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Oxidative stress‐induced apoptosis and matrix loss of chondrocytes is inhibited by eicosapentaenoic acid
Author(s) -
Sakata Shuhei,
Hayashi Shinya,
Fujishiro Takaaki,
Kawakita Kohei,
Kanzaki Noriyuki,
Hashimoto Shingo,
Iwasa Kenjiro,
Chinzei Nobuaki,
Kihara Shinsuke,
Haneda Masahiko,
Ueha Takeshi,
Nishiyama Takayuki,
Kuroda Ryosuke,
Kurosaka Masahiro
Publication year - 2015
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.22767
Subject(s) - chondrocyte , apoptosis , oxidative stress , eicosapentaenoic acid , matrix metalloproteinase , chemistry , poly adp ribose polymerase , microbiology and biotechnology , biochemistry , polyunsaturated fatty acid , biology , fatty acid , polymerase , enzyme , in vitro
Eicosapentaenoic acid (EPA) is an antioxidant and n‐3 polyunsaturated fatty acid that reduces the production of inflammatory cytokines. We evaluated the role of EPA in chondrocyte apoptosis and degeneration. Normal human chondrocytes were treated with EPA and sodium nitroprusside (SNP). Expression of metalloproteinases (MMPs) was detected by real‐time polymerase chain reaction (PCR) and that of apoptosis‐related proteins was detected by western blotting. Chondrocyte apoptosis was detected by flow cytometry. C57BL/6J mice were used for the detection of MMP expression by immunohistochemistry and for investigation of chondrocyte apoptosis. EPA inhibited SNP‐induced chondrocyte apoptosis, caspase 3 and poly(ADP‐ribose) polymerase cleavage, phosphorylation of p38 MAPK and p53, and expression of MMP3 and MMP13. Intra‐articular injection of EPA prevented the progression of osteoarthritis (OA) by inhibiting MMP13 expression and chondrocyte apoptosis. EPA treatment can control oxidative stress‐induced OA progression, and thus may be a new approach for OA therapy. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:???–???, 2015.