Abstract
Evaluate the effect of the extract of Ginkgo biloba in the bone alkaline phosphatase, bone mineral density, in the mechanical properties of the tibia in rats with glucocorticoid-induced-osteoporosis. After osteoporosis induction, the rats were divided into five groups: Osteoporosis; EGb1 (28 mg/Kg); EGb2 (56 mg/Kg); alendronate (0.2 mg/animal) and control. The animals were treated during 20 and 30 days. The control group was compared with the osteoporosis's (Student's t-test), while the other were analyzed by ANOVA test followed by Tukey/Dunnett'T3 (p<0.05). In the osteoporosis group the bone alkaline phosphatase, bone mineral density, the bone stiffness, the maximum load and the resilience were reduced. The bone alkaline phosphatase values increased in the EGb1 and EGb2 groups (30 days). In addition, in the EGb2 and alendronate groups (20 and 30 days) the bone mineral density increased. The extract of Ginkgo biloba restored bone alkaline phosphatase and bone mineral density using dual-energy x-ray absorptiometry.
Highlights
The low bone mass is associated with genetic, nutritional and lifestyle factors, as well as estrogen levels and the use of some drugs (Johnell 1996)
A few pre-clinical studies have been conducted to evaluate the effects of EGb in osteoporosis; the majority of them, employed as a model for osteoporosis induction, ovariectomized rats
The values of bone alkaline phosphatase (BAP) in the present study were significantly reduced in the osteoporosis group and in the EGb1, EGb2 groups the levels of BAP increased significantly
Summary
The low bone mass is associated with genetic, nutritional and lifestyle factors, as well as estrogen levels and the use of some drugs (Johnell 1996). Among these drugs, glucocorticoids have potent anti-inflamatory effects and were used for decades in the treatment of chronic diseases, as well as in prophylaxis or treatment (Cruse et al 2006, Feldstein et al 2005). The Bcl-2 gene family encodes a large number of proteins, including Bax, a pro-apoptotic protein member of the Bcl-2 gene family that participates in programmed cell death (Verborgt et al 2002)
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