Gonadotropin-releasing hormone treatment improves locomotor activity, urinary function and neurofilament protein expression after spinal cord injury in ovariectomized rats

Calderón-Vallejo, Denisse; Quintanar, J. Luis

doi:10.1016/j.neulet.2012.03.052

Cited by 27 publications

(22 citation statements)

References 25 publications

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“…Our results confirm that the administration of LA reduces the severity of clinical signs of locomotion in EAE animals [4], as does GnRH [3]. Experimental work developed in an animal model of spinal cord injury demonstrated that GnRH administration starting 1 day after the lesion significantly improved locomotor activity, achieved micturition reflex control and increased the expression of neurofilaments in rats [27]. Taking all these results together suggests an action of GnRH and its analogs as possible neurotrophic factors.…”

Section: Discussionsupporting

confidence: 78%

Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-κB Activation

Guzmán-Soto

Salinas

2015

Neuroimmunomodulation

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Objective: Recent findings have shown that gonadotropin-releasing hormone (GnRH) administration in an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis, EAE) improves clinical signs of locomotion. The present study was designed to determine whether the administration of the synthetic analog of GnRH, leuprolide acetate (LA) - besides its effects on clinical signs of locomotion - also has an effect on the activation/expression levels of molecular markers of EAE, namely transcription nuclear factor (NF)-κB and the proinflammatory cytokines IL-1ß, IL-17A, IL-23 and TNF-a. Methods: EAE spinal cords were collected from control and LA-administered rats. Lumbar sections were processed at four different time points during the course of the disease to analyze NF-κB activation by chemiluminescent Western blot, and during the EAE recovery phase to evaluate proinflammatory cytokine levels by quantitative real-time PCR. Results: It was found that LA administration to EAE rats promoted a significant reduction of NF-κB activation during the course of the disease and also decreased the mRNA expression levels of the proinflammatory cytokines IL-1ß, IL-17A and TNF-a in the EAE recovery phase; both effects are consistent with the decrease in the severity of clinical signs of locomotion induced by the treatment. Conclusion: LA causes a reduction in the severity of locomotor activity, as well as in the activation of NF-κB and the number of proinflammatory markers in rats with EAE. These results suggest the use of this agonist as a potential therapeutic approach for multiple sclerosis.

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Section: Discussionsupporting

confidence: 78%

Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-κB Activation

Guzmán-Soto

Salinas

2015

Neuroimmunomodulation

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“…These data suggest possible roles of GnRH3 systems on locomotion or movement. Interestingly, studies on spinal cord injury also support locomotor effects of GnRH systems, showing that GnRH treatment to rats with experimentally induced spinal cord injury improves recovery, increases locomotor activity, and decreases histopathological damage in the injured spinal cord of rats (Calderon-Vallejo et al, 2015;Calderon-Vallejo and Quintanar, 2012).…”

Section: Introductionmentioning

confidence: 94%

Low dose exposure to Bisphenol A alters development of gonadotropin-releasing hormone 3 neurons and larval locomotor behavior in Japanese Medaka

et al. 2016

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“…This agonist has been previously used for the same purposes as those mentioned above (7). Furthermore, it has been used as a neurological recovery factor in experimental autoimmune encephalomyelitis and in spinal cord injury (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

“…Studies in humans and experimental models have evidenced that therapeutic application of GnRH or administration of agonists thereof has the secondary effect of increasing body weight (8,9,11). The mechanisms involved in this process remain elusive; however, in the last two decades, different Changes in body composition and mRNA expression of ghrelin and lipoprotein lipase in rats treated with leuprolide acetate, a GnRH agonist approaches have been proposed to elucidate the association between energy balance and adipogenesis with the aim of correlating endocrine and metabolic pathways.…”

Section: Introductionmentioning

confidence: 99%

Changes in body composition and mRNA expression of ghrelin and lipoprotein lipase in rats treated with leuprolide acetate, a GnRH agonist

et al. 2017

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Abstract. Leuprolide acetate (LA), a gonadotropin-releasing hormone (GnRH) agonist, was identified to cause changes in body weight in experimental and clinical trials; however, to date, the effect of LA on the body composition has not been properly assessed. The aim of the present study was to evaluate the long-term effect of LA administration on body composition and the mRNA expression of ghrelin and lipoprotein lipase (LPL) in rats. Ovariectomized (OVX), ovariectomized and LA-treated (OVX+LA), non-ovariectomized (CTRL) and non-ovariectomized but LA-treated (LA) rats were used. LA treatment was performed by intramuscular injection at 5 µg/kg every 72 h over 120 days. Analysis of body composition and mRNA expression of ghrelin and lipoprotein lipase were performed. The results indicated significant changes in body composition after treatment; in the OVX, LA, OVX+LA and CTRL group, the body weight was increased by 216.1, 183.7, 175.4 and 150.1%, respectively, compared with baseline. The fat mass in the LA group was 14% higher than that in the CTRL group, while that in the OVX group was 19% higher than that in the OVX+LA, and the fat-free mass was similar between the LA and CTRL as well as the OVX and OVX+LA groups. Following 120 days of treatment, the mRNA expression of ghrelin and LPL in the LA group was ~20% higher than that in the CTRL group, while that in the OVX+LA was downregulated in comparison with that in the OVX group. The results of the present study confirmed changes in body composition and mRNA expression of ghrelin and LPL caused by long-term administration of LA. LA may contribute to regulate food consumption and exert control over adipogenesis.

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Gonadotropin-releasing hormone treatment improves locomotor activity, urinary function and neurofilament protein expression after spinal cord injury in ovariectomized rats

Cited by 27 publications

References 25 publications

Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-κB Activation

Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-κB Activation

Low dose exposure to Bisphenol A alters development of gonadotropin-releasing hormone 3 neurons and larval locomotor behavior in Japanese Medaka

Changes in body composition and mRNA expression of ghrelin and lipoprotein lipase in rats treated with leuprolide acetate, a GnRH agonist

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Gonadotropin-releasing hormone treatment improves locomotor activity, urinary function and neurofilament protein expression after spinal cord injury in ovariectomized rats

Cited by 27 publications

References 25 publications

Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-&#954;B Activation

Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-&#954;B Activation

Low dose exposure to Bisphenol A alters development of gonadotropin-releasing hormone 3 neurons and larval locomotor behavior in Japanese Medaka

Changes in body composition and mRNA expression of ghrelin and lipoprotein lipase in rats treated with leuprolide acetate, a GnRH agonist

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Resources

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Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-κB Activation

Leuprolide Acetate Inhibits Spinal Cord Inflammatory Response in Experimental Autoimmune Encephalomyelitis by Suppressing NF-κB Activation