Abstract

ing to the superoxide group. Our own previous studies have shown that P. sarmentosum has the ability to inhibit the 11-β-hydroxysteroid dehydrogenase (11-βHSD) enzyme, an enzyme important in the synthesis of cortisol. Based on this and also its antioxidant property, we hypothesize that P. sarmentosum will be able to prevent osteoporosis in a rat model of excess glucocorticoids. Forty male Sprague–Dawley rats, aged 3 months and weighing between 200 and 250 g were used. Twenty-four animals were adrenalectomized and replaced with intramuscular dexamethasone 120 μg/kg/day. They were simultaneously given either P. sarmentosum 0.125 g/kg/day, glycyrrhizic acid (GCA) 240 μg/kg/day or vehicle distilled water (adrx-control group) daily by oral gavage. A group of eight animals were sham-operated and given vehicle daily, i.e. intramuscular olive and oral distilled water. The treatment was given for 8 weeks. The group given GCA was used as a comparison since GCA had been proven to inhibit 11-βHSD enzyme, therefore reducing serum cortisol levels. A baseline control group was used to determine whether any significant stress was induced in the sham-control group. The results after eight weeks showed increased serum cortisol levels in the adrx-control group compared to the sham-control group. However, in the groups treated with P. sarmentosum and GCA, the serum cortisol levels were maintained at sham-control levels. Plasma pyridinoline (bone resorption marker) levels were lower in the P. sarmentosum and GCA groups compared to the adrx-control group. No difference in serum osteocalcin levels were detected between all the groups. In conclusion, the results showed that P. sarmentosum was as effective as GCA in preventing the increased cortisol levels seen in adrenalectomised rats treated with dexamethasone. This was associated with reduced bone resorption activity. Therefore, this suggests that P. sarmentosum is potentially useful in prevention of osteoporosis induced by long-term glucocorticoid therapy.

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