阿托伐他汀钙对糖尿病骨质疏松大鼠骨代谢的影响

Effect of atorvastatin calcium on bone metabolism in diabetic rats with osteoporosis

目的观察糖尿病大鼠应用他汀类药物阿托伐他汀钙(商品名立普妥Lipitor)治疗后骨组织形态学改变以及血中Ⅰ型胶原氨基端肽(PINP)水平变化,为骨质疏松的防治提供依据。方法3月龄雄性SD大鼠30只,单纯随机分为糖尿病组(D)、立普妥治疗组(L),空白对照组(C),每组10只。D组和L组大鼠经鼠尾静脉注射链尿佐菌素造成糖尿病大鼠模型,C组大鼠注射生理盐水。L组大鼠予立普妥灌胃。9周及14周分别处死大鼠,取骨与血行骨组织形态计量法分析及应用放免方法检测PINP水平。结果9周末,D组和L组光镜下见骨质疏松表现,PINP水平:C组(63±7)μg/L,D组(67±3)μg/L,L组(100±11)μg/L,D组和C组无差异,L组明显增高(P<0.05)。14周末D组仍见骨质疏松征象,而L组微观结构较9周末明显改善;PINP水平:C组(60±11)μg/L,D组(62±8)μg/L,L组(92±6)μg/L,D组与C组无差异,L组显著增高(P<0.01)。结论立普妥可以促进糖尿病大鼠骨质的形成,抑制糖尿病大鼠骨质疏松的发生发展。

Aim To observe the effects of atorvastatin calcium(Lipitor) on bone tis sue morphology and the level of PINP as the basis of the prevention for osteopor osisbone in diabetic rats. Methods Thirty male SD rats, aged 3 months, were rand omly divided into three groups of 10 rats: diabetic group(DG) without treatment, Lipitor treatment group (LG) injected with Lipitor and control group(CG) inject ed with normal saline. Except 10 rats in the control group, the other 20 rats we re injected with streptozotocin via caudal vein of rats to establish the diabeti c rat models. Four and six rats were killed at the end of 9 and 14 weeks respect ively in each group, and lumbar spine was taken out for morphological analysis, and blood was taken out for detection of the propeptide of procollagen(PINP ) wi th radioimmunoassay. Results After 9 weeks, osteoporosis was found in DG and LG. The levels of PINP were (63±7)μg/L in CG,(67±3)μg/L in DG and (100±11)μg /L in the LG respectively, with no significant difference between the DG and CG and with a significant increase in the LP (P< 0.05). After 14 weeks, osteoporosi s was also found in the DG and LG and the microstructure of LG improved signific antly, compared with that at the end of 9 weeks. The levels of PINP were (60±11 )μg/L, (62±8)μg/L and (92±6)μg/L in the three groups respectively after 14 weeks,with no difference between the CG and DG and with a significant increase in the LP(P< 0.01). Conclusion Lipitor improves the bone matrix formation in dia betic rats, and inhibits the occurrence and development of osteoporosis in diabe tic rats.