| Literature DB >> 33582913 |
Guang-Tao Han1, Wei-Song Cai1, Yu-Biao Zhang1, Si-Qi Zhou1, Bin He1, Hao-Huan Li2.
Abstract
Osteoarthritis (OA) is a degenerative disease characterized by matrix degradation and cell death leading to a gradual loss of articular cartilage integrity. As a bacterial synthesis of quinine, pyrroloquinoline quinone (PQQ) is a strong redox cofactor with a variety of biological benefits, including antioxidant, anti-inflammation-induced mitochondrial metabolism regulation. This study was designed to investigate the effect of PQQ on TNF-α-induced mitochondrial damage in chondrocytes. Chondrocytes isolated from C57BL/6 mice were exposed to TNF-α 50 ng/mL, TNF-α 50 ng/mL + PQQ 10 µmol/L for 24 h. Then, morphological study, functional study and mechanism study were taken. The results revealed TNF-α-induced chondrocyte mitochondrion damage could be reduced by application of PQQ, evidenced by elevated number of mitochondria, well-kept mtDNA integrity, preserved ATP level, reestablished mitochondrial membrane potential, and prevented mitochondrial function. The present work strongly suggests that the mitochondrion is an important target for OA chondrocyte damage induced by TNF-α and the PQQ protection from this damage ameliorates mitochondrial dysfunction induced by TNF-α. PQQ might be a potential chemical for OA intervention.Entities:
Keywords: TNF-α; chondrocyte; mitochondrial injury; osteoarthritis; pyrroloquinoline quinone
Year: 2021 PMID: 33582913 DOI: 10.1007/s11596-020-2248-3
Source DB: PubMed Journal: Curr Med Sci ISSN: 2523-899X