
Infrapatellar fat pads participate in the development of knee osteoarthritis in obese patients via the activation of the NF‑κB signaling pathway
Author(s) -
Lijun Duan,
Yuan Ma,
Yonggui Wang,
Jijun Liu,
Zeen Tan,
Qi Wu,
Yi-Feng Wu,
Xing Yu
Publication year - 2020
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2020.4739
Subject(s) - adipokine , medicine , osteoarthritis , leptin , tumor necrosis factor alpha , interleukin 6 , proinflammatory cytokine , western blot , immunohistochemistry , cytokine , endocrinology , body mass index , inflammation , obesity , pathology , biology , alternative medicine , biochemistry , gene
The aim of the present study was to assess the activation of nuclear factor‑κB (NF‑κB) in the infrapatellar fat pads (IPFPs) of obese patients with knee osteoarthritis (KOA). For this purpose, 32 patients (22 obese patients with KOA and 10 patients with KOA with a healthy weight) treated with total knee arthroplasty (TKA) were selected. The expression levels of pro‑inflammatory cytokines and adipocytokines, and the activation of NF‑κB were detected in both the cases and controls by enzyme‑linked immunosorbent assay (ELISA), western blot analysis and immunohistochemistry where appropriate. SPSS 18.0 software was used for statistical analysis to determine the correlation between obesity and the detected cytokine levels. It was found that in patients with KOA, the expression of leptin in the synovial fluid positively correlated with body mass index (BMI; P<0.05), and the expression of interleukin (IL)‑6 in serum significantly correlated with the IL‑1β, leptin and tumor necrosis factor (TNF)‑α levels (P<0.05). Furthermore, the expression of inflammatory cytokines and adipocytokines in IPFPs differed significantly between the obese and non‑obese patients with KOA (P<0.05). By evaluating the expression of IKKβ and IκBα and the nuclear translocation ability of p‑p65, it was concluded that NF‑κB signaling was activated to a higher degree in the IPFP tissues of obese patients with KOA than in those of patients with KOA with a healthy weight. On the whole, the findings of the present study suggested that the NF‑κB signaling pathway was activated and that there were changes in the expression in levels of inflammatory cytokines and adipocytokines in the IPFP tissues of obese patients with KOA.