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Wpływ flufenazyny i risperidonu na przebudowę kości u szczurów owariektomizowanych

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Pytlik M., Fronczek-Sokół J.
Annales Academiae Medicae Silesiensis
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2012
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vol. 66
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issue 3
34-43
EN
INTRODUC TION Typical neuroleptics (fl uphenazine), and to a less extent atypical neuroleptics (risperidone), can induce osteoporosis because of the increased secretion of prolactin. The available literature lacks experimental results on the effect of neuroleptics on the skeletal system in conditions of estrogen deficiency. The aim of this study was to investigate the effect of fluphenazine and risperidone on bone remodeling in ovariectomized rats. MATERIAL AND METHODS The experiments were conducted on female Wistar rats divided into groups: NOVX – non-ovariectomized control rats, OVX – ovariectomized control rats, OVX+R – ovariectomized rats receiving risperidone (1 mg/kg), OVX+F1 – ovariectomized rats receiving fluphenazine (1 mg/kg), OVX+F5 – ovariectomized rats receiving fluphenazine (5 mg/kg). The tested drugs were administered by a stomach tube (po) once daily for 28 days. Bone remodeling after the use of neuroleptics was assessed based on the bone mass, bone mineral mass, macrometric parameters and histomorphometric parameters. RESULTS Fluphenazine administered at the dose of 5 mg/kg, compared with the results obtained in ovariectomized control rats (OVX), signifi cantly decreased mass of the femur, tibia and L-4 vertebra, as well as periosteal transverse growth and width of periosteal osteoid in the tibial diaphysis and the width of trabeculae in the femoral epiphysis. Fluphenazine in both doses caused statistically signifi cant reduction of the transverse cross-section area of the tibial diaphysis, and decreases in bone mineral mass in the femur, tibia and L-4 vertebra. After risperidone administration no statistically signifi cant differences in the examined bone parameters were observed in comparison to the ovariectomized control rats. CONCLUSIONS Fluphenazine dose dependently augmented the changes in the skeletal system caused by estrogen defi ciency in both cancellous and cortical bone. Risperidone did not intensify changes in the rats bones induced by estrogen deficiency.
PL
WSTĘP Neuroleptyki typowe (flufenazyna) oraz w mniejszym stopniu atypowe (risperidon) na skutek zwiększonego wydzielania prolaktyny mogą powodować rozwój osteoporozy. W dostępnym piśmiennictwie brakuje wyników badań eksperymentalnych dotyczących działania neuroleptyków na układ kostny w warunkach niedoboru estrogenów. Celem pracy było zbadanie wpływu flufenazyny i risperidonu na przebudowę kości u szczurów owariektomizowanych. MATERIAŁ I METODY Badania przeprowadzono na samicach szczurów szczepu Wistar podzielonych na grupy: NOVX – szczury kontrolne nieowariektomizowane; OVX – szczury kontrolne owariektomizowane; OVX+R – szczury owariektomizowane otrzymujące risperidon w dawce 1 mg/kg; OVX+F1 – szczury owariektomizowane otrzymujące flufenazynę w dawce 1 mg/kg; OVX+F5 – szczury owariektomizowane otrzymujące flufenazynę w dawce 5 mg/kg. Leki podawano sondą dożołądkowo (po) raz dziennie przez 28 dni. Przebudowę kości po stosowaniu neuroleptyków oceniano na podstawie masy kości, masy substancji mineralnych oraz parametrów makrometrycznych i histomorfometrycznych. WYNIKI Flufenazyna podawana w dawce 5 mg/kg, w porównaniu z wynikami uzyskanymi w grupie szczurów kontrolnych owariektomizowanych (OVX), spowodowała znaczący statystycznie spadek masy kości udowej, kości piszczelowej i kręgu L-4, a także przyrostu na grubość i szerokości osteoidu od strony okostnej w trzonie kości piszczelowej oraz szerokości beleczek kostnych w nasadzie kości udowej. W obu badanych dawkach flufenazyna wykazała znaczący statystycznie spadek pola powierzchni przekroju poprzecznego trzonu kości piszczelowej, a także masy substancji mineralnych w kości udowej, piszczelowej oraz kręgu L-4. Risperidon u szczurów z niedoborem estrogenów nie wykazał istotnych statystycznie zmian w ocenianych parametrach kości w odniesieniu do grupy kontrolnej owariektomizowanej. WNIOSKI Flufenazyna nasiliła zmiany w układzie kostnym wywołane niedoborem estrogenów w kości o strukturze gąbczastej oraz zbitej w sposób zależny od dawki. Risperidon nie intensyfikował zmian w układzie kostnym szczurów wywołanych niedoborem estrogenów.
2
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Fenoterol did not enhance glucocorticoid-induced skeletal changes in male rats

61%
Folwarczna J., Nowińska B., Śliwiński L., Pytlik M., Cegieła U., Betka A.
Acta Biochimica Polonica
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2011
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vol. 58
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issue 3
313-319
EN
Glucocorticoids and β2-adrenergic receptor agonists are the most commonly used drugs in the treatment of asthma. Both therapies are potentially dangerous to the skeletal system. The aim of the present study was to investigate the effects of fenoterol, a β2-receptor agonist, on the development of bone changes induced by glucocorticoid (prednisolone) administration in mature male rats. The experiments were carried out on 24-week-old male Wistar rats. The effects of prednisolone 21-hemisuccinate sodium salt (7 mg/kg s.c. daily) or/and fenoterol hydrobromide (1.4 mg/kg i.p. daily), administered for 4 weeks, on the skeletal system were studied. Bone turnover markers, geometric parameters, mass, mass of bone mineral in the tibia, femur and L-4 vertebra, bone histomorphometric parameters and mechanical properties of tibial metaphysis, femoral diaphysis and femoral neck were determined. Both prednisolone and fenoterol had damaging effects on the skeletal system of mature male rats. However, concurrent administration of fenoterol and prednisolone did not result in the intensification of the deleterious skeletal effect of either drug administered separately.
3
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Effect of diosgenin, a steroidal sapogenin, on the rat skeletal system

52%
Folwarczna J., Zych M., Nowińska B., Pytlik M., Bialik M., Jagusiak A., Lipecka-Karcz M., Matysiak M.
Acta Biochimica Polonica
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2016
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vol. 63
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issue 2
287-295
EN
Diosgenin is a steroidal sapogenin present in fenugreek and Dioscorea spp. as glycosides (saponins). Diosgenin has already been reported to inhibit osteoclastogenesis and to stimulate osteogenic activity of osteoblastic cells in vitro, and to exert some antiosteoporotic effects in rats in vivo. The aim of the present study was to investigate the effects of diosgenin administration on the skeletal system of rats with normal estrogen level and with estrogen deficiency induced by bilateral ovariectomy. The experiments were carried out on 3-month-old non-ovariectomized and ovariectomized Wistar rats, divided into control rats and rats receiving diosgenin (50 mg/kg p.o. daily) for 4 weeks. Serum bone turnover markers, bone mass and mineralization, histomorphometric parameters and mechanical properties were studied. Diosgenin improved some investigated parameters in both non-ovariectomized and ovariectomized rats, in which estrogen deficiency induced osteoporotic changes. Diosgenin increased compact bone formation and probably inhibited cancellous bone resorption, which led to improvement of mechanical properties of compact and cancellous bone. In conclusion, this in vivo study demonstrated that diosgenin may be one of sparse compounds increasing bone formation.
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A comparative study of the effects of genistein, estradiol and raloxifene on the murine skeletal system

52%
Śliwiński L., Folwarczna J., Nowińska B., Cegieła U., Pytlik M., Kaczmarczyk-Sedlak I., Trzeciak H., Trzeciak H. I.
Acta Biochimica Polonica
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2009
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vol. 56
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issue 2
261-270
EN
Genistein, a major phytoestrogen of soy, is considered a potential drug for prevention and treatment of postmenopausal osteoporosis. The aim of the present study was to compare the effects of genistein, estradiol and raloxifene on the skeletal system in vivo and in vitro. Genistein (5 mg/kg), estradiol (0.1 mg/kg) or raloxifene hydrochloride (5 mg/kg) were administered daily by a stomach tube to mature ovariectomized Wistar rats for 4 weeks. Bone mass, mineral and calcium content, macrometric parameters and mechanical properties were examined. Also the effects of genistein, estradiol and raloxifene (10-9-10-7 M) on the formation of osteoclasts from neonatal mouse bone marrow cells and the activity of osteoblasts isolated from neonatal mouse calvariae were compared. In vivo, estrogen deficiency resulted in the impairment of bone mineralization and bone mechanical properties. Raloxifene but not estradiol or genistein improved bone mineralization. Estradiol fully normalized the bone mechanical properties, whereas genistein augmented the deleterious effect of estrogen-deficiency on bone strength. In vitro, genistein, estradiol and raloxifene inhibited osteoclast formation from mouse bone marrow cells, decreasing the ratio of RANKL mRNA to osteoprotegerin mRNA expression in osteoblasts. Genistein, but not estradiol or raloxifene, decreased the ratio of alkaline phosphatase mRNA to ectonucleotide pyrophosphatase phosphodiesterase 1 mRNA expression in osteoblasts. This difference may explain the lack of genistein effect on bone mineralization observed in ovariectomized rats in the in vivo study. Concluding, our experiments demonstrated profound differences between the activities of genistein, estradiol and raloxifene towards the osseous tissue in experimental conditions.
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