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Effects of oral glucosamine hydrochloride and mucopolysaccharide protein in a rabbit model of osteoarthritis

Authors
홍일화Jeong, DH (Jeong, Da-Hee)Ullah, HMA (Ullah, H. M. ArifGoo, MJ (Goo, Moon-Jung)Ghim, SG (Ghim, Soong-Gu)Kim, AY (Kim, Ah-Young)Jeon, SM (Jeon, Sun-Min)Choi, MS (Choi, Myung-Sook)Elfadl, AK (Elfadl, Ahmed K.)Chung, MJ (Chung, Myung-Jin)Lee, EJ (Lee, Eun-Joo)Kim, YD (Kim, Yong D.)Kim, JH (Kim, Jun-Hyung)Kim, SY (Kim, Shin-Yoon)Jeong, KS (Jeong, Kyu-Shik)..
Issue Date
Mar-2018
Publisher
WILEY
Citation
INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, v.21, no.3, pp 620 - 628
Pages
9
Indexed
SCIE
SCOPUS
Journal Title
INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES
Volume
21
Number
3
Start Page
620
End Page
628
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/11829
ISSN
1756-1841
1756-185X
Abstract
AimThe aim was to study whether oral glucosamine hydrochloride (GlcN.HCl) or mucopolysaccharide protein (MucoP) has a structure-modifying effect on an anterior cruciate ligament transection (ACLT) rabbit model of osteoarthritis (OA). MethodsOA was surgically induced in the right knees of rabbits by transection of the ACLT. The left knees served as a sham-operated control. The animals were divided into four groups (n = 6 each): negative control (phosphate buffered saline, orally), positive control (oral celecoxib 10 mg/kg body weight/day), GlcN.HCl (oral 100 mg/kg/day) and MucoP (oral 100 mg/kg/day). Experimental animals were sacrificed after 8 weeks of treatment and the distal femur was removed for macroscopic examination, histological assessment, and terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) assay of the OA rabbits. ResultsOn gross morphology, severe lesions were observed in articular cartilage in the negative control group. In the GlcN.HCl and MucoP treatment groups, fibrillations and cartilaginous lesions were significantly (P < 0.05) decreased compared to the negative control group. In particular, degenerative changes in cartilage and chondrocyte cellularity were significantly reduced (P < 0.05) in the positive control (celecoxib) group, GlcN.HCl treatment group and MucoP treatment group compared with the negative control group. TUNEL assay showed that apoptotic chondrocytes were significantly suppressed in the celecoxib group. Similar significant (P < 0.05) results were seen in the GlcN.HCl group and MucoP group but apoptosis of chondrocytes were high in the negative control group. ConclusionThese data suggest that the protective effects of GlcN.HCl and MucoP may play a useful role in the clinical treatment of OA.
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