Abstract
Postmenopausal osteoporosis is a common disorder resulting from increased osteoclastic activity. To determine the effect of Panax ginseng on postmenopausal osteoporosis, ovariectomized (OVX) mice were treated with 500 mg/kg/day P. ginseng extract (Pg) alone or in combination with hot water extract of Brassica oleracea (Bo) daily for 10 weeks, and the effect of the treatments on OVX-induced bone loss was examined. Bone weight, bone mineral density (BMD), osteoclast (OC) formation, OC marker expression, and biochemical parameters in blood were determined. OVX significantly increased body weight and decreased bone weight compared with those in the Sham group (p < 0.01). Pg or Bo alone did not affect OVX-induced bone loss, but a combination of Pg and Bo (Pg:Bo) recovered bone weight. The bones of OVX mice showed lower BMD than that of Sham mice, and the Pg:Bo = 3:1 restored the decreased BMD. Single treatment with Pg or Bo did not alter OC formation; however, the Pg:Bo = 3:1 inhibited OC formation. In addition, Pg and Bo lowered the OVX-induced elevation in blood glucose level. Thus, we suggest that Pg in combination with proper materials, such as Bo, might be a potential candidate treatment with minimal side effects protect against postmenopausal osteoporosis.
Highlights
Osteoporosis (OP) is a disorder characterized by low bone mass and structural deterioration of the bone microarchitecture, and it leads to an increased risk of bone fragility and fracture
Mice in the OVX group were heavier than those in the Sham group, which were lighter than those in the Normal group. These results suggested that OVX surgery affected body weight and that estrogen deficiency caused weight gain
Treatment with Pg500, Bo500, and P. ginseng extract (Pg):Brassica oleracea (Bo) combination showed no effect on body weight; this result is contradictory to the reports that showed a significant recovery of body weight in OVX mice following treatment with P. ginseng
Summary
Osteoporosis (OP) is a disorder characterized by low bone mass and structural deterioration of the bone microarchitecture, and it leads to an increased risk of bone fragility and fracture. Over 75 million people worldwide suffer from OP, of which 80% are postmenopausal women [1], and there is a direct relationship between the lack of estrogen and OP development [2]. The two major causes of bone loss are menopause-induced estrogen deficiency and aging. Postmenopausal OP generally develops when, after menopause, estrogen levels drop precipitously. Senile OP is related to aging and it results from deficiencies in dietary calcium and vitamin D, and increased activity of the parathyroid glands. Calcium and vitamin D are implicated in gynecologic and reproductive conditions [3,4], and improve vasomotor disturbances, quality of life, and sexual function in menopausal women [5]
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