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目的探讨鹿骨多肽对地塞米松诱导的骨质疏松模型大鼠骨微结构的影响。方法以im地塞米松诱导糖皮质激素性骨质疏松(glucocorticoid-induced osteoporosis,GIOP)模型。同时ig不同剂量(250、125、62.5 mg/kg)的鹿骨多肽,连续75 d。检测血清生化指标;采用micro CT方法对胫骨近端骨小梁结构进行三维分析;HE染色观察股骨远端组织病理形态。结果鹿骨多肽可以增加GIOP模型大鼠血清Ca~(2+)、骨钙素(BGP)水平,使血清P3+、碱性磷酸酶(ALP)和甲状旁腺激素(PTH)水平下降。鹿骨多肽虽有降低GIOP模型大鼠血清降钙素(CT)的趋势,但与模型组比较没有统计学意义。GIOP大鼠骨小梁变细,中断、游离端增多,数量减少,间隙增宽,空间结构破坏增加,而鹿骨多肽的干预能明显改善上述骨显微结构指标。结论鹿骨多肽能够抑制地塞米松诱导的钙磷代谢失衡,降低ALP,升高BGP,抑制骨吸收和促进骨形成,并且改善GIOP大鼠病理学改变和显微结构,对骨质疏松大鼠具有保护作用。
Objective To investigate the effect of deer bone polypeptide on the bone microarchitecture induced by dexamethasone in osteoporosis model rats. Methods Im-dexamethasone induced glucocorticoid-induced osteoporosis (GIOP) model. At the same time ig different doses of deer bone polypeptide (250,125,62.5 mg / kg) for 75 days. Serum biochemical parameters were measured. Micro-CT was used to analyze the trabecular structure of the proximal tibia. HE staining was used to observe the histopathology of distal femur. Results Deer bone polypeptide could increase serum levels of Ca2 + and BGP and decrease serum levels of P3 +, ALP and PTH in GIOP model rats. Although deer bone polypeptide decreased the serum calcitonin (CT) in GIOP model rats, it was not statistically significant compared with model group. GIOP rat trabecular bone thinning, interrupted, free end increased, the number decreased, the gap widened, the increase in spatial structure damage, and deer bone polypeptide intervention can significantly improve the above bone microstructure indicators. Conclusion Deer bone polypeptide can inhibit dexamethasone-induced imbalance of calcium and phosphorus metabolism, reduce ALP, increase BGP, inhibit bone resorption and promote bone formation, and improve GIOP pathological changes and microstructure in rats with osteoporosis Protective effects.