Abstract
Objective To explore bone formation markers in dexamethasone intervention osteocalcin (OC), bone alkaline phosphatase (BAKP), and type I original amino terminal propeptide (PINP) relationship with bone longitudinal growth. Methods The selected thirty-three 4-week-old male Sprague-Dawley (SD) rats were randomly divided into two groups: the dexamethasone group (n=18) and the control group (n=15). The rats in the dexamethasone group received dexamethasone (200 μg/100 g) by intraperitoneal injection for 10 days. The rats in the control group received matching volume sodium chloride solution. All rats were weighed everyday. The rats were killed by using 10% chloral hydration at 8 AM of 11th day. The length of tibiae was measured. The proximal tibiae were excised, fixed and decaleified. After paraffin embedded, sections in 5 μm thick were cut. The growth plate sections were stained by haematoxylin-eosin (HE) histochemistry method. Total height of growth plate was measured. The rats decaptitating and the blood were collected. Serum was separated and stored in -80 ℃ refrigerator for analysis. Enzyme-linked immuno sorbent assay (ELISA) method was used to detect the rat OC, BAKP and PINP values. Results The length of growth plate and tibiae of dexamethasone group were significantly decreased contrast the control group: the length of growth plate (P=0.001), and the length of tibiae (P=0.000). There were no significant differences between two groups of the value of OC, BAKP and PINP: OC (P=0.056), BAKP (P=0.122), and PINP (P=0.169). There was positive correlation between the serum OC and the length of tibiae (r=0.454, P=0.08) in control group, the PINP and OC (r=0.521, P=0.026) in dexamethasone group. Conclusions Glucocorticoid inhibit the longitudinal bone growth, to the osteoblasts (OC, BAKP and PINP) of growing rats is not obvious. Key words: Glucocorticoids/PD; Dexamethasone/PD; Osteocalcin; Alkaline phosphatase; Collagen type I; Skeleton; Growth and development
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