytes, Monocytes, Granulocytes, RBC, HGB, and HCT of both SAM P6 and SAM P1 during the aging process. Plasma albumin, glucose, alkaline phosphatase, calcium, creatinine, inorganic phosphate, urea concentrations were also measured at the same time. In addition to these, plasma concentrations of cortisol, total T3, and total T4 were analyzed by Chemiluminescent Immunoassay. There were no change in CBC counts of SAM R1 and SAM P6 during this study. Plasma concentratins of albumin and glucose decreased significantly in SAM R1. However, plasma alkaline phosphatases and creatinine concentration in SAM P6 decreased significantly at 16 week after birth comparing to the control. Total T4 levels were siginificantly increased although cortisol and total T3 concentrations were the same in SAM R1 groups. Especially, the after birth of creatinine, alkaline phosphatase, T4 of SAM P6 at 16 week were significantly different form those of SAM R1. At 12 week after birth, pilose antler extract was given 5g/kg/day p.o. for 0, 7, 14, 21, and 30 days each in both SAM R1 and SAM P6. The RBC, HGB, and HCT levels started to increase significantly from 7 days after the dose at SAM P6 only. Total T4 conectrations were elevated gradually during the study although the antler extract administration did not prevent or inhibit the increase in total T4 concentration during the study. Therefore, the elevation of erythrocytes after administration of the extract needs to be studied in future.

• Animal Bioscience
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• v.37 no.8
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• pp.1377-1386
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• 2024

Objective: Embryonic interferon-tau (IFNT) and progesterone affect expression of interferon-stimulated genes (ISGs), progesterone receptor (PGR) and progesterone-induced blocking factor (PIBF) in the ovine thyroid. Methods: Thyroids of ewes were sampled at day 16 of nonpregnancy, days 13, 16, and 25 of pregnancy, and real-time quantitative polymerase chain reaction assay, western blot and immunohistochemistry were used to detect expression of ISGs, PGR, and PIBF. Results: Free ISG15 protein was undetected, but ISG15 conjugated proteins upregulated at day 16 of pregnancy, and expression levels of ISG15 conjugated proteins, PGR isoform (70 kDa), PIBF, interferon-gamma-inducible protein 10 and myxovirusresistance protein 1 peaked, but expression level of signal transducer and activator of transcription 1 was the lowest at day 16 of pregnancy. In addition, the expression levels of PGR isoform (70 kDa) and signal transducer and activator of transcription 1 (STAT1) decreased, but levels of PGR isoform (43 kDa), 2',5'-oligoadenylate synthetase, IP-10 and MX1 increased at day 25 of pregnancy comparing with day 16 of the estrous cycle. Conclusion: Early pregnancy affects expression of ISGs, PGR, and PIBF in maternal thyroid through IFNT and progesterone, which may regulate thyroid autoimmunity and thyroid hormone secretion in ewes.