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水飞蓟宾在治疗链脲佐菌素诱导的大鼠糖尿病性骨质疏松症中的保护作用。

The protective effects of silibinin in the treatment of streptozotocin-induced diabetic osteoporosis in rats.

机构信息

Department of Orthopaedic Surgery, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325000, China.

Department of Endocrinology, Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine, Wenzhou 325000, China.

出版信息

Biomed Pharmacother. 2017 May;89:681-688. doi: 10.1016/j.biopha.2017.02.018. Epub 2017 Mar 6.

DOI:10.1016/j.biopha.2017.02.018
PMID:28273632
Abstract

Diabetic osteoporosis (DO) is a complication of diabetes mellitus. Our previous study showed that silibinin can attenuate high glucose mediated human bone marrow stem cells dysfunction through antioxidant effect. However, no study has yet investigated the effect of silibinin in diabetic rats. Therefore, we assessed the effects of silibinin on bone characteristics in streptozotocin-induced diabetic rats. The aim of our study was to determine whether providing silibinin in the different supplementation could prevent bone loss in diabetic rats or not. Rats were randomly divided into four groups: (1) control group (CG) (n=10); (2) diabetic group (DG) (n=10); (3) diabetic group with 50mgkgday of silibinin orally (DG-50) (n=10); and (4) diabetic group with 100mgkgday of silibinin orally (DG-100) (n=10). 12 weeks after streptozotocin (STZ) injection, the femora from all rats were assessed and oxidative stress was evaluated. Bone mineral density was significantly decreased in diabetic rats; these effects were prevented by treatment with silibinin (100mgkgday orally). Similarly, in the DG and DG-50 groups, changes in microarchitecture of femoral metaphysis assessed by microcomputed tomography demonstrated simultaneous existence of diabetic osteoporosis; these impairments were prevented by silibinin (100mgkgday orally). In conclusion, silibinin supplementation may have potential use as a possible therapy for maintaining skeletal health and these results can enhance the understanding of diabetic osteoporosis induced by diabetes.

摘要

糖尿病性骨质疏松症(DO)是糖尿病的一种并发症。我们之前的研究表明,水飞蓟素可以通过抗氧化作用来减轻高葡萄糖介导的人骨髓基质细胞功能障碍。然而,目前还没有研究调查水飞蓟素对糖尿病大鼠的影响。因此,我们评估了水飞蓟素对链脲佐菌素诱导的糖尿病大鼠骨特征的影响。我们的研究目的是确定在不同补充剂中提供水飞蓟素是否可以防止糖尿病大鼠的骨丢失。大鼠被随机分为四组:(1)对照组(CG)(n=10);(2)糖尿病组(DG)(n=10);(3)糖尿病组每天口服 50mg/kg 水飞蓟素(DG-50)(n=10);和(4)糖尿病组每天口服 100mg/kg 水飞蓟素(DG-100)(n=10)。链脲佐菌素(STZ)注射 12 周后,评估所有大鼠的股骨并评估氧化应激。糖尿病大鼠的骨密度明显降低;水飞蓟素(100mg/kg 每天口服)治疗可预防这些影响。同样,在 DG 和 DG-50 组中,通过微计算机断层扫描评估的股骨干骺端微结构变化表明同时存在糖尿病性骨质疏松症;水飞蓟素(100mg/kg 每天口服)可预防这些损伤。总之,水飞蓟素补充剂可能具有作为维持骨骼健康的潜在治疗方法的用途,这些结果可以增强对糖尿病引起的糖尿病性骨质疏松症的理解。

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