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柚皮苷可预防1型糖尿病大鼠模型中的骨质流失。

Naringin prevents bone loss in a rat model of type 1 Diabetes mellitus.

作者信息

Rivoira M, Rodríguez V, Picotto G, Battaglino R, Tolosa de Talamoni N

机构信息

Laboratorio "Dr. Cañas", Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA (CONICET-Universidad Nacional de Córdoba), Córdoba, Argentina.

Department of Physical Medicine and Rehabilitation, School of Medicine, University of Colorado, Aurora, USA.

出版信息

Arch Biochem Biophys. 2018 Jan 1;637:56-63. doi: 10.1016/j.abb.2017.12.001. Epub 2017 Dec 5.

DOI:10.1016/j.abb.2017.12.001
PMID:29208404
Abstract

The aim of this work was to know whether naringin (NA) could prevent the bone complications in a model of streptozotocin (STZ) induced diabetes. Rats were divided in: 1) controls, 2) STZ-rats, 3) STZ-rats treated with 40 mg NA/kg, and 4) STZ-rats treated with 80 mg NA/kg. BMD and BMC were performed by DEXA. Bone histomorphometry and histology as well as TRAP staining were done in tibia. Osteocalcin (OCN) was determined in bone and serum. Glutathione content and SOD and catalase activities were assayed in bone marrow from femur. The data showed that NA80 increased the BMD and BMC from the long bones of STZ-rats. Both NA40 and NA80 normalized the trabecular number and the trabecular separations. An increase in the number of adipocytes and TRAP(+) cells in tibia from STZ-rats was blocked by NA. NA40 treatment increased the number of OCN(+) cells, but only the NA80 treatment allowed to reach the control values. NA normalized the SOD and catalase activities in bone marrow of femur from STZ-rats. In conclusion, NA avoids alterations in the physical properties and microstructure of bone from STZ-rats probably by stimulation of osteoblastogenesis, inhibition of the osteoclastogenesis and adipogenesis via blocking the oxidative stress.

摘要

这项工作的目的是了解柚皮苷(NA)是否能预防链脲佐菌素(STZ)诱导的糖尿病模型中的骨并发症。大鼠被分为:1)对照组,2)STZ诱导的糖尿病大鼠组,3)用40mg NA/kg治疗的STZ诱导的糖尿病大鼠组,4)用80mg NA/kg治疗的STZ诱导的糖尿病大鼠组。通过双能X线吸收法(DEXA)测量骨密度(BMD)和骨矿含量(BMC)。对胫骨进行骨组织形态计量学、组织学以及抗酒石酸酸性磷酸酶(TRAP)染色。测定骨和血清中的骨钙素(OCN)。检测股骨骨髓中的谷胱甘肽含量以及超氧化物歧化酶(SOD)和过氧化氢酶活性。数据显示,80mg/kg的NA增加了STZ诱导的糖尿病大鼠长骨的BMD和BMC。40mg/kg和80mg/kg的NA均使骨小梁数量和骨小梁间距恢复正常。NA阻止了STZ诱导的糖尿病大鼠胫骨中脂肪细胞和TRAP(+)细胞数量的增加。40mg/kg的NA治疗增加了OCN(+)细胞的数量,但只有80mg/kg的NA治疗使OCN水平达到对照值。NA使STZ诱导的糖尿病大鼠股骨骨髓中的SOD和过氧化氢酶活性恢复正常。总之,NA可能通过刺激成骨细胞生成、抑制破骨细胞生成和脂肪生成以及阻断氧化应激,避免了STZ诱导的糖尿病大鼠骨骼物理性质和微观结构的改变。

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