ABSTRACT
OBJECTIVE: Prednisolone-induced osteoporosis model using zebrafish was used to evaluate the antiosteoporotic activity of micro amount icariin and epimedin B. METHODS: Zebrafish larvae were co-exposed with 25 μmol·L-1 prednisolone and a series of icariin and epimedin B solutions with a range of concentration (0.2, 1, 5 and 10 μmol·L-1) from 4 to 9 days post fertilization(dpf), 25 μmol·L-1 prednisolone was selected as model group, 15 μg·mL-1 etidronate disodium with 25 μmol·L-1 prednisolone as positive group, 0.5% DMSO as the vehicle control group, the medium as a negative blank control group, all groups were incubated in 24-well plates (28.5°C) until 9 dpf. The medium/solution was changed half every day. Zebrafish skeleton at 9 dpf were anesthetized and fixed for staining with alizarin red. Quantitative analysis of the stained area was performed by microscopic inspection and digital imaging methods to reflect the amount of zebrafish head skeleton mineralization. RESULTS: The results indicated head skeleton mineral aera and integrated optical density (IOD) of 25 μmol·L-1 prednisolone model group were significantly decreased when compared with vehicle control group and negative control group; and 15 μg·mL-1 etidronate disodium can increase the mineralized matrix of zebrafish head skeleton when compared with model group and prevent osteoporosis induced by prednisolone; head skeleton mineral area and IOD of 10 and 5 μmol·L-1 icariin groups and 1μmol·L-1 epimedin B groups were significantly increased when compared with model group, which indicated that icariin and epimedin B can prevent zebrafish osteoporosis induced by prednisolone. CONCLUSION: This novel osteoporosis model using zebrafish has advantages of simple, high efficiency, far less amount of compound needed and easy to perform, and it was successfully applied in quickly evaluating the antiosteoporosis activity of micro amount compounds such as icariin and epimedin B.
ABSTRACT
OBJECTIVE: To evaluate the effects of etidronate disodium on bone and soft tissue, especially on bone mineral density, and mucosal changes of the aorta and esophagus. METHOD: Male Sprague-Dawley rats were randomly divided into 2 separate groups: one with etidronate disodium and one without etidronate disodium. Bone mineral density (BMD) in lumbar vertebrae, femur, and a simple X-ray of the whole body were obtained. The abdominal aorta and esophagus were assessed histopathologically in post treatment. RESULTS: In post treatment for 12 weeks, the extent of decrease in BMD of the group with etidronate disodium was less than that of the group without etidronate disodium (p<0.05). There was no evidence of aorta and heart valve calcification in the simple X-ray, nor was there intima-media thickening, atheroma formation and calcification in aorta and esophageal irritation findings in pathologic examinations in both groups. CONCLUSION: The results suggested that etidronate disodium had an inhibitory effect on bone mineral loss and had the esophageal tolerability and safety, but no difference in aorta calcification and antiarthrogenic effects, including aorta wall thickness in this study.
Subject(s)
Humans , Male , Aorta , Aorta, Abdominal , Bone Density , Esophagus , Etidronic Acid , Femur , Heart Valves , Lumbar Vertebrae , Plaque, Atherosclerotic , Rats, Sprague-DawleyABSTRACT
Heterotopic ossification(HO) is a formation of ectopic bone around joints in the soft tissues. It often occurs after the central nervous system injuries, burns, and joint replacements. It causes an important morbidity in the rehabilitation population. The etiology, pathogenesis, prophylaxis, and treatment of HO are still unclear even though there have been many investigation on the prevention of HO among the patients with spinal cord injury. The prevention effect of EHDP on HO formation still remains controversial. A randomized clinical trial was performed to assess the prevention effect of EHDP on HO formation in 73 patients (control group: 40 cases, study group: 33 cases) as a prospective study. EHDP was given to the study group for 12 weeks; 20 mg /kg /day for 2 weeks followed by 10 mg/kg/day for 10 weeks. The patients were followed up with the serial physical examinations, serum alkaline phosphatase levels, and plane radiographs for one year period after the injury. The results revealed that HO developed in eight cases(20.0%) among the control group and two cases(9.1%) among the study group. There was no significant difference in the incidence of HO between two groups(p>0.05). The mean duration from the injury to the detection of HO was 113 days. Twelve of 15 HO sites(80.0%) were detected within the 6 months after injury. Seven patients developed the HO in one site, two in two sites, and one in three sites. The sites of HO were 6 in hips, 4 in knees, 2 in shoulders, 2 in pelvis, and one in elbow. The results of this study do not support the prevention effect of EHDP on HO formation among the patients with spinal cord injury.
Subject(s)
Humans , Alkaline Phosphatase , Burns , Central Nervous System , Elbow , Etidronic Acid , Hip , Incidence , Joints , Knee , Ossification, Heterotopic , Pelvis , Physical Examination , Prospective Studies , Rehabilitation , Shoulder , Spinal Cord Injuries , Spinal CordABSTRACT
Objective To evaluate the clinical efficacy of domestic bisphosphonates (etidronate and alendronate) in the treatment of postmenopausal osteoporosis. Methods Eighty three patients with postmenopausal osteoporosis were divided randomly into three groups: group Ⅰ(37 cases),group Ⅱ(15 cases) and group Ⅲ(31 cases). Etidronate(400 mg/d) and placebo were given with intermittent cyclical therapy in group Ⅰ and group Ⅲ respectively, and alendronate(10 mg/d) was given continuously in groupⅡ for 9 months. Eeach group was given calcium agents(equal to elementary calcium 500 mg/d). Before and after treatment, the bone mineral density(BMD) was measured by dual energy X ray absorptiometry. The biochemical markers such as blood calcium, phosphate, alkaline phosphatase and urine calcium/creatinin were examined. Results After treatment the BMD of groupⅠ and groupⅡ wee increased obviously(P0.05). The BMD of group Ⅱ was increased more than that of groupⅠ(P