Background and Aims: It has been suggested that thyrotropin-releasing hormone (TRH) may have functions beyond its fundamental regulating function. Previous studies have demonstrated that TRH promotes wound healing. We aimed to perform an in vitro study in fibroblasts to assess the role of TRH in wounds that frequently occur in diabetes. Thus, we investigated the effects of TRH in wound healing both under normoglycemic and hyperglycemic-conditions. Methods: L929 mouse fibroblast cell line was used in the experiments. The cell viability was confirmed with XTT. Then the scratch migration assay was used for assessing the wound healing. TRH was added to both control and hyperglycemia groups at 100 nM after the scratch was created. The wound areas were measured after 24 and 48 hours after the scratch. Results: TRH and/or hyperglycemia did not affect the cellular activity after 48 hours. TRH reduced the wound areas (42.6%) compared to the control (52.2%) after 24 hours. In the hyperglycemia group the wound area was 64.3% and 61.0% of initial area at the 24 th and 48 th hours respectively. TRH incubation reduced these wound areas to 55.2% and 47.1% of initial areas. Conclusion: TRH treatment accelerated wound healing in hyperglycemia, which indicates the positive effects of TRH in wounds, may occur in diabetes.
The cardiopulmonary diseases are very common in the population. They are high-cost diseases and there are still no definitive treatments. The roles of members of the calcitonin-gene-related peptide (CGRP) family in the cardiopulmonary diseases have been studied for many years and promising results are obtained. Especially in recent years, two important members of the family, adrenomedullin and adrenomedullin2/intermedin, are considered as new treatment targets in cardiopulmonary diseases. In this review, the roles of CGRP family peptides in cardiopulmonary diseases has been investigated according to the studies that were performed to the present day.
How to cite this article: Telli G, Tel BC, Büyükafşar K, Gümüşel B. Effects of GPER-1 receptor activation on the reactivity of pulmonary vascular bed and its possible protective role on ischemia /reperfusion injury. Marmara Pharm J. ABSTRACT: Estrogens have remarkable roles in various diseases and physiological events. The recent studies indicate that estrogens exhibit rapid effects such as calcium influx or release of nitric oxide via receptors on the cell membrane or on endoplasmic reticulum. This receptor is called GPER-1 (G protein-coupled estrogen receptor-1). In many previous studies, acute administration of GPER-1 selective agonist G1 reduced ischemia/reperfusion (I/R) injury in heart. In this study, the effect of G1 on the pulmonary vascular bed was investigated using isolated organ bath and isolated lung perfusion. The effect of pre-ischemic acute G1 treatment on lung I/R injury was assessed with post-I/R acetylcholine (ACh) or sodium nitroprusside (SNP) administration. Lungs wet/dry weight ratios were measured to determine the role of acute G1 administration on lung edema due to I/R injury. G1 was not cause a vasorelaxation in precontracted pulmonary arteries. The acute G1 pre-administration was increased the responses of ACh and SNP in I/R injury, however this increase was not statistically significant compared to control. There was no change on lung wet/dry weight ratio between the treatment and control groups. The vasorelaxation responses to ACh and SNP were not different between male and female rats. In our study, G1 caused a slight vasorelaxation in pulmonary vascular bed. There was no significant increase in the vasorelaxations with G1 treatment after I/R injury. Our results suggest that considering the presence of GPER-1 in lung tissue, GPER-1 should be evaluated in detail with further studies.
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