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Teneligliptin inhibits IL‐1β‐induced degradation of extracellular matrix in human chondrocytes
Author(s) -
Gao Feng,
Wang Yanbing,
Wu Minfei
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29662
Subject(s) - matrix metalloproteinase , tumor necrosis factor alpha , extracellular matrix , microbiology and biotechnology , chemistry , pharmacology , cancer research , p38 mitogen activated protein kinases , kinase , interleukin , protein kinase a , medicine , immunology , cytokine , biochemistry , biology
The mechanisms driving the pathologic progression of osteoarthritis (OA) have not yet to be fully elucidated. Excessive and irreversible breakdown of the extracellular matrix is the main hallmark of OA. Inhibitors of DPP‐4 have been widely used for over a decade as a treatment for type‐2 diabetes, but the promising function of DPP‐4 inhibitors in chronic inflammatory diseases has only begun to receive attention. Here, we treated human chondrocytes with interleukin‐1β (IL‐1β) with or without teneligliptin to assess the role of DPP‐4 in the enzyme‐driven reduction of type II collagen. Treatment with teneligliptin significantly reduced IL‐1β‐induced expression of tumor necrosis factor α, IL‐6, and IL‐8, generation of reactive oxygen species, increase in metalloproteinase 3 (MMP‐3) and MMP‐13, reduction of tissue inhibitors of matrix metalloproteinase 1 (TIMP‐1) and TIMP‐2, release of lactate dehydrogenase, and activation of the mitogen‐activated protein kinase p38 and nuclear factor κB intracellular signaling pathways, among other things. These findings demonstrate that treatment with teneligliptin may act as a novel therapy to slow or halt disease progression in patients with OA.