S-allylcysteine inhibits chondrocyte inflammation to reduce human osteoarthritis via targeting RAGE, TLR4, JNK, and Nrf2 signaling: comparison with colchicine

Elmazoglu Z., AYDIN BEK Z., Saribas S. G., Ozogul C., GÖKER B., Bitik B., ...Daha Fazla

BIOCHEMISTRY AND CELL BIOLOGY, cilt.99, sa.5, ss.645-654, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 99 Sayı: 5
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1139/bcb-2021-0004
  • Dergi Adı: BIOCHEMISTRY AND CELL BIOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Agricultural & Environmental Science Database, BIOSIS, Biotechnology Research Abstracts, CAB Abstracts, Chemical Abstracts Core, Compendex, EMBASE, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.645-654
  • Anahtar Kelimeler: osteoarthritis, chondrocytes, S-allylcysteine, colchicine, toll-like receptor-4, redox signaling, inflammation, nuclear factor erythroid 2-related factor 2, oxidative stress, ENDOPLASMIC-RETICULUM STRESS, INDUCED NEURONAL DEATH, KNEE OSTEOARTHRITIS, LIPID-PEROXIDATION, CARTILAGE, MATRIX, PHOSPHORYLATION, DEGRADATION, MANAGEMENT, CYSTEINE
  • Gazi Üniversitesi Adresli: Evet

Özet

The discovery of new pharmacological agents is needed to control the progression of osteoarthritis (OA), characterized by joint cartilage damage. Human OA chondrocyte (OAC) cultures were either applied to S-allylcysteine (SAC), a sulfur-containing amino acid derivative, or colchicine, an ancient anti-inflammatory therapeutic, for 24 h. SAC or colchicine did not change viability at 1 nM-10 mu M but inhibited p-JNK/pan-JNK. While SAC seems to be more effective, both agents inhibited reactive oxygen species (ROS), 3-nitrotyrosine (3-NT), lipid hydroperoxides (LPO), advanced lipoxidation end-products (ALEs as 4-hydroxy-2-nonenal, HNE), advanced glycation end-products (AGEs), and increased glutathione peroxidase (GPx) and type-II-collagen (COL2). IL-1 beta, IL-6, and osteopontin (OPN) were more strongly inhibited by SAC than by colchicine. In contrast, TNF-alpha was inhibited only by SAC, and COX2 was only inhibited by colchicine. Casp-1/ICE, GM-CSF, receptor for advanced glycation end-products (RAGE), and toll-like receptors (TLR4) were inhibited by both agents, but bone morphogenetic protein 7 (BMP7) was partially inhibited by SAC and induced by colchicine. Nuclear factor erythroid 2-related factor 2 (Nrf2) was induced by SAC; in contrast, it was inhibited by colchicine. Although they exert opposite effects on TNF-alpha, COX2, BMP7, andNrf2, SAC and colchicine exhibit anti-osteoarthritic properties in OAC by modulating redox-sensitive inflammatory signaling.