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

被引：34
作者：
Rivoira, M. [1 ]
Rodriguez, V. [1 ]
Picotto, G. [1 ]
Battaglino, R. [2 ]
Tolosa de Talamoni, N. [1 ]
机构：
[1] Univ Nacl Cordoba, CONICET, Fac Ciencias Med, Lab Dr Canas,Catedra Bioquim & Biol Mol,INICSA, Cordoba, Argentina
[2] Univ Colorado, Sch Med, Dept Phys Med & Rehabil, Aurora, CO USA
来源：
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 2018年 / 637卷
基金：
美国国家科学基金会;
关键词：
Type; 1; D.m; Naringin; Oxidative stress; Bone mineral density; TRAP(+) cells; Adipocytes; OXIDATIVE STRESS; VITAMIN-D; MECHANISMS; PATHWAY; MICE; OSTEOPOROSIS; STIMULATION; METABOLISM; EXPRESSION; RESORPTION;
D O I：
10.1016/j.abb.2017.12.001
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：56 / 63
页数：8
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