Effects of propranolol on the development of glucocorticoid-induced osteoporosis in male rats

Folwarczna, Joanna; Pytlik, Maria; Śliwiński, Leszek; Cegieła, Urszula; Nowińska, Barbara; Rajda, Monika

doi:10.1016/s1734-1140(11)70620-x

Cited by 19 publications

(12 citation statements)

References 36 publications

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“…These results suggest that autophagy, induced by glucocorticoid therapy, was self-protective in the maintenance of BMSCs. A previous study using similar methods established that the bone density, the trabecular bone mass and the capacity to form new bone were reduced in GIOP model rats compared with controls (17). In the current study, the proliferative ability of GIOP-BMSCs was observed to be impaired, suggesting that long-term oral glucocorticoid therapy impairs the functional activity of BMSCs.…”

Section: Discussionsupporting

confidence: 56%

Glucocorticoids induce autophagy in rat bone marrow mesenchymal stem cells

Wang

Fan

Lin

et al. 2014

Molecular Medicine Reports

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Glucocorticoid‑induced osteoporosis (GIOP) is a widespread clinical complication following glucocorticoid therapy. This irreversible damage to bone‑forming and ‑resorbing cells is essential in the pathogenesis of osteoporosis. Autophagy is a physiological process involved in the regulation of cells and their responses to diverse stimuli, however, the role of autophagy in glucocorticoid‑induced damage to bone marrow mesenchymal stem cells (BMSCs) remains unclear. The current study confirmed that glucocorticoid administration impaired the proliferation of BMSCs. Transmission electron microscopy, immunohistochemistry and western blot analysis detected autophagy in vitro and in GIOP model rats (in vivo). With the addition of the autophagy inhibitor 3‑methyladenine, the proliferative ability of BMSCs was further reduced, while the number of apoptotic BMSCs was significantly increased. The data suggests that in response to glucocorticoid administration, induced autophagy aids to maintain proliferation and prevent apoptosis of BMSCs. Thus, it is hypothesized that autophagy may be a novel target in the treatment or prevention of osteoporosis.

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Section: Discussionsupporting

confidence: 56%

Glucocorticoids induce autophagy in rat bone marrow mesenchymal stem cells

Wang

Fan

Lin

et al. 2014

Molecular Medicine Reports

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“…PROP, a non-selective βAR antagonist, blocks activity of both β1 and β2 AR. Although epinephrine is a potent agonist of virtually all AR (Molinoff et al, 1984), in this study we focused only on the role of βAR activity since these receptors are enriched in cardiopulmonary tissues and have a major role in autonomic regulation and innate immune homeostatic balance (Bible et al, 2015;Folwarczna et al, 2011;Hegstrand and Eichelman, 1983;Kolmus et al, 2015;Sato et al, 2010). MIFE, a GR antagonist, has been widely used to antagonize the GR in psychiatric disorders (Howland, 2013) and adrenal hyper-production of cortisol (Morgan and Laufgraben, 2013).…”

Section: Discussionmentioning

confidence: 99%

Adrenergic and glucocorticoid receptor antagonists reduce ozone-induced lung injury and inflammation

Henriquez

Snow

Schladweiler

et al. 2018

Toxicology and Applied Pharmacology

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Recent studies showed that the circulating stress hormones, epinephrine and corticosterone/cortisol, are involved in mediating ozone-induced pulmonary effects through the activation of the sympathetic-adrenal-medullary (SAM) and hypothalamus-pituitary-adrenal (HPA) axes. Hence, we examined the role of adrenergic and glucocorticoid receptor inhibition in ozone-induced pulmonary injury and inflammation. Male 12-week old Wistar-Kyoto rats were pretreated daily for 7days with propranolol (PROP; a non-selective β adrenergic receptor [AR] antagonist, 10mg/kg, i.p.), mifepristone (MIFE; a glucocorticoid receptor [GR] antagonist, 30mg/kg, s.c.), both drugs (PROP+MIFE), or respective vehicles, and then exposed to air or ozone (0.8ppm), 4h/d for 1 or 2 consecutive days while continuing drug treatment. Ozone exposure alone led to increased peak expiratory flow rates and enhanced pause (Penh); with greater increases by day 2. Receptors blockade minimally affected ventilation in either air- or ozone-exposed rats. Ozone exposure alone was also associated with marked increases in pulmonary vascular leakage, macrophage activation, neutrophilic inflammation and lymphopenia. Notably, PROP, MIFE and PROP+MIFE pretreatments significantly reduced ozone-induced pulmonary vascular leakage; whereas PROP or PROP+MIFE reduced neutrophilic inflammation. PROP also reduced ozone-induced increases in bronchoalveolar lavage fluid (BALF) IL-6 and TNF-α proteins and/or lung Il6 and Tnfα mRNA. MIFE and PROP+MIFE pretreatments reduced ozone-induced increases in BALF N-acetyl glucosaminidase activity, and lymphopenia. We conclude that stress hormones released after ozone exposure modulate pulmonary injury and inflammatory effects through AR and GR in a receptor-specific manner. Individuals with pulmonary diseases receiving AR and GR-related therapy might experience changed sensitivity to air pollution.

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“…The mechanical strength of the femoral neck was studied using a compression test. The bone was prepared for measurement by fixing the diaphysis, which was cut at the mid‐length of the femur, in a methacrylate plate . The load was applied to the head of the femur along the long axis of the femur (preload of 1 N, displacement rate of 0.01 mm/s).…”

Section: Methodsmentioning

confidence: 99%

“…The data were analyzed by Bluehill 2 version 2.14 software (Instron). Mechanical properties of the diaphysis of the left femurs were studied using a three-point bending test as previously described [29][30][31][32]. The distance between the points supporting the femur was 16 mm.…”

Section: Bone Mechanical Properties Studiesmentioning

confidence: 99%