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Long‐term oral administration of glucosamine or chondroitin sulfate reduces destruction of cartilage and up‐regulation of MMP‐3 mRNA in a model of spontaneous osteoarthritis in Hartley guinea pigs
Author(s) -
Taniguchi Shin,
Ryu Junnosuke,
Seki Masayuki,
Sumino Takanobu,
Tokuhashi Yasuaki,
Esumi Mariko
Publication year - 2012
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.22003
Subject(s) - glucosamine , osteoarthritis , chondroitin sulfate , cartilage , aggrecan , messenger rna , guinea pig , type ii collagen , chondrocyte , chemistry , endocrinology , medicine , immunology , glycosaminoglycan , biochemistry , pathology , articular cartilage , anatomy , gene , alternative medicine
Histological and molecular changes were examined to investigate the effects of long‐term administration of glucosamine (GlcN) and chondroitin sulfate (CS) in a model of spontaneous osteoarthritis (OA) in Hartley guinea pigs. Three groups of female 3‐week‐old Hartley guinea pigs received GlcN, CS, and neither agent, respectively. Five animals in each group were sacrificed at 8, 12, and 18 months of age. At 8 months of age, Hartley guinea pigs had severe degeneration of knee joint cartilage, chondrocyte apoptosis, marked reduction of tissue total RNA, decreases of aggrecan and collagen type 2 mRNAs, and increases in MMP‐3 and MMP‐8 mRNAs. Long‐term administration of GlcN and CS reduced cartilage degeneration at 8 months of age. The marked loss of total RNA and the increase in MMP‐3 mRNA were also inhibited by GlcN and CS. Thus, long‐term oral administration of GlcN or CS inhibits OA progression, maintains total RNA and down‐regulates MMP‐3 mRNA in a spontaneous OA model in Hartley guinea pigs. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:673–678, 2012