Effects of Combined Long-Term Treatment with a Growth Hormone-Releasing Hormone Analogue and a Growth Hormone Secretagogue in the Growth Hormone-Releasing Hormone Knock Out Mouse

2005 ◽  
Vol 82 (3-4) ◽  
pp. 198-207 ◽  
Author(s):  
Danilo Fintini ◽  
Maria Alba ◽  
Andrew V. Schally ◽  
Cyril Y. Bowers ◽  
A.F. Parlow ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Term Treatment ◽  
Growth Hormone Releasing Hormone ◽  
Hormone Analogue ◽  
Growth Hormone Secretagogue ◽  
Knock Out ◽  
Releasing Hormone ◽  
Long Term Treatment ◽  
Knock Out Mouse

Agonistic analog of growth hormone–releasing hormone promotes neurofunctional recovery and neural regeneration in ischemic stroke

2021 ◽  
Vol 118 (47) ◽  
pp. e2109600118
Author(s):  
Yueyang Liu ◽  
Jingyu Yang ◽  
Xiaohang Che ◽  
Jianhua Huang ◽  
Xianyang Zhang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Ischemic Stroke ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Term Treatment ◽  
Neural Regeneration ◽  
Growth Hormone Releasing Hormone ◽  
Neuroprotective Effects ◽  
Releasing Hormone ◽  
Long Term Treatment

Ischemic stroke can induce neurogenesis. However, most stroke-generated newborn neurons cannot survive. It has been shown that MR-409, a potent synthetic agonistic analog of growth hormone–releasing hormone (GHRH), can protect against some life-threatening pathological conditions by promoting cell proliferation and survival. The present study shows that long-term treatment with MR-409 (5 or 10 μg/mouse/d) by subcutaneous (s.c.) injection significantly reduces the mortality, ischemic insult, and hippocampal atrophy, and improves neurological functional recovery in mice operated on for transient middle cerebral artery occlusion (tMCAO). Besides, MR-409 can stimulate endogenous neurogenesis and improve the tMCAO-induced loss of neuroplasticity. MR-409 also enhances the proliferation and inhibits apoptosis of neural stem cells treated with oxygen and glucose deprivation–reperfusion. The neuroprotective effects of MR-409 are closely related to the activation of AKT/CREB and BDNF/TrkB pathways. In conclusion, the present study demonstrates that GHRH agonist MR-409 has remarkable neuroprotective effects through enhancing endogenous neurogenesis in cerebral ischemic mice.

scholarly journals Hormonal and Volumetric Long Term Control of a Growth Hormone-Releasing Hormone-Producing Carcinoid Tumor

1999 ◽  
Vol 84 (9) ◽  
pp. 3162-3169 ◽  
Author(s):  
A. Van den Bruel ◽  
J. Fevery ◽  
J. Van Dorpe ◽  
L. Hofland ◽  
R. Bouillon
Keyword(s):  
Growth Hormone ◽  
Carcinoid Tumor ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone

Hormonal changes in gilts receiving bromocriptine orally during gestation

2000 ◽  
Vol 80 (2) ◽  
pp. 373-376 ◽  
Author(s):  
S. Horth ◽  
C. Farmer
Keyword(s):  
Growth Hormone ◽  
Key Words ◽  
Initial Treatment ◽  
Term Treatment ◽  
Hormonal Changes ◽  
Long Term Treatment ◽  
Blood Profiles

Pregnant gilts received a placebo (CTL; n = 7) or 10 mg of bromocriptine orally (Bromo; n = 7) thrice daily from days 70 to 107 of gestation. Blood profiles of prolactin (PRL), growth hormone (GH) and cortisol were obtained on day 70, after the first treatment with bromocriptine, and on day 107 of gestation. On day 70, concentrations of PRL, GH and cortisol were not affected (P > 0.1) by bromocriptine. By day 107, bromocriptine decreased concentrations of PRL (P < 0.01) whereas concentrations of GH and cortisol were not affected (P > 0.1). Results indicate that long-term treatment with bromocriptine inhibits PRL secretion without affecting GH and cortisol concentrations, while no changes are present within 8 h of initial treatment. Key words: Gilt, gestation, bromocriptine, prolactin

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