摘要
研究生、制首乌正己烷提取物对维甲酸致小鼠骨质疏松的防治作用,并探讨其主要作用机制。采用维甲酸(105 mg·kg-1)致小鼠骨质疏松模型,生首乌正己烷提取物高、低剂量组48、24 mg·kg-1,清蒸制首乌正己烷提取物高、低剂量组48、24 mg·kg-1,黑豆制何首乌正己烷提取物高、低剂量组48、24 mg·kg-1,灌胃给药,2周后以比色法测定血清钙、磷含量和碱性磷酸酶(ALP)、抗酒石酸酸性磷酸酶(TRAP)活性,竞争放射免疫法测定血清中骨钙素(BGP)和雌二醇(E2)含量,取股骨进行骨组织形态学观察。结果表明:维甲酸可引起高转换型骨质疏松,与模型组比较,生、制首乌各剂量组可显著升高s-E2的水平(P <0. 05),降低s-ALP、s-TRAP和s-BGP的水平(P <0. 05,P <0. 01);生、制首乌各组与模型组比较,骨组织形态均有不同程度的改善,骨小梁数明显增加。从以上结果可知,生、制首乌正己烷提取物对维甲酸致小鼠骨质疏松有明显的治疗作用,其机制可能与减缓雌激素水平降低,抑制骨高转换有关。
We investigated the anti-osteoporosis effect and the possible mechanism of PM-HE( Hexane extract from Raw and Processed Polygonum multiflorum) in animal model. Kunming mice were randomly divided into 9 groups:Control group( normal saline),model group,nilestriol group(2 mg/kg),PM-HE groups(48,24 mg/kg). The mice osteoporosis was induced by given retinoic acid intragastrically. After oral administration for 14 days,the features of bones and biochemicals in serum were determined to evaluate the anti-osteoporosis effects of PM-HE. The results showed:PM-HE can induce high conversion of osteoporosis. The levels of ALP,TRAP and BGP in the PM-HE groups were lower than those in the model group( P < 0. 05,P < 0. 01),whereas the E2 level was higher than that of the model group( P < 0. 05). PMHE can prevent the loss bone in the experimental mice. The mechanism may be the inhibition of estrogen decrease and the high bone turnover.
引文
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