AIMTo know the effect of cysteamine (CS) on the plasma levels of somatostatin (SS) and some metabolic hormones in adult geese.

METHODSFourteen adult crossbred geese (Chuan white x Tai lake) fitted with chronic wing vein cannulas were used in this study to evaluate the effect of CS on SS, TSH, T3 and T4 levels. The experiment was consisted of control and treated phase. The diet was added CS at dosage of 100 mg/kg bw on the first day of the treated phase. The blood samples were collected from the cannulas and analyzed by radioimmunoassay.

RESULTSThe plasma SS concentration was (1.87 +/- 0.10) microg/L in control phase. Whereas SS concentrations on day 1, 3, 5, 7 of treated phase were decreased markedly (P < 0.05 or P < 0.01). Thereafter it was rose on the seventh day, however it was still lower than that of control. The thyroid stimulating hormone (TSH) content (2.45 +/- 0.31 mIU/L) was significantly decreased by 21.63% (P < 0.01) on day 1, and 18.37% (P > 0.05) on day 3 and day 5. Comparing with control phase (5.41 +/- 0.98 microg/L), T4 contents were elevated by 60.26% (P < 0.01), 43.25% (P < 0.01), 37.15% (P < 0.01) and 16. 82% (P < 0.01) respectively on day 1, 3, 5, 7. T3 level was (1.05 +/- 0.06) microg/L in control phase, whereas the levels was significantly increased by 36.19% (P < 0.01) on day 3. Also, the insulin concentration was higher than that of control (4.43 +/- 0.41 mU/ L) by 18.28% (P < 0.05) on the day 5.

CONCLUSIONThese results indicate that CS can decrease the plasma SS and TSH levels, whereas increase the levels of T4, T3 and insulin, therefore change metabolism, improve the nutrition transform and accelerate the growth in geese.

Animals ; Cysteamine ; pharmacology ; Diet ; Geese ; Insulin ; blood ; Somatostatin ; blood ; Thyrotropin ; blood ; Thyroxine ; blood ; Triiodothyronine ; blood

OBJECTIVETo investigate the neonatal umbilical cord blood thyroid stimulating hormone (TSH) level in the universal iodized salt areas and put forward the cut-point, then analyze its application.

METHODSSeven provinces were selected where the pregnant women having satisfied urinary iodine levels, then the urinary samples of pregnant women and the neonates cord blood were collected for urine iodine and TSH tests, and the relative factors were also recorded.

RESULTSTotal 1 524 urine and cord blood samples were collected from pregnant women and their new borns respectively. The median urinary iodine of pregnant women was 246.0 micro g/L, and the median TSH was 3.58 mU/L. The TSH level among seven areas and the neonatal delivery type varied significantly.

CONCLUSIONSThe neonatal cord blood TSH was influenced by several factors and could not be controlled, thus not be suitable as a iodine deficiency disorders surveillance indicator.

Delivery, Obstetric ; Female ; Fetal Blood ; drug effects ; metabolism ; Humans ; Iodine ; pharmacology ; urine ; Pregnancy ; Thyrotropin ; blood

Animals ; Gallbladder ; physiology ; Rabbits ; Solitary Nucleus ; drug effects ; Thyrotropin-Releasing Hormone ; pharmacology ; Vagus Nerve ; drug effects ; physiology

OBJECTIVETo observe the improvement of thyroid function and changes of Akt, p-Akt, mammalian target of rapamycin (mTOR), and para-mTOR (p-mTOR) expression in Graves' disease (GD) mice after intervened by Jiakangning Capsule (JC), and to explore possible mechanism for JC in treating GD.

METHODSGD model was established by immunizing female BALB/c mice with thyroid stimulating hormone receptor A subunit (Ad-TSHRα-289). Totally 70 successfully modeled mice were divided into the model group (n =20), the JC intervened group (n =25), the Methimazole Tablet intervened group (n =25) according to random digit table. A normal control group (n =15) and a vehicle control group (n =20, injected with Ad-null) were also set up. Mice in the JC intervened group were administered with JC suspension at the daily dose of 1. 5 g/kg by gastrogavag. Mice in the Methimazole intervened group were administered with Methimazole suspension at the daily dose of 2. 5 g/kg by gastrogavage. Equal volume of normal saline was administered to mice in the rest 3 groups by gastrogavage. All intervention lasted for 5 weeks. Six mice were selected from each group to observe pathological changes of thyroid tissues. Serum levels of thyroxine (T4), triiodothyronine (T3), thyroid stimulating hormone (TSH), and thyrotropin receptor antibody (TRAb) were analyzed by radioimmunoassay. Expression levels of Akt, p-Akt, mTOR, and p-mTOR in thyroid tissues were etermined by Western blot.

RESULTS(1) The thyroid gland in the GD model group showed proliferative changes, with enlarged follicles of various sizes. Interstitial stroma was filled with blood vessels. Structures of thyroid tissues in the JC intervened group and the Methimazole intervened group were significantly restored, and follicular hyperplasia was relieved. (2) Compared with the normal control group and the vehicle control group, levels of TRAb, T4, and T3 increased; ratios of P-Akt/β-actin, p-Akt/Akt, p-mTOR/β-actin, and p-mTOR/mTOR also increased in the model group (all P <0. 01). Compared with the model group, levels of TRAb, T4, and T3 decreased in the JC intervened group and the Methimazole intervened group (P <0. 01); ratios of p-mTOR/β-actin and pmTOR/mTOR decreased in the JC intervened group (P <0.01); ratios of P-Akt/β-actin, p-Akt/Akt, p-mTOR/β-actin, and p-mTOR/mTOR decreased in the Methimazole intervened group (P <0. 05, P <0. 01). Conclusion JC could reduce thyroid hormonc levels of GD mice and lower expression levels of mTOR, and its mechanism for improving thyroid function of GD mice might be associated with this influence.

Actins ; Animals ; Capsules ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Graves Disease ; drug therapy ; pathology ; Methimazole ; Mice ; Mice, Inbred BALB C ; Receptors, Thyrotropin ; Signal Transduction ; TOR Serine-Threonine Kinases ; Thyrotropin ; Thyroxine ; Triiodothyronine

OBJECTIVETo investigate the early effect of thyrotropin-releasing hormone (TRH) on cerebral free radical reactions after acute brain injury in rabbits.

METHODS30 healthy white rabbits were randomly divided into three groups: Group A (n=10), Group B (n=12) and Group C (n=8). The rabbits in Group A and Group B were injured by direct hit. At 0.5-4 hours after injury, the rabbits in Group A were injected with TRH (8 mg/kg body weight) through a vein and the rabbits in Group B were injected with normal saline of equal volume. The rabbits in Group C served as the normal control. Then all the rabbits were killed and brain tissues were obtained. The content of lipoperoxide (LPO), the activity of superoxide dismutase (SOD) and the water content of the brain tissues were measured.

RESULTSThe contents of LPO and water in brain tissues in Group A were lower and the activity of SOD was higher than those of Group B (P<0.05). After injury, intracranial pressure (ICP) rose rapidly and continuously with time passing by. When TRH was given to the animals in Group A, the rising speed of ICP slowed down significantly.

CONCLUSIONSTRH can decrease the cerebral free radical reactions and cerebral edema after acute brain injury in rats.

Animals ; Brain Edema ; etiology ; prevention & control ; Brain Injuries ; complications ; metabolism ; Female ; Free Radicals ; metabolism ; Intracranial Pressure ; Lipid Peroxidation ; Male ; Rabbits ; Superoxide Dismutase ; metabolism ; Thyrotropin-Releasing Hormone ; pharmacology

AIMTo investigate the effect of hypothalamic thyrotropin-releasing hormone (TRH) on cardiac function and its mechanism.

METHODSThe Sprague-Dawley rats were mounted in a stereotaxic apparatus and a guide cannula placed in the left hypophysiotropic area, through which TRH were microinjected in presence or absence of L-NAME and atropine. The left ventricular systolic pressure (LVSP), heart rate (HR) and the maximum velocity of ascending or descending in intraventricular pressure (+/- dp/dt(max)) were recorded.

RESULTS(1) TRH microinjected into the hypophysiotropic area induced a significant increase of LVSP, HR, dp/dt and-dp/dt(max) (P < 0.05, P < 0.01). (2) L-NAME significant increased LVSP and pretreatment with L-NAME inhibited the positive effects induced by TRH. (3) Atropine increased LVSP and dp/dt(max) (P < 0.05), but it significantly descended heart rate (P < 0.05). Pretreatment with atropine weakened the tachycardiac response induced by TRH.

CONCLUSION(1) Hypothalamic TRH can produce positive inotropic and chronotropic response to myocardium. (2) Hypothalamic endogenous NO can descend LVSP, but has no effects on HR, dp/dt(max), and-dp/dt(max). The effect of TRH is through nitric oxide-dependent pathway. (3) Hypothalamic endogenous cholinergic transmitter can produce negative chronotropic and positive inotropic response to myocardium. Hypothalamic TRH mediates cardiac function maybe partly through cholinergic M receptor.

Animals ; Blood Pressure ; Heart Rate ; Heart Ventricles ; drug effects ; Hypothalamus ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley ; Thyrotropin-Releasing Hormone ; administration & dosage ; pharmacology ; Ventricular Function, Left ; drug effects

OBJECTIVE: To explore the mechanism of Radix Scrophulariae (RS) extracts in the treatment of hyperthyroidism rats by regulating proliferation, apoptosis, and autophagy of thyroid cell through the mammalian sterile 20-like kinase 1 (MST1)/Hippo pathway. METHODS: Twenty-four rats were randomly divided into 4 groups according to a random number table: control, model group, RS, and RS+Hippo inhibitor (XMU-MP-1) groups (n=6 per group). Rats were gavaged with levothyroxine sodium tablet suspension (LST, 8 μ g/kg) for 21 days except for the control group. Afterwards, rats in the RS group were gavaged with RS extracts at the dose of 1,350 mg/kg, and rats in the RS+XMU-MP-1 group were gavaged with 1,350 mg/kg RS extracts and 1 mg/kg XMU-MP-1. After 15 days of administration, thyroid gland was taken for gross observation, and histopathological changes were observed by hematoxylin-eosin staining. The structure of Golgi secretory vesicles in thyroid tissues was observed by transmission electron microscopy. The expression of thyrotropin receptor (TSH-R) was observed by immunohistochemistry. Terminal-deoxynucleoitidyl transferase mediated nick end labeling assay was used to detect cell apoptosis in thyroid tissues. Real-time quantity primer chain reaction and Western blot were used to detect the expressions of MST1, p-large tumor suppressor gene 1 (LATS1), p-Yes1 associated transcriptional regulator (YAP), proliferating cell nuclear antigen (PCNA), G₁/S-specific cyclin-D1 (Cyclin D1), B-cell lymphoma-2 (Bcl-2), Caspase-3, microtubule-associated proeins light chain 3 II/I (LC3-II/I), and recombinant human autophagy related 5 (ATG5). Thyroxine (T4) level was detected by enzyme-linked immunosorbent assay. RESULTS: The thyroid volume of rats in the model group was significantly increased compared to the normal control group (P<0.01), and pathological changes such as uneven size of follicular epithelial cells, disorderly arrangement, and irregular morphology occurred. The secretion of small vesicles by Golgi apparatus was reduced, and the expressions of receptor protein TSH-R and T4 were significantly increased (P<0.01), while the expressions of MST1, p-LATS1, p-YAP, Caspase-3, LC3-II/I, and ATG5 were significantly decreased (P<0.01). The expressions of Bcl-2, PCNA, and cyclin D1 were significantly increased (P<0.01). Compared with the model group, RS extracts reduced the volume of thyroid gland, improved pathological condition of the thyroid gland, promoted secretion of the secretory vesicles with double-layer membrane structure in thyroid Golgi, significantly inhibited the expression of TSH-R and T4 levels (P<0.01), upregulated MST1, p-LATS1, p-YAP, Caspase-3, LC3-II/I, and ATG5 expressions (P<0.01), and downregulated Bcl-2, PCNA, and Cyclin D1 expressions (P<0.01). XMU-MP-1 inhibited the intervention effects of RS extracts (P<0.01). CONCLUSION RS extracts could inhibit proliferation and promote apoptosis and autophagy in thyroid tissues through MST1/Hippo pathway for treating hyperthyroidism.
Rats ; Humans ; Animals ; Hippo Signaling Pathway ; Proliferating Cell Nuclear Antigen/metabolism* ; Cyclin D1/pharmacology* ; Caspase 3/metabolism* ; Protein Serine-Threonine Kinases/pharmacology* ; Apoptosis ; Hyperthyroidism/drug therapy* ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Thyrotropin/pharmacology* ; Mammals/metabolism*

Ammonium perchlorate (AP), mainly used as solid propellants, was reported to interfere with homeostasis via competitive inhibition of iodide uptake. However, detailed mechanisms remain to be elucidated. In this study, AP was administered at 0, 130, 260 and 520 mg/kg every day to 24 male SD rats for 13 weeks. The concentrations of iodine in urine, serum thyroid hormones levels, total iodine, relative iodine and total protein, and malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activity in thyroid tissues were measured, respectively. Our results showed that high-dose perchlorate induced a significant increase in urinary iodine and serum thyroid stimulating hormone (TSH), with a decrease of total iodine and relative iodine content. Meanwhile, free thyroxine (FT4) was decreased and CAT activity was remarkably increased. Particularly, the CAT activity was increased in a dose-dependent manner. These results suggested that CAT might be enhanced to promote the synthesis of iodine, resulting in elevated urinary iodine level. Furthermore, these findings suggested that iodine in the urine and CAT activity in the thyroid might be used as biomarkers for exposure to AP, associated with thyroid hormone indicators such as TSH, FT4.
Analysis of Variance ; Animals ; Catalase ; metabolism ; Dose-Response Relationship, Drug ; Homeostasis ; drug effects ; Iodine ; metabolism ; urine ; Male ; Malondialdehyde ; metabolism ; Perchlorates ; pharmacology ; Quaternary Ammonium Compounds ; pharmacology ; Radioimmunoassay ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Thyroid Gland ; metabolism ; Thyrotropin ; blood ; Thyroxine ; blood ; Triiodothyronine ; blood

TSH secretion is controlled by the stimulatory action of hypothalamic TRH and the inhibition via central dopaminergic and somatostatinergic mechanisms as well as by a hypothalamic inhibitory action of thyroid hormones. Metoclopramide is DA2 receptor blockade which can accelerate to elevate the concentration of serum TSH in hypothyroidism, which is accompanied by a progressive loss of dopaminergic tone as demonstrated by a progressive increase in prolaction serum levels, especially in patients with differentiated thyroid carcinoma(DTC). So the period of L-thyroxine withdrawal is contracted and the symptoms of hypothyroidism is released. It's important to monitor and treat DTC patients with radioactive iodide.
Dopamine Antagonists ; pharmacology ; Humans ; Hyperthyroidism ; blood ; drug therapy ; Hypothalamo-Hypophyseal System ; drug effects ; physiology ; Hypothyroidism ; blood ; drug therapy ; Metoclopramide ; chemistry ; pharmacology ; Thyroid Gland ; drug effects ; physiology ; Thyroid Hormones ; blood ; Thyrotropin ; blood

Both fertilization promoting peptide and adenosine stimulate capacitation but inhibit spontaneous acrosome loss by modulation of the adenylyl cyclase (AC)/cAMP signal transduction pathway. This is a review aimed at analyzing the function of fertilization promoting peptide during this process. The possible molecular basis is also discussed.
Acrosome ; drug effects ; Adenylyl Cyclases ; metabolism ; Animals ; Cyclic AMP ; metabolism ; Humans ; Male ; Pyrrolidonecarboxylic Acid ; analogs & derivatives ; Signal Transduction ; drug effects ; Spermatozoa ; drug effects ; physiology ; Thyrotropin-Releasing Hormone ; analogs & derivatives ; pharmacology